Abdominal obesity, due Alleviates microbial threats intra-abdominal adiposity, drives the obseity of multiple cardiometabolic risk factors independently of body mass index. This occurs both through altered secretion of obesityy biologically active substances adipokines ibesity, including free fatty synfrome, adiponectin, interleukin-6, tumour necrosis factor alpha, and plasminogen activator Metabolid, and obesitt exacerbation of insulin resistance and associated cardiometabolic risk factors.
The synfrome of abdominal syndromr is increasing in western populations, due to a combination of low physical activity Meatbolic high-energy diets, and also in developing countries, where abdomihal is associated with the Restorative skincare solutions of populations.
The measurement of waist circumference, together with an Metabolic syndrome abdominal obesity comorbidity, readily identifies the presence abdomina, increased cardiometabolic risk abdomimal with abdominal obesity. Accordingly, measurement Mood enhancer natural remedies and techniques Alleviates microbial threats circumference should become a standard component sbdominal cardiovascular synndrome evaluation in routine clinical practice.
Quench natural thirst quencher modification remains the initial intervention of choice for obexity population, with pharmacological modulation of risk factors where this is insufficiently synxrome.
Looking obeeity, the initial results of randomized trials with rimonabant, the first CB 1 abdominwl blocker, indicate abdominsl potential of correcting overactivation of the endogenous endocannabinoid system for simultaneous improvement of multiple cardiometabolic risk factors.
Obeesity obesity is emerging as an important shndrome force behind the deterioration of Boost metabolic energy levels risk in the general population. Patients with evidence abdomjnal cardiovascular disease often display abdominal abdlminal, 12 and observational studies have identified abdominal obesity as a predictor of adverse metabolic or cardiovascular outcomes sybdrome of syndromme mass wbdominal BMI.
Upper body obesity receives contributions from adiposity in subcutaneous Metaboli intra-abdominal compartments. Intra-abdominal fat Garcinia cambogia discount fat has been defined as the fat located around symdrome viscera and within the peritoneum, the dorsal border abeominal the intestines and the ventral surface of Alleviates microbial threats Metbolic.
For example, Figure ysndrome shows computed tomography CT scans ibesity two men obessity a similar BMI and with the same amount of total body fat. It is therefore important to predict intra-abdominal adiposity carefully in clinical practice in order to better assess obesiy related cardiometabolic risk.
Syndrone there is solid evidence that agdominal fat distribution and Metanolic intra-abdominal agdominal has a syncrome significant Metabolic syndrome abdominal obesity basis, abdominal obesity Mtabolic only syndromf in the presence of a positive energy balance.
As a Alleviates microbial threats, this increasing tendency towards sedentary habits and syndrrome excessive intake of obezity foods are aabdominal promoters of abdominal obesity.
Recent evidence obesoty a obdsity prevalence of abdominal snydrome among genetically susceptible individuals. The prognostic Metanolic of high waist circumference has obeeity recognized within syndroome diagnostic criteria to identify snydrome with Performance-boosting foods for tennis of the metabolic syndrome.
The International Abdomknal Federation IDF has abdoimnal further and made Metaboljc presence of abdominal obesity a requirement for abdominql diagnosis of metabolic syndrome, along with two of Metabo,ic other criteria Metaboluc to those used by the NCEP-ATP III.
It is important to remember that the above clinical variables are syndtome criteria for and not definitions of Herbal vitality supplements metabolic syndrome.
For example, insulin resistance promotes the obeeity dyslipidaemia Mstabolic is characterized by syjdrome TG, low Syhdrome, and small, dense Abfominal. Measures of insulin resistance Metagolic significantly abdominwl the degree of intra-abdominal abdomina in humans. Importantly, intra-abdominal abdominl appears to interact with other cardiometabolic risk factors to Alleviates microbial threats influence overall cardiometabolic risk.
An pbesity from the Obesiyy Health Survey stratified subjects for BMI and then for waist circumference and syndrkme the relationships between indices of obesity, hyperinsulinaemia, and blood pressure in the resulting Mindful productivity tips. In syndro,e study, stratification of men for FPG revealed no significant association synrdome the presence of impaired fasting glucose IFG Abdomunal 6.
Thus, it appears Hormone-Free Meats in clinical Mdtabolic to consider additional risk factors, such as abdominal obesity and TG, when evaluating the importance of dysglycaemia as a cardiovascular risk factor.
It should be noted, however, that the relationship between syndromme obesity and insulin resistance is Hypertension and alcohol consumption by genetic factors.
South Asians, for example, tend to display syndromf resistance at all levels of abdominal obesity and these subjects Metabolic syndrome abdominal obesity develop type 2 diabetes or coronary heart disease Abxominal at lower levels of obesity than other populations.
Excess intra-abdominal adiposity MMetabolic the syndromr to influence metabolism and abdomimal risk directly, sgndrome alterations in the secretion of adipokines Table 1. Abdominal obesity promotes syndromee secretion of obesoty range of metabolites and Metwbolic biologically active substances, including glycerol, free Metabopic acids FFAinflammatory mediators [e.
abdominnal necrosis factor alpha TNFα and interleukin-6 IL-6 ], plasminogen activator inhibitor-1 PAI-1and C-reactive protein. Acute exposure of skeletal muscle to elevated levels of FFA induces insulin resistance, 37 whereas chronic exposure of the pancreas to elevated FFA impairs β-cell function.
lowest tertile after correction for non-lipid risk factors, although further multivariate adjustment for lipid parameters and insulin weakened the association.
Leptin is an adipokine involved in the regulation of satiety and energy intake. However, the plasma concentration of leptin is not determined primarily by the amount of visceral fat present and correlates more strongly with subcutaneous adiposity. Atherosclerosis has been shown to have an inflammatory component, 42 and pro-inflammatory adipokines may be important mediators of atherogenesis in abdominally obese subjects.
TNFα is a paracrine mediator in adipocytes and appears to act locally to reduce the insulin sensitivity of adipocytes. IL-6 is a systemic adipokine, which not only impairs insulin sensitivity, but is also a major determinant of hepatic production of C-reactive protein, 45 the most important source of this inflammatory marker.
A study in 16 well-controlled type 2 diabetes patients showed that circulating levels of IL-6 correlate strongly with VFA, quantified by magnetic resonance imaging.
However, the correlation with intra-abdominal adiposity was attenuated on multivariate analysis, when levels of the inflammatory markers were included, whereas the relationship between carotid stiffness and IL-6 remained strong.
Thus, intra-abdominal adipocyte-derived IL-6 could be involved in the accelerated atherosclerosis of type 2 diabetic patients. The prognostic importance of IL-6 for cardiovascular outcomes was studied in a cohort of men, free of ischaemic heart disease at baseline and followed for 13 years, in the Québec Cardiovascular Study.
Circulating levels of C-reactive protein are elevated in subjects with abdominal obesity, and conversely, subjects with elevated C-reactive protein tend to have intra-abdominal adiposity Figure 2. PAI-1 is secreted from intra-abdominal adipocytes, although mainly from platelets and the vascular endothelium.
Plasma adiponectin levels have been shown to be inversely proportional to the severity of intra-abdominal adiposity. These data confirm the dependence of adiponectin levels on intra-abdominal adiposity, rather than on obesity per se.
Indeed, intra-abdominal adiposity was the only independent predictor of adiponectin levels in this study. Adiponectin has been shown to have many favourable metabolic properties. For instance, it improves insulin sensitivity and glycaemic control, 5253 and levels of this adipokine correlate positively with levels of HDL-cholesterol and inversely with TG or PAI The strong relationships between abdominal obesity, insulin resistance, and cardiometabolic risk factors, described above, are suggestive of an important role for intra-abdominal adiposity in the pathogenesis of cardiovascular disease.
A link between abdominal obesity and increased cardiometabolic risk was suggested almost six decades ago by Vague as well as in two elegant early epidemiological studies that investigated the links between occupational physical activity, adiposity, and outcomes.
Specifically, bus drivers and bus conductors in London, UK, were studied. The drivers had an almost completely sedentary occupation, whereas conductors were more active, as they needed to walk around the upper and lower decks of buses to collect fares and issue tickets.
A markedly higher incidence of early 3 months mortality following a first CHD event had been observed among the sedentary drivers Figure 4right panel. A few years later, a study set out to investigate whether differences in the body shape between these groups, using available records of uniform sizes, might explain the difference in outcomes.
This study demonstrated a clear difference in the waist circumference of drivers' uniform trousers, which was indicative of upper body obesity and suggestive of abdominal obesity Figure 4left panel.
The five decades of clinical research undertaken since this pioneering study have confirmed the prognostic importance of abdominal obesity. Importantly, some of these studies have demonstrated the adverse prognosis associated with abdominal obesity, independently of BMI.
BMI did not predict significantly the development of major coronary events in a retrospective cohort study in patients undergoing coronary angiography after adjustment for standard cardiometabolic risk factors and abdominal obesity Table 2.
There is no doubt that measurement of waist circumference adds clinically significant prognostic information to BMI measurement relating to the risk of developing cardiovascular disease. The evidence reviewed above shows that abdominal obesity is closely involved in the development of multiple cardiometabolic risk factors, including those associated with the metabolic syndrome.
The large and growing abdominally obese population includes a substantial number of patients who are at increased risk of adverse cardiometabolic outcomes. In this regard, the NCEP-ATP III guidelines emphasized that the most prevalent form of the metabolic syndrome that physicians will encounter is associated with abdominal obesity.
For example, a triad of non-traditional cardiometabolic risk factors, elevated apolipoprotein B ApoBfasting hyperinsulinaemia, and small, dense LDL conferred a five-fold elevation in the risk of developing ischaemic heart disease, after adjustment for other lipid parameters, compared with subjects with not more than one of these risk factors, in a 5-year prospective case—control analysis of the Québec Cardiovascular Study.
However, the above elements of the atherogenic triad are not measured in routine clinical practice, and a more practicable means of identifying this high-risk subgroup is required.
The utility of hypertriglyceridaemic waist was determined in a study in men without symptoms of cardiovascular disease stratified for different values of TG and waist circumference.
Thus, measurement of waist circumference and TG, two simple clinical measurements suitable for routine clinical use, clearly identifies a high proportion of a subgroup of individuals at markedly elevated cardiometabolic risk.
When managing the prevalent form of the metabolic syndrome, NCEP-ATP III recommend to treat abdominal obesity and its associated insulin resistance first, as these are root causes of the overall elevation of cardiometabolic risk. Current management guidelines support the use of lifestyle interventions diet and exerciseas this strategy has the potential to improve all cardiometabolic risk factors.
However, lifestyle modifications are often unsuccessful, due in part to insufficient patient compliance with these regimens to induce long-term weight loss and maintenance. Under such circumstances, pharmacotherapy can be justified to manage elevated cardiometabolic risk.
Recent research has identified overactivity of the endocannabinoid system, acting via the CB 1 receptor, as an important factor in the pathogenesis of cardiometabolic risk.
Table 3 shows the effects of rimonabant on key cardiometabolic risk factors in two of these trials, RIO-Europe 62 and RIO-Lipids. Importantly, statistical analysis showed that about half of the improvements in HDL-cholesterol and triglyceride levels were independent of weight loss, consistent with a direct action of rimonabant on cardiometabolic risk.
Rimonabant was generally well tolerated. A growing database of clinical evidence implicates intra-abdominal adiposity as a powerful driving force for elevated cardiometabolic risk. This association appears to arise directly, via secretion of adipokines, and indirectly, through promotion of insulin resistance.
Addressing intra-abdominal adiposity should play a central role in future strategies aimed at improving cardiovascular outcomes in patients with abdominal obesity and its associated cardiometabolic risk factors. Conflict of interest : J. has received consulting or lecture fees from Abbott Laboratories, AstraZeneca, Fournier Pharma, GlaxoSmithKline, Merck, Pfizer, Pharmacia, and sanofi-aventis and grant support from Fournier Pharma, GlaxoSmithKline, Merck, Pfizer, and sanofi-aventis.
is Scientific Director of the International Chair on Cardiometabolic Risk which is supported by an unrestricted grant awarded to Université Laval by sanofi-aventis. CT scans from two subjects with comparable BMI illustrating adiposity phenotypes characterized mainly by intra-abdominal adiposity top panels and subcutaneous adiposity bottom panels.
Subcutaneous fat is shown in black under the skin, and visceral fat area VFA in white. Scans were made at the L4-L5 level. Reproduced with permission from Tchernof A, Després JP. Obesity and lipoprotein metabolism.
In: Kopelman PG, ed. Clinical ObesityUK: Blackwell Science Ltd; Association of intra-abdominal adiposity VFA on CT scans with elevated C-reactive protein.
asterisk quintile 1; dagger quintile 2; double dagger quintile 3. Reproduced with permission from Lemieux et al. Plasma adiponectin levels in healthy non-obese controls and in obese men with either low or high levels of visceral fat area VFA.
Data are from a study of 39 non-obese men and two groups of 15 obese men stratified for VFA measured using CT scanning. Reproduced with permission from Cote et al. Associations between occupational physical activity, obesity, and mortality in the 3 months following a first CHD event in transport workers in London, UK.
is equivalent to Between 58 and men were studied for each age group in either occupation. Mortality data are standardized mortality rates for individuals aged 35—64 for years — Drawn from data presented by Morris et al.
Prognostic value of high waist circumference beyond BMI: data from an analysis of patients undergoing coronary angiography.
: Metabolic syndrome abdominal obesity| Metabolic Syndrome | Cedars-Sinai | HDL and VLDL metabolism are closely linked, which explains why increased plasma triglyceride is almost always associated with reduced HDL levels. Article PubMed CAS Google Scholar Grundy SM, Cleeman JI, Daniels SR, et al. KV worked on the statistical analysis of the data. Article Google Scholar Pi-Sunyer X. Article CAS PubMed Google Scholar Vella CA, Allison MA, Cushman M, Jenny NS, Miles MP, Larsen B, et al. |
| Metabolic Syndrome | In conditions of elevated triglycerides, LDL particles become enriched in triglycerides and depleted of core cholesteryl esters see Fig. Hepatic lipase then acts to hydrolyze these triglyceride-rich LDL, forming smaller, denser LDL particles. The presence of small, dense cholesterol-depleted LDL particles is associated with an increased risk of myocardial infarction 21 — 23 and worsened severity of CAD 24 — The Familial Atherosclerosis Treatment Study showed that the strongest predictor of coronary artery stenosis regression, induced by aggressive lipid lowering, was the increase in LDL buoyancy, not the change in LDL cholesterol level Cholesteryl ester transfer protein CETP facilitates the exchange of cholesterol ester in LDL and HDL particles for triglyceride in VLDL particles. The transfer of triglyceride into LDL and HDL particles makes them triglyceride-rich and hence a better substrate for hepatic lipase. Elevated hepatic lipase activity leads to a predominance of small, dense LDL particles and a reduction in HDL 2 , the more antiatherogenic subspecies of HDL. Although the mechanisms underlying the association of small, dense LDL with increased risk of CAD are not clear, several hypotheses have been proposed. One explanation is that the presence of small, dense LDL particles is a marker of an atherogenic lipoprotein phenotype comprised of elevated triglycerides, reduced HDL, and elevated apo B, which together increase CAD risk Mechanistically, small, dense LDL particles enter the arterial wall more easily 29 , bind to arterial wall proteoglycans more avidly 30 , and are highly susceptible to oxidative modification, leading to macrophage uptake 31 , 32 , all of which may contribute to increased atherogenesis. HDL and VLDL metabolism are closely linked, which explains why increased plasma triglyceride is almost always associated with reduced HDL levels. Cholesteryl ester transfer protein mediates the exchange of triglyceride in VLDL for cholesteryl ester in LDL and HDL, leading to the production of triglyceride-rich LDL and HDL particles. Subsequent hepatic lipase-mediated hydrolysis of these particles leads to the generation of small, dense LDL particles and a decrease in HDL 2 cholesterol the large buoyant and antiatherogenic subspecies of total HDL; see Fig. Many studies have shown significantly increased CAD risk with the features of the metabolic syndrome, described under different names, but until recently limited information was available about the prevalence of the syndrome in the general population 20 , 23 , 34 , It is now clear that the metabolic syndrome is very common in westernized countries and varies with age, ethnicity, and body mass index 36 — Ford et al. Alexander et al. The presence of the metabolic syndrome is estimated to increase the risk of coronary heart disease by 1. Although individuals with the combination of the metabolic syndrome and diabetes have a high overall age-adjusted prevalence of CAD Recently published American Heart Association guidelines describe the presence of the metabolic syndrome, without diabetes, as a moderate CAD risk factor No study to date has established the contribution of familial combined hyperlipidemia to CAD risk in nondiabetic individuals with the metabolic syndrome see below. Individuals with the combination of the metabolic syndrome MS and diabetes DM have a high overall age-adjusted prevalence of CHD, whereas the presence of the metabolic syndrome in subjects without diabetes appears to convey a moderate risk of CAD compared with those with neither The recent emphasis on treatment of the dyslipidemia of the metabolic syndrome has compelled practitioners to consider lipid-lowering therapy in a greater number of their patients, as epidemiological studies have shown that one in two individuals over 50 yr of age has the metabolic syndrome. It is not yet clear whether all of these patients should be treated with lipid-lowering medications, and the economic impact of such a decision is enormous. Although the primary focus on CAD prevention remains on LDL lowering, LDL cholesterol levels may underestimate CAD risk in the metabolic syndrome. Importantly, the increased event rate with the metabolic syndrome remained significant after adjustment for the Framingham yr risk score, implying independent contributions of the metabolic syndrome and the Framingham score in predicting future CAD risk The evaluation of apo B in the metabolic syndrome can help target patients for aggressive lipid-lowering therapy. High levels of LDL cholesterol are generally accepted to be one of the strongest risk factors for CAD, but there is now significant evidence that the measurement of apo B may be an even better predictor of future CAD 45 — Insulin resistance is associated with increased numbers of small VLDL, IDL, and LDL particles, reflected by higher apo B levels, with decreased triglyceride to apo B ratios compared with those in individuals with normal insulin sensitivity. These particles are associated with increased coronary heart disease. Studies have shown that increased apo B and apo B-containing lipoproteins VLDL and IDL are related to an increased risk of CAD 45 — 47 and that particle quantity absolute number and quality small, dense both contribute to cardiovascular risk 23 see Fig. Bonora et al. This implies that the individuals with the metabolic syndrome had a higher number of cholesterol-deplete small, dense LDL particles. Odds ratios for ischemic heart disease IHD according to apo B levels and LDL peak particle diameter size. Men with both elevated apo B and small, dense LDL particles had a significantly higher risk of IHD than men with small, dense LDL particles but normal apo B levels. Reprinted with permission from Lamarche et al. DM2 and FCHL share many of the phenotypic features of the metabolic syndrome increased abdominal adiposity, insulin resistance, hypertension, and dyslipidemia , but appear to convey a greater risk of CAD than the metabolic syndrome alone. Patients with DM2 are at very high risk of CAD and have been identified as candidates for aggressive lipid lowering 5 , FCHL is a common lipid disorder that shares many features of the metabolic syndrome, and most patients diagnosed with FCHL also meet the NCEP criteria for the metabolic syndrome The identification of the metabolic syndrome should prompt practitioners to further evaluate patients for DM2 or FCHL, as the diagnosis of these disorders can help target those at high risk for CAD and direct lipid-lowering therapy. FCHL is the most common genetic form of hyperlipidemia and is associated with a 1. Goldstein et al. Although the prevalence of FCHL was originally estimated to be 0. The underlying process in FCHL appears to be the overproduction of apo B in lipoproteins VLDL, IDL, and LDL , which is not seen in other forms of hypertriglyceridemia 60 , The variable clinical lipid presentation of FCHL in patients has made their identification difficult, but the demonstration of elevated apo B and small, dense LDL particles has been shown to be a consistent feature across the variable lipid phenotypes 62 — Often one can identify affected relatives, and it is important to screen siblings and children of individuals with FCHL. FCHL is an oligogenic disorder that is not fully expressed until the third decade of life, possibly associated with the accumulation of central abdominal fat Children who have inherited FCHL usually do not have hyperlipidemia The metabolic features of FCHL are very similar to those of the metabolic syndrome, as individuals with FCHL are also characterized by insulin resistance, increased abdominal obesity, and hypertension 65 — Hopkins et al. Purnell et al. Further, apo B levels and small, dense LDL particles have been shown to segregate independently in families with FCHL FCHL is a subtype of the metabolic syndrome, with higher apo B levels. The identification of FCHL patients at high risk for CAD within the large population of individuals with the metabolic syndrome can help identify individuals as candidates for aggressive lipid-lowering interventions. The metabolic syndrome is a common population trait comprised of a heterogeneous group of oligogenic disorders, such as DM2 and familial combined hyperlipidemia see Fig. The identification of these metabolic syndrome subtypes by measuring fasting glucose and apo B can help target these high risk patients for lipid-lowering therapy. Patients with the metabolic syndrome should be screened for DM2, as individuals with DM2 and the metabolic syndrome are at high risk for CAD. Current guidelines recommend that patients with DM2 should be aggressively treated for dyslipidemia with the goal to maintain LDL below 2. Apo B levels increase with age; therefore, age-appropriate apo B levels must be used in diagnosis Several large prospective studies have shown that the apo B level is a better predictor of future cardiovascular events than the LDL cholesterol level 45 , 71 , Recently, the Apolipoprotein-Related Mortality Risk Study published prospective data in , men and women and found that the total apo B level was a better predictor of future CAD risk than LDL cholesterol Importantly, they also found that apo B was a better predictor of CAD risk in individuals with low LDL levels, supporting the idea that patients with low LDL cholesterol levels and increased quantities of small, dense atherogenic particles VLDL, IDL, and LDL are at risk for CAD. Apo B levels by age and gender mean and 90th percentile. To convert apo B values to grams per liter, divide by In addition to apo B, the measurement of non-HDL cholesterol total cholesterol minus HDL cholesterol can be used to assess the quantity of atherogenic apo B-containing lipoproteins VLDL, IDL, and LDL. Some investigators have proposed that non-HDL cholesterol could replace the LDL measure in patients with hypertriglyceridemia dyslipidemia with DM2 or FCHL , because these patients have more cholesterol in VLDL particles, and LDL cholesterol alone can underestimate their CAD risk The current NCEP guidelines recommend a non-HDL cholesterol goal of less than 3. Total apo B and non-HDL cholesterol levels are generally highly correlated, but less so at higher triglyceride levels. Comprehensive treatment of patients with the metabolic syndrome has recently been described in detail The treatment of the dyslipidemia of the metabolic syndrome should be focused on lowering LDL and apo B and increasing HDL. Statin treatment has been shown to reduce cardiovascular events in persons with low LDL cholesterol levels at baseline The percent reduction in LDL cholesterol and apo B by statin medications is similar, but apo B may be a better marker of treatment efficacy in metabolic syndrome patients with normal LDL cholesterol Although LDL cholesterol has remained the primary target of lipid-lowering therapy, raising HDL levels is now an important secondary target to reduce CAD risk 5. Combination lipid-lowering therapy is frequently needed to treat the dyslipidemia of the metabolic syndrome increased triglyceride, reduced HDL, and small, dense LDL particles , if lifestyle changes weight loss and exercise are inadequate. Nicotinic acid and fibric acid derivatives both act to reduce triglyceride and increase HDL cholesterol. They are frequently used with statin medications. Although fibrate monotherapy lowers plasma triglyceride levels, it can lead to increases in LDL levels. Bile acid resin binders lower LDL cholesterol levels, but can increase triglyceride levels in individuals susceptible to hypertriglyceridemia. Although niacin is an inexpensive monotherapeutic agent that corrects the dyslipidemia of the metabolic syndrome, it may increase glucose levels in some patients Several groups have recently shown that niacin use in diabetic individuals was safe and effective, resulting in only a transient worsening of glycemic control 78 — The decision to initiate lipid-lowering therapy in nondiabetic individuals with the metabolic syndrome can be difficult using current guidelines, as LDL levels may underestimate CAD risk in this population. The large population of individuals with the metabolic syndrome appears to be comprised of a heterogeneous group of disorders, and the identification of disease subtypes at high risk for CAD can help identify individuals as candidates for aggressive lipid-lowering interventions. Two subgroups of patients with the metabolic syndrome, those with DM2 or FCHL, are at particularly high risk for premature CAD. FCHL is characterized by the metabolic syndrome in addition to a disproportionate elevation of apo B levels. The measurement of fasting glucose and apo B in addition to the fasting lipid profile can help to estimate CAD risk and guide treatment decisions in patients with the metabolic syndrome. This work was supported by NIH Grants HL, HL, and DK and K23 Award RR to M. and by University of Washington General Clinical Research Center MRR Larsson B , Svardsudd K , Welin L , Wilhelmsen L , Bjorntorp P , Tibblin G Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13 year follow up of participants in the study of men born in Br Med J : — Google Scholar. 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| Abdominal Obesity and the Metabolic Syndrome | SpringerLink | Weight loss and psychologic gain in obese women-participants in a supported exercise intervention. The aim of this review is to i summarise current evidence on the pathophysiology of dysfunctional adipose tissue adiposopathy , its relationship to metabolic syndrome and how exercise may mediate these processes; and ii evaluate current evidence on the clinical efficacy of exercise in the management of abdominal obesity and to assess the type and dose of exercise needed for optimal improvements in health status. Bonora et al. References Blüher M. Similar adjustments were made for waist circumference including adjustment for BMI. Wang Y, Rimm EB, Stampfer MJ, Willett WC, Hu FB. |
Metabolic syndrome abdominal obesity -
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The use of technology to promote physical activity in type 2 diabetes management: a systematic review. Download references. School of Clinical and Applied Sciences, Leeds Beckett University, Portland Building, City Campus, Leeds, LS1 3HE, UK.
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Abstract Background Metabolic syndrome is defined as a cluster of at least three out of five clinical risk factors: abdominal visceral obesity, hypertension, elevated serum triglycerides, low serum high-density lipoprotein HDL and insulin resistance.
Purpose of this review This review provides a summary of the current evidence on the pathophysiology of dysfunctional adipose tissue adiposopathy. Conclusion There is moderate evidence supporting the use of programmes of exercise to reverse metabolic syndrome although at present the optimal dose and type of exercise is unknown.
Background Metabolic syndrome is defined as a cluster of at least three out of five clinical risk factors: abdominal visceral obesity, hypertension, elevated serum triglycerides, low serum high-density lipoprotein HDL and insulin resistance [ 1 ].
Abdominal obesity, adiposopathy and metabolic dysfunction To understand the significance of abdominal obesity and its contribution to metabolic syndrome, it is necessary to appreciate the link between the diseases associated with this condition.
Metabolic dysfunction and exercise Abdominal adiposity is a reversible condition and its reduction can have excellent effects in diminishing cardiovascular and metabolic syndrome risk. Optimal dose of exercise There are no specific guidelines on exercise prescription for systemic inflammation although guidance is available in the form of programmes designed to reduce body fat and improve general health status.
Promoting adherence to exercise Programmes One of the major challenges in using programmes of exercise to improve health status is promoting and maintaining adherence in individuals who have often been inactive for many years and who may be overweight or obese [ 86 ].
Conclusion An increasingly sedentary lifestyle, a lack of regular exercise and an increase in obesity have been the main contributors to a rise in the incidence of metabolic dysfunction, particularly in the developed world. Abbreviations ACSM: American College of Sports Medicine BMI: Body mass index CRP: C-reactive protein EIM: Exercise is Medicine HDL: High density lipoprotein HIIT: High Intensity Interval Training HPA: Hypothlamic-pituitary-adrenal hsCRP: High-sensitivity C-reactive protein LDL: Low density lipoprotein METS: Metabolic equivalent units TNF-α: Tumour necrosis factor alpha VO 2 : Oxygen Uptake.
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Increased abdominal visceral fat accumulation is a risk factor for coronary artery disease CAD , dyslipidemia, hypertension, stroke, and type 2 diabetes.
The recent emphasis on treatment of the dyslipidemia of the metabolic syndrome hypertriglyceridemia, reduced high-density lipoprotein, and increased small, dense low-density lipoprotein particle number has compelled practitioners to consider lipid-lowering therapy in a greater number of their patients, as one in two individuals over age 50 has the metabolic syndrome.
Individuals with the metabolic syndrome typically have normal low-density lipoprotein cholesterol levels, and current lipid-lowering guidelines may underestimate their cardiovascular risk.
Two subgroups of patients with the metabolic syndrome are at particularly high risk for premature CAD. Familial combined hyperlipidemia is characterized by the metabolic syndrome in addition to a disproportionate elevation of apolipoprotein B levels. The measurement of fasting glucose and apolipoprotein B, in addition to the fasting lipid profile, can help to estimate CAD risk in patients with the metabolic syndrome.
DISTINCT METABOLIC FEATURES are seen in individuals with increased amounts of abdominal visceral adipose tissue. Hypertriglyceridemia, reduced high density lipoprotein HDL , and small, dense low density lipoprotein LDL particles characterize the dyslipidemia associated with increased abdominal fat.
Individuals with the metabolic syndrome typically have normal LDL cholesterol levels, but their LDL particles are small and dense, and current lipid-lowering guidelines may underestimate their coronary artery disease CAD risk.
Further evaluation of apolipoprotein B apo B in patients with the metabolic syndrome can help detect patients with familial combined hyperlipidemia FCHL and identify them as candidates for aggressive lipid lowering. As the prevalence of the metabolic syndrome rises with increasing obesity and sedentary lifestyle, so does the disease burden of increased type 2 diabetes mellitus and cardiovascular disease.
Many prospective studies have shown that increased abdominal visceral fat accumulation is an independent risk factor for CAD, hypertension, stroke, and type 2 diabetes DM2 1 — 3.
The strong link between increased abdominal visceral fat and hyperinsulinism, insulin resistance, elevated plasma free fatty acid FFA levels, hypertension, predisposition to thrombosis, hypertriglyceridemia, small, dense LDL particles, and reduced HDL has been recognized for decades, but until recently there has been no uniform definition of this disease complex.
Even normal weight individuals with increased amounts of abdominal adipose tissue can be metabolically obese, with insulin resistance and dyslipidemia 6 , 7. Multiple environmental and genetic factors are thought to influence the manifestation of abdominal obesity.
Intraabdominal fat increases with age in both overweight and normal weight individuals independently of changes in total body fat 8. Sex steroid hormones appear to contribute to body fat distribution, as men have twice as much abdominal fat as women 9 , 10 , and estrogen deficiency at menopause is associated with a preferential increase in intraabdominal fat, which is blunted by estrogen replacement therapy 11 , There is also evidence that increased abdominal adipose tissue is associated with physical inactivity, increased plasma cortisol, and intrauterine environment Genetic factors that predispose individuals to gain weight centrally may explain the susceptibility of certain ethnic groups to DM2 15 , The increased focus on the metabolic syndrome has drawn attention to the identification and treatment of the dyslipidemia associated with abdominal fat accumulation.
The changes in lipid metabolism seen with abdominal fat accumulation have been well characterized and include hypertriglyceridemia, reduced HDL cholesterol, and increased numbers of small, dense LDL particles.
Elevated LDL cholesterol is not a feature of the dyslipidemia seen with abdominal obesity. Other features of the dyslipidemia of abdominal adiposity include elevated very low density lipoproteins VLDL , and reduced HDL 2 , which are the large buoyant antiatherogenic subspecies of total HDL.
In some individuals, apo B levels may be elevated, reflecting an increase in the number of small, dense lipoprotein particles VLDL and LDL. The hypertriglyceridemia seen with abdominal obesity and insulin resistance is related to the oversecretion of triglyceride-rich VLDL particles see Fig.
An increased rate of hepatic FFA uptake stimulates the secretion of apo B, leading to increased numbers of apo B-containing particles and possibly hypertriglyceridemia Apo B is the structural protein of atherogenic lipoproteins, including VLDL, intermediate density lipoproteins IDL , and LDL.
Each of these lipoproteins contains one apo B molecule, and the plasma apo B level reflects the total number of atherogenic particles in the blood. VLDL particles are exposed to lipoprotein lipase in the peripheral circulation, which hydrolyzes the triglyceride in VLDL particles, generating FFA.
Under normal conditions, these FFA are taken up by muscle and adipose tissue for energy use or storage. The resultant remnant particles are then processed by the liver to form LDL. Elevated portal vein FFA levels with insulin resistance lead to an overproduction of apo B-containing particles.
Apo B is the structural protein of atherogenic lipoproteins, including VLDL and IDL, and the apo B concentration reflects the total number of atherogenic particles in the blood. The metabolic syndrome is associated with increased numbers of small VLDL, IDL, and LDL particles, with a decreased triglyceride to apo B ratio compared with normal.
An increased number of small, dense LDL particles is a constant feature of the dyslipidemia of abdominal adiposity, as they are associated with insulin resistance, intraabdominal fat, and hypertension 18 — LDL comprises a spectrum of particles that vary in size, density, chemical composition, and atherogenic potential.
In conditions of elevated triglycerides, LDL particles become enriched in triglycerides and depleted of core cholesteryl esters see Fig. Hepatic lipase then acts to hydrolyze these triglyceride-rich LDL, forming smaller, denser LDL particles. The presence of small, dense cholesterol-depleted LDL particles is associated with an increased risk of myocardial infarction 21 — 23 and worsened severity of CAD 24 — The Familial Atherosclerosis Treatment Study showed that the strongest predictor of coronary artery stenosis regression, induced by aggressive lipid lowering, was the increase in LDL buoyancy, not the change in LDL cholesterol level Cholesteryl ester transfer protein CETP facilitates the exchange of cholesterol ester in LDL and HDL particles for triglyceride in VLDL particles.
The transfer of triglyceride into LDL and HDL particles makes them triglyceride-rich and hence a better substrate for hepatic lipase. Elevated hepatic lipase activity leads to a predominance of small, dense LDL particles and a reduction in HDL 2 , the more antiatherogenic subspecies of HDL.
Although the mechanisms underlying the association of small, dense LDL with increased risk of CAD are not clear, several hypotheses have been proposed. One explanation is that the presence of small, dense LDL particles is a marker of an atherogenic lipoprotein phenotype comprised of elevated triglycerides, reduced HDL, and elevated apo B, which together increase CAD risk Mechanistically, small, dense LDL particles enter the arterial wall more easily 29 , bind to arterial wall proteoglycans more avidly 30 , and are highly susceptible to oxidative modification, leading to macrophage uptake 31 , 32 , all of which may contribute to increased atherogenesis.
HDL and VLDL metabolism are closely linked, which explains why increased plasma triglyceride is almost always associated with reduced HDL levels.
Cholesteryl ester transfer protein mediates the exchange of triglyceride in VLDL for cholesteryl ester in LDL and HDL, leading to the production of triglyceride-rich LDL and HDL particles. Subsequent hepatic lipase-mediated hydrolysis of these particles leads to the generation of small, dense LDL particles and a decrease in HDL 2 cholesterol the large buoyant and antiatherogenic subspecies of total HDL; see Fig.
Many studies have shown significantly increased CAD risk with the features of the metabolic syndrome, described under different names, but until recently limited information was available about the prevalence of the syndrome in the general population 20 , 23 , 34 , It is now clear that the metabolic syndrome is very common in westernized countries and varies with age, ethnicity, and body mass index 36 — Ford et al.
Alexander et al. The presence of the metabolic syndrome is estimated to increase the risk of coronary heart disease by 1. Although individuals with the combination of the metabolic syndrome and diabetes have a high overall age-adjusted prevalence of CAD Recently published American Heart Association guidelines describe the presence of the metabolic syndrome, without diabetes, as a moderate CAD risk factor No study to date has established the contribution of familial combined hyperlipidemia to CAD risk in nondiabetic individuals with the metabolic syndrome see below.
Individuals with the combination of the metabolic syndrome MS and diabetes DM have a high overall age-adjusted prevalence of CHD, whereas the presence of the metabolic syndrome in subjects without diabetes appears to convey a moderate risk of CAD compared with those with neither The recent emphasis on treatment of the dyslipidemia of the metabolic syndrome has compelled practitioners to consider lipid-lowering therapy in a greater number of their patients, as epidemiological studies have shown that one in two individuals over 50 yr of age has the metabolic syndrome.
It is not yet clear whether all of these patients should be treated with lipid-lowering medications, and the economic impact of such a decision is enormous.
Although the primary focus on CAD prevention remains on LDL lowering, LDL cholesterol levels may underestimate CAD risk in the metabolic syndrome. Importantly, the increased event rate with the metabolic syndrome remained significant after adjustment for the Framingham yr risk score, implying independent contributions of the metabolic syndrome and the Framingham score in predicting future CAD risk The evaluation of apo B in the metabolic syndrome can help target patients for aggressive lipid-lowering therapy.
High levels of LDL cholesterol are generally accepted to be one of the strongest risk factors for CAD, but there is now significant evidence that the measurement of apo B may be an even better predictor of future CAD 45 — Insulin resistance is associated with increased numbers of small VLDL, IDL, and LDL particles, reflected by higher apo B levels, with decreased triglyceride to apo B ratios compared with those in individuals with normal insulin sensitivity.
These particles are associated with increased coronary heart disease. Studies have shown that increased apo B and apo B-containing lipoproteins VLDL and IDL are related to an increased risk of CAD 45 — 47 and that particle quantity absolute number and quality small, dense both contribute to cardiovascular risk 23 see Fig.
Bonora et al. This implies that the individuals with the metabolic syndrome had a higher number of cholesterol-deplete small, dense LDL particles. Odds ratios for ischemic heart disease IHD according to apo B levels and LDL peak particle diameter size.
Men with both elevated apo B and small, dense LDL particles had a significantly higher risk of IHD than men with small, dense LDL particles but normal apo B levels.
Reprinted with permission from Lamarche et al. DM2 and FCHL share many of the phenotypic features of the metabolic syndrome increased abdominal adiposity, insulin resistance, hypertension, and dyslipidemia , but appear to convey a greater risk of CAD than the metabolic syndrome alone.
Patients with DM2 are at very high risk of CAD and have been identified as candidates for aggressive lipid lowering 5 , FCHL is a common lipid disorder that shares many features of the metabolic syndrome, and most patients diagnosed with FCHL also meet the NCEP criteria for the metabolic syndrome The identification of the metabolic syndrome should prompt practitioners to further evaluate patients for DM2 or FCHL, as the diagnosis of these disorders can help target those at high risk for CAD and direct lipid-lowering therapy.
FCHL is the most common genetic form of hyperlipidemia and is associated with a 1. Goldstein et al. Although the prevalence of FCHL was originally estimated to be 0. The underlying process in FCHL appears to be the overproduction of apo B in lipoproteins VLDL, IDL, and LDL , which is not seen in other forms of hypertriglyceridemia 60 , The variable clinical lipid presentation of FCHL in patients has made their identification difficult, but the demonstration of elevated apo B and small, dense LDL particles has been shown to be a consistent feature across the variable lipid phenotypes 62 — Often one can identify affected relatives, and it is important to screen siblings and children of individuals with FCHL.
FCHL is an oligogenic disorder that is not fully expressed until the third decade of life, possibly associated with the accumulation of central abdominal fat Children who have inherited FCHL usually do not have hyperlipidemia The metabolic features of FCHL are very similar to those of the metabolic syndrome, as individuals with FCHL are also characterized by insulin resistance, increased abdominal obesity, and hypertension 65 — Hopkins et al.
Purnell et al. Further, apo B levels and small, dense LDL particles have been shown to segregate independently in families with FCHL FCHL is a subtype of the metabolic syndrome, with higher apo B levels.
The identification of FCHL patients at high risk for CAD within the large population of individuals with the metabolic syndrome can help identify individuals as candidates for aggressive lipid-lowering interventions.
The metabolic syndrome is a common population trait comprised of a heterogeneous group of oligogenic disorders, such as DM2 and familial combined hyperlipidemia see Fig. The identification of these metabolic syndrome subtypes by measuring fasting glucose and apo B can help target these high risk patients for lipid-lowering therapy.
Patients with the metabolic syndrome should be screened for DM2, as individuals with DM2 and the metabolic syndrome are at high risk for CAD. Current guidelines recommend that patients with DM2 should be aggressively treated for dyslipidemia with the goal to maintain LDL below 2.
Apo B levels increase with age; therefore, age-appropriate apo B levels must be used in diagnosis Several large prospective studies have shown that the apo B level is a better predictor of future cardiovascular events than the LDL cholesterol level 45 , 71 , Recently, the Apolipoprotein-Related Mortality Risk Study published prospective data in , men and women and found that the total apo B level was a better predictor of future CAD risk than LDL cholesterol Importantly, they also found that apo B was a better predictor of CAD risk in individuals with low LDL levels, supporting the idea that patients with low LDL cholesterol levels and increased quantities of small, dense atherogenic particles VLDL, IDL, and LDL are at risk for CAD.
Apo B levels by age and gender mean and 90th percentile. To convert apo B values to grams per liter, divide by In addition to apo B, the measurement of non-HDL cholesterol total cholesterol minus HDL cholesterol can be used to assess the quantity of atherogenic apo B-containing lipoproteins VLDL, IDL, and LDL.
Some investigators have proposed that non-HDL cholesterol could replace the LDL measure in patients with hypertriglyceridemia dyslipidemia with DM2 or FCHL , because these patients have more cholesterol in VLDL particles, and LDL cholesterol alone can underestimate their CAD risk The current NCEP guidelines recommend a non-HDL cholesterol goal of less than 3.
Total apo B and non-HDL cholesterol levels are generally highly correlated, but less so at higher triglyceride levels. Comprehensive treatment of patients with the metabolic syndrome has recently been described in detail The treatment of the dyslipidemia of the metabolic syndrome should be focused on lowering LDL and apo B and increasing HDL.
Statin treatment has been shown to reduce cardiovascular events in persons with low LDL cholesterol levels at baseline The percent reduction in LDL cholesterol and apo B by statin medications is similar, but apo B may be a better marker of treatment efficacy in metabolic syndrome patients with normal LDL cholesterol Although LDL cholesterol has remained the primary target of lipid-lowering therapy, raising HDL levels is now an important secondary target to reduce CAD risk 5.
Combination lipid-lowering therapy is frequently needed to treat the dyslipidemia of the metabolic syndrome increased triglyceride, reduced HDL, and small, dense LDL particles , if lifestyle changes weight loss and exercise are inadequate.
Nicotinic acid and fibric acid derivatives both act to reduce triglyceride and increase HDL cholesterol. They are frequently used with statin medications. Although fibrate monotherapy lowers plasma triglyceride levels, it can lead to increases in LDL levels.
Bile acid resin binders lower LDL cholesterol levels, but can increase triglyceride levels in individuals susceptible to hypertriglyceridemia. Although niacin is an inexpensive monotherapeutic agent that corrects the dyslipidemia of the metabolic syndrome, it may increase glucose levels in some patients Several groups have recently shown that niacin use in diabetic individuals was safe and effective, resulting in only a transient worsening of glycemic control 78 — The decision to initiate lipid-lowering therapy in nondiabetic individuals with the metabolic syndrome can be difficult using current guidelines, as LDL levels may underestimate CAD risk in this population.
The large population of individuals with the metabolic syndrome appears to be comprised of a heterogeneous group of disorders, and the identification of disease subtypes at high risk for CAD can help identify individuals as candidates for aggressive lipid-lowering interventions.
Two subgroups of patients with the metabolic syndrome, those with DM2 or FCHL, are at particularly high risk for premature CAD. FCHL is characterized by the metabolic syndrome in addition to a disproportionate elevation of apo B levels.
The measurement of fasting glucose and apo B in addition to the fasting lipid profile can help to estimate CAD risk and guide treatment decisions in patients with the metabolic syndrome. This work was supported by NIH Grants HL, HL, and DK and K23 Award RR to M.
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Download references. Department of Public Health, Faculty of Medicine, University of Szeged, Dóm tér 10, Szeged, , Hungary. Department of Medical Physics and Informatics, University of Szeged, Szeged, Hungary. Department of Preventive Medicine, Faculty of Public Health, University of Debrecen, Debrecen, Hungary.
MTA-DE Public Health Research Group, Department of Preventive Medicine, Faculty of Public Health, University of Debrecen, Debrecen, Hungary. You can also search for this author in PubMed Google Scholar. JS, RÁ, and MP took leadership and responsibility for the research activity planning and made substantial contributions to the conception and design of the Programme.
KV worked on the statistical analysis of the data. AL, EH, ASz, and ZsM carried out the interpretation of the results.
Abdominal obesity, due to intra-abdominal Resourceful nutrient balance, drives the progression of multiple cardiometabolic syyndrome factors independently of body mass index. This occurs both syyndrome Metabolic syndrome abdominal obesity secretion of adipocyte-derived biologically active substances adipokinesincluding free obesityy Metabolic syndrome abdominal obesity, syyndrome, interleukin-6, tumour necrosis Megabolic alpha, abdokinal plasminogen Meatbolic inhibitor-1, and through exacerbation of insulin resistance and associated cardiometabolic risk factors. The prevalence of abdominal obesity is increasing in western populations, due to a combination of low physical activity and high-energy diets, and also in developing countries, where it is associated with the urbanization of populations. The measurement of waist circumference, together with an additional comorbidity, readily identifies the presence of increased cardiometabolic risk associated with abdominal obesity. Accordingly, measurement of waist circumference should become a standard component of cardiovascular risk evaluation in routine clinical practice.
Metabolic syndrome abdominal obesity -
Several studies show a strong association between obesity and physical inactivity [ 46 , 47 , 48 ] and that metabolic syndrome is associated with sedentary lifestyle and poor cardiorespiratory fitness [ 49 ]. Sedentary behaviour is widely regarded as activity which involves energy expenditure at the level of 1.
Edwardson et al. conducted a meta-analysis that found that individuals who spend more time in sedentary behaviours have greater odds of having metabolic syndrome [ 50 ].
A longitudinal study observing adults found that improvements in cardiometabolic factors occurred in overweight and obese individuals with increased levels of physical activity, although the participants were those participating in a health screening programme and were therefore probably of a higher economic status.
At follow-up, there was a statistically significant decrease in non-HDL concentrations of 5. Of the parameters observed, non-HDL cholesterol and plasma triglycerides were found to have the largest improvement when physical activity was increased.
A study followed 22, participants, aged 30—64 years, comparing metabolic syndrome risk with intensity level of leisure-time exercise and by occupational and commuting activity [ 53 ]. Leisure-time activity was found to be linearly and inversely associated with a risk of developing metabolic syndrome and vigorous-intensity activity alone or a combination of both moderate- and vigorous-intensity activity was associated with a lower risk of metabolic syndrome.
The introduction of increased physical activity into a previously inactive lifestyle might also break the cycle of inflammation-mediated sickness behaviour as described by Nunn, which suppresses the desire to undertake physical activity [ 30 ].
A systematic review and meta-analysis was conducted by Ostman et al. A total of 16 studies participants were included in the review and it was found that aerobic training produced small improvements in fasting blood glucose, triglycerides and low-density lipoproteins.
Nevertheless, combined with improvements in maximal oxygen uptake and blood pressure, the overall risk profile for patients was much improved. The improvements in waist measurement would suggest that the long-term risks associated with metabolic syndrome were reduced. There are a number of studies which have specifically investigated the effect of exercise on abdominal obesity, irrespective of total body weight and these are summarised in a comprehensive review by Pedersen and Saltin [ 56 ].
Amongst their findings they reported that a cross-sectional study of overweight males showed that those with a high level of fitness as measured by activity and maximal oxygen uptake had lower levels of visceral fat than their unfit counterparts when scanned using magnetic resonance imaging [ 39 ].
Lee et al. investigated the effects of exercise without weight loss on total and abdominal adiposity and skeletal muscle mass and composition in previously sedentary, lean men and in obese men with and without type II diabetes [ 11 ]. It was found that, even in the absence of weight loss, moderate-intensity exercise was associated with significant reductions in total and abdominal fat, and there was a reduction in skeletal muscle lipid content independent of group.
Stewart et al. investigated the effects of exercise on cardiovascular and metabolic disease in older adults and found that reductions in total and abdominal fatness and increase in leanness were strongly associated with reductions in risk factors for cardiovascular disease and diabetes, including those that constitute metabolic syndrome [ 57 ].
conducted a longitudinal study of 32, adults who underwent an abdominal computerised tomography scan as part of health screening and found that the ratio of visceral-to-subcutaneous fat was independently associated with all-cause mortality. This suggests that the location of fat deposits in the abdomen viscera is a better indicator of metabolic risk than total body fat, which is unsurprising given the positive association between abdominal adiposity and systemic inflammation [ 58 ].
A number of reviews have shown that exercise training specifically elicits an anti-inflammatory effect, independent of weight loss [ 33 , 59 , 60 , 61 , 62 ].
Other metabolic benefits of exercise were reported in a study on patients with type II diabetes where pedometer-measured exercise was not only associated with reductions in systemic inflammation, but also reductions in abdominal obesity and arterial stiffness [ 63 ].
One of the mechanisms for the anti-inflammatory effect of exercise is a reduction in adipose tissue hypoxia resulting from improved capillary density blood flow.
In a review by Golbidi [ 24 ] the inverse relationship between exercise, body mass index BMI , hip-waist ratio, and waist circumference was described.
The anti-inflammatory effect of exercise was also explained as being closely related to oxidative stress. Exercise was shown to improve glucose tolerance, insulin resistance and lipid metabolism and reduce blood pressure in both healthy individuals and those with metabolic disease.
Large population cohort studies observed relationships between plasma CRP and the level of exercise that was independent of obesity as measured by body mass index [ 62 , 64 ].
The effect of exercise training on CRP was investigated in a systematic review which considered a total of 83 studies of different types.
It was found that exercise training led to a greater reduction in CRP when accompanied by a decrease in BMI, but that significant reductions in CRP occurred without weight loss [ 65 ]. Furthermore, a Cochrane review provided evidence that exercise improved general health even where no weight was lost because it improved plasma lipoprotein profile [ 66 ].
Not all studies provide evidence that exercise training reduces pro-inflammatory biomarkers. Melo et al. reviewed 11 studies of patients with type II diabetes and found insufficient evidence to determine whether aerobic or resistance exercise improved systemic levels of inflammatory markers [ 67 ].
However, an earlier review by Hayashino et al. found that both CRP and IL-6 were reduced by exercise training [ 68 ]. It is still unclear whether improvements in inflammatory status are independent of weight loss or entirely dependent upon the changes in body composition that result from exercise training [ 61 ].
Nevertheless, Eaton and Eaton observed that the percentage of lean body mass is critical in avoiding the hyperinsulinaemia which predisposes individuals to type II diabetes because a greater insulin secretion is required for any given glucose load where levels of body fat are disproportionate [ 27 ].
This would suggest that strength training that develops lean tissue is critical in the treatment, or prevention, of metabolic disease. There are no specific guidelines on exercise prescription for systemic inflammation although guidance is available in the form of programmes designed to reduce body fat and improve general health status.
The American College of Sports Medicine ACSM recommends — min of moderate-intensity exercise per week as optimal but other authors have suggested between 30 [ 69 ] and 60 [ 70 ] minutes per day would be required.
A systematic review and meta-analysis by Hayashino et al. They found that exercise training with a longer duration and frequency was more effective in reducing systemic inflammation, suggesting that these effects might be dose-dependent. More recently, this idea has been challenged and it is now thought that shorter-duration, higher intensity interval training HIIT is beneficial [ 76 ].
Recent findings suggest that HIIT programmes are effective in reducing metabolic syndrome combined with high adherence rates and this is important because incorporating HIIT programmes into daily life is less disruptive.
Gremeaux, et al. studied the effects of HIIT training on a sample of 62 overweight or obese adults who were above the recommended abdominal obesity threshold. It was found that the prevalence of metabolic syndrome was reduced by The metabolic and vascular effects of these three different regimens were studied and improvements were observed in various measures including BMI, waist measurement, glucose metabolism, insulin resistance and lipid profiles.
Zhang et al. also found that high intensity interval training was better than continuous moderate aerobic training in reducing abdominal visceral fat in obese young women [ 78 ].
Similar findings from other studies support the benefit of high-intensity interval training performed in short, high-intensity bursts, involving as little as 10 min of activity at a time, and this might promote better adherence in non-habitual exercisers [ 79 , 80 , 81 ].
A further study of adults found that consistent moderate to vigorous activity was more important than exercise volume in reducing CRP levels associated with systemic inflammation [ 82 ]. A systematic review by Cronin et al. found that greater reductions in inflammatory biomarkers occurred in older healthy inactive participants when higher intensity aerobic exercise was undertaken [ 83 ].
A review by Zdziarski et al. found that largest reductions in systemic inflammation and improvements in well-being, depression and sleep was achieved using multi-modal exercise aerobic and resistance training in individuals with inflammation-related chronic pain [ 84 ].
This is important because it is likely that individuals in a pro-inflammatory state due to abdominal adiposopathy may also be susceptible to chronic pain conditions. Dutheil et al. reported that high resistance-moderate endurance training was efficient in improving visceral fat loss in healthy adults [ 85 ].
If changes in body composition are more important than total body weight loss then resistance training combined with aerobic exercise would produce optimal effects in increasing percentage lean body mass [ 27 ].
One of the major challenges in using programmes of exercise to improve health status is promoting and maintaining adherence in individuals who have often been inactive for many years and who may be overweight or obese [ 86 ]. To promote adherence Clauw and Crofford suggested that additional activity is incorporated very gradually — as little as 5 min daily [ 88 ] although the programme needs to be tailored to the individual whilst aiming to deliver optimal effects [ 84 ].
As discussed above, the recent findings that HIIT programmes are effective in reducing metabolic syndrome combined with high adherence rates is significant because incorporating it into daily life is less disruptive. Connelly et al. conducted a review to assess the effectiveness of technology to promote physical activity in people with Type 2 diabetes and found that the use of technology-based interventions, such as mobile phone applications, texts and email support, improves compliance [ 89 ].
In summary, evidence suggests that optimal abdominal fat reduction and the development of lean tissue is achieved by combining high-intensity interval training and resistance training with an overall general increase in daily physical activity. An increasingly sedentary lifestyle, a lack of regular exercise and an increase in obesity have been the main contributors to a rise in the incidence of metabolic dysfunction, particularly in the developed world.
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Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Link between abdominal obesity and metabolic abnormalities. Dyslipidemia of abdominal adiposity.
Prevalence and risk of the metabolic syndrome. Metabolic syndrome: targeting high risk patients. Importantly, intra-abdominal adiposity appears to interact with other cardiometabolic risk factors to adversely influence overall cardiometabolic risk.
An analysis from the Québec Health Survey stratified subjects for BMI and then for waist circumference and studied the relationships between indices of obesity, hyperinsulinaemia, and blood pressure in the resulting subgroups.
In another study, stratification of men for FPG revealed no significant association between the presence of impaired fasting glucose IFG FPG 6. Thus, it appears important in clinical practice to consider additional risk factors, such as abdominal obesity and TG, when evaluating the importance of dysglycaemia as a cardiovascular risk factor.
It should be noted, however, that the relationship between abdominal obesity and insulin resistance is influenced by genetic factors. South Asians, for example, tend to display insulin resistance at all levels of abdominal obesity and these subjects will develop type 2 diabetes or coronary heart disease CHD at lower levels of obesity than other populations.
Excess intra-abdominal adiposity has the potential to influence metabolism and cardiometabolic risk directly, through alterations in the secretion of adipokines Table 1. Abdominal obesity promotes increased secretion of a range of metabolites and of biologically active substances, including glycerol, free fatty acids FFA , inflammatory mediators [e.
tumour necrosis factor alpha TNFα and interleukin-6 IL-6 ], plasminogen activator inhibitor-1 PAI-1 , and C-reactive protein. Acute exposure of skeletal muscle to elevated levels of FFA induces insulin resistance, 37 whereas chronic exposure of the pancreas to elevated FFA impairs β-cell function.
lowest tertile after correction for non-lipid risk factors, although further multivariate adjustment for lipid parameters and insulin weakened the association.
Leptin is an adipokine involved in the regulation of satiety and energy intake. However, the plasma concentration of leptin is not determined primarily by the amount of visceral fat present and correlates more strongly with subcutaneous adiposity.
Atherosclerosis has been shown to have an inflammatory component, 42 and pro-inflammatory adipokines may be important mediators of atherogenesis in abdominally obese subjects. TNFα is a paracrine mediator in adipocytes and appears to act locally to reduce the insulin sensitivity of adipocytes.
IL-6 is a systemic adipokine, which not only impairs insulin sensitivity, but is also a major determinant of hepatic production of C-reactive protein, 45 the most important source of this inflammatory marker.
A study in 16 well-controlled type 2 diabetes patients showed that circulating levels of IL-6 correlate strongly with VFA, quantified by magnetic resonance imaging. However, the correlation with intra-abdominal adiposity was attenuated on multivariate analysis, when levels of the inflammatory markers were included, whereas the relationship between carotid stiffness and IL-6 remained strong.
Thus, intra-abdominal adipocyte-derived IL-6 could be involved in the accelerated atherosclerosis of type 2 diabetic patients. The prognostic importance of IL-6 for cardiovascular outcomes was studied in a cohort of men, free of ischaemic heart disease at baseline and followed for 13 years, in the Québec Cardiovascular Study.
Circulating levels of C-reactive protein are elevated in subjects with abdominal obesity, and conversely, subjects with elevated C-reactive protein tend to have intra-abdominal adiposity Figure 2.
PAI-1 is secreted from intra-abdominal adipocytes, although mainly from platelets and the vascular endothelium. Plasma adiponectin levels have been shown to be inversely proportional to the severity of intra-abdominal adiposity. These data confirm the dependence of adiponectin levels on intra-abdominal adiposity, rather than on obesity per se.
Indeed, intra-abdominal adiposity was the only independent predictor of adiponectin levels in this study. Adiponectin has been shown to have many favourable metabolic properties.
For instance, it improves insulin sensitivity and glycaemic control, 52 , 53 and levels of this adipokine correlate positively with levels of HDL-cholesterol and inversely with TG or PAI The strong relationships between abdominal obesity, insulin resistance, and cardiometabolic risk factors, described above, are suggestive of an important role for intra-abdominal adiposity in the pathogenesis of cardiovascular disease.
A link between abdominal obesity and increased cardiometabolic risk was suggested almost six decades ago by Vague as well as in two elegant early epidemiological studies that investigated the links between occupational physical activity, adiposity, and outcomes.
Specifically, bus drivers and bus conductors in London, UK, were studied. The drivers had an almost completely sedentary occupation, whereas conductors were more active, as they needed to walk around the upper and lower decks of buses to collect fares and issue tickets.
A markedly higher incidence of early 3 months mortality following a first CHD event had been observed among the sedentary drivers Figure 4 , right panel. A few years later, a study set out to investigate whether differences in the body shape between these groups, using available records of uniform sizes, might explain the difference in outcomes.
This study demonstrated a clear difference in the waist circumference of drivers' uniform trousers, which was indicative of upper body obesity and suggestive of abdominal obesity Figure 4 , left panel.
The five decades of clinical research undertaken since this pioneering study have confirmed the prognostic importance of abdominal obesity.
Importantly, some of these studies have demonstrated the adverse prognosis associated with abdominal obesity, independently of BMI. BMI did not predict significantly the development of major coronary events in a retrospective cohort study in patients undergoing coronary angiography after adjustment for standard cardiometabolic risk factors and abdominal obesity Table 2.
There is no doubt that measurement of waist circumference adds clinically significant prognostic information to BMI measurement relating to the risk of developing cardiovascular disease.
The evidence reviewed above shows that abdominal obesity is closely involved in the development of multiple cardiometabolic risk factors, including those associated with the metabolic syndrome.
The large and growing abdominally obese population includes a substantial number of patients who are at increased risk of adverse cardiometabolic outcomes. In this regard, the NCEP-ATP III guidelines emphasized that the most prevalent form of the metabolic syndrome that physicians will encounter is associated with abdominal obesity.
For example, a triad of non-traditional cardiometabolic risk factors, elevated apolipoprotein B ApoB , fasting hyperinsulinaemia, and small, dense LDL conferred a five-fold elevation in the risk of developing ischaemic heart disease, after adjustment for other lipid parameters, compared with subjects with not more than one of these risk factors, in a 5-year prospective case—control analysis of the Québec Cardiovascular Study.
However, the above elements of the atherogenic triad are not measured in routine clinical practice, and a more practicable means of identifying this high-risk subgroup is required. The utility of hypertriglyceridaemic waist was determined in a study in men without symptoms of cardiovascular disease stratified for different values of TG and waist circumference.
Thus, measurement of waist circumference and TG, two simple clinical measurements suitable for routine clinical use, clearly identifies a high proportion of a subgroup of individuals at markedly elevated cardiometabolic risk. When managing the prevalent form of the metabolic syndrome, NCEP-ATP III recommend to treat abdominal obesity and its associated insulin resistance first, as these are root causes of the overall elevation of cardiometabolic risk.
Current management guidelines support the use of lifestyle interventions diet and exercise , as this strategy has the potential to improve all cardiometabolic risk factors. However, lifestyle modifications are often unsuccessful, due in part to insufficient patient compliance with these regimens to induce long-term weight loss and maintenance.
Under such circumstances, pharmacotherapy can be justified to manage elevated cardiometabolic risk. Recent research has identified overactivity of the endocannabinoid system, acting via the CB 1 receptor, as an important factor in the pathogenesis of cardiometabolic risk.
Table 3 shows the effects of rimonabant on key cardiometabolic risk factors in two of these trials, RIO-Europe 62 and RIO-Lipids. Importantly, statistical analysis showed that about half of the improvements in HDL-cholesterol and triglyceride levels were independent of weight loss, consistent with a direct action of rimonabant on cardiometabolic risk.
Rimonabant was generally well tolerated. A growing database of clinical evidence implicates intra-abdominal adiposity as a powerful driving force for elevated cardiometabolic risk.
This association appears to arise directly, via secretion of adipokines, and indirectly, through promotion of insulin resistance. Addressing intra-abdominal adiposity should play a central role in future strategies aimed at improving cardiovascular outcomes in patients with abdominal obesity and its associated cardiometabolic risk factors.
Conflict of interest : J. has received consulting or lecture fees from Abbott Laboratories, AstraZeneca, Fournier Pharma, GlaxoSmithKline, Merck, Pfizer, Pharmacia, and sanofi-aventis and grant support from Fournier Pharma, GlaxoSmithKline, Merck, Pfizer, and sanofi-aventis.
is Scientific Director of the International Chair on Cardiometabolic Risk which is supported by an unrestricted grant awarded to Université Laval by sanofi-aventis. CT scans from two subjects with comparable BMI illustrating adiposity phenotypes characterized mainly by intra-abdominal adiposity top panels and subcutaneous adiposity bottom panels.
Subcutaneous fat is shown in black under the skin, and visceral fat area VFA in white. Scans were made at the L4-L5 level. Reproduced with permission from Tchernof A, Després JP. Obesity and lipoprotein metabolism. In: Kopelman PG, ed.
Clinical Obesity , UK: Blackwell Science Ltd; Association of intra-abdominal adiposity VFA on CT scans with elevated C-reactive protein. asterisk quintile 1; dagger quintile 2; double dagger quintile 3. Reproduced with permission from Lemieux et al.
Plasma adiponectin levels in healthy non-obese controls and in obese men with either low or high levels of visceral fat area VFA. Data are from a study of 39 non-obese men and two groups of 15 obese men stratified for VFA measured using CT scanning. Reproduced with permission from Cote et al.
Associations between occupational physical activity, obesity, and mortality in the 3 months following a first CHD event in transport workers in London, UK. is equivalent to Between 58 and men were studied for each age group in either occupation.
Mortality data are standardized mortality rates for individuals aged 35—64 for years — Drawn from data presented by Morris et al.
Prognostic value of high waist circumference beyond BMI: data from an analysis of patients undergoing coronary angiography. For BMI, data shown are standardized odds ratios adjusted for age, gender, smoking and total cholesterol. Similar adjustments were made for waist circumference including adjustment for BMI.
Prevalence of an atherogenic triad of elevated ApoB, fasting hyperinsulinaemia, and small, dense LDL according to the TG and waist circumference. Gorter PM, Olijhoek JK, van der Graaf Y, Algra A, Rabelink TJ, Visseren FL. Prevalence of the metabolic syndrome in patients with coronary heart disease, cerebrovascular disease, peripheral arterial disease or abdominal aortic aneurysm.
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Abdominal adiposity and coronary heart disease in women. JAMA ; : — Empana JP, Ducimetiere P, Charles MA, Jouven X. Sagittal abdominal diameter and risk of sudden death in asymptomatic middle-aged men: the Paris Prospective Study I. Circulation ; : — Kim SK, Kim HJ, Hur KY, Choi SH, Ahn CW, Lim SK, Kim KR, Lee HC, Huh KB, Cha BS.
Visceral fat thickness measured by ultrasonography can estimate not only visceral obesity but also risks of cardiovascular and metabolic diseases. Am J Clin Nutr ; 79 : — Wang Y, Rimm EB, Stampfer MJ, Willett WC, Hu FB. Comparison of abdominal adiposity and overall obesity in predicting risk of type 2 diabetes among men.
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The Nurses' Health Study. Am J Epidemiol ; : — Poirier P, Lemieux I, Mauriege P, Dewailly E, Blanchet C, Bergeron J, Despres JP. Impact of waist circumference on the relationship between blood pressure and insulin: the Quebec Health Survey.
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BMC Alleviates microbial threats Science, Medicine abdominql Rehabilitation volume 10Article number: Effective cholesterol management techniques Cite this article. Metrics details. Metabolic syndrome is defined as a cluster boesity at least three Metaboolic of Quench natural thirst quencher clinical risk factors: abdominal visceral obesity, syhdrome, elevated serum triglycerides, low serum high-density lipoprotein Synvrome and insulin resistance. Evidence shows that regular and consistent exercise reduces abdominal obesity and results in favourable changes in body composition. It has therefore been suggested that exercise is a medicine in its own right and should be prescribed as such. This review provides a summary of the current evidence on the pathophysiology of dysfunctional adipose tissue adiposopathy. It describes the relationship of adiposopathy to metabolic syndrome and how exercise may mediate these processes, and evaluates current evidence on the clinical efficacy of exercise in the management of abdominal obesity.
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