Uncontrolled diabetes poses a significantly increased risk of developing macrovascular disease, especially coronary, cerebrovascular, and peripheral vascular disease. It also increases the chances of microvascular disease, including retinopathy, nephropathy, and neuropathy.

Diagram of the relationship between the processes of carbohydrate metabolism, including glycolysis, gluconeogenesis, glycogenesis, glycogenolysis, fructose metabolism, and galactose metabolism Contributed by Wikimedia User: Eschopp, CC BY-SA 4.

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Author Information and Affiliations Authors Mihir N. Affiliations 1 Nova Southeastern University. Introduction Glucose is central to energy consumption. We can summarize blood glucose regulation and its clinical significance in the following ways: The liver serves as a buffer for blood glucose concentration.

Cellular Level Following are the critical steps in the utilization of glucose at the cellular level- Transport of glucose through the cell membrane. Development In a developing fetus, regulated glucose exposure is imperative to normal growth because glucose is the primary energy form used by the placenta.

Organ Systems Involved Nervous system: The pancreas performs autonomic function through the sympathetic and parasympathetic innervation of the pancreas. The brain itself also houses insulin receptors in multiple regions, including the hypothalamus, cerebellum, hippocampus, among other areas.

Pancreas: The pancreas is behind the stomach in the right upper quadrant of the abdomen. The endocrine functionality of the pancreas regulates glucose homeostasis.

Liver: Glycogenesis and gluconeogenesis are the storing and releasing of glucose, respectively. These processes occur using insulin, glucagon, and hepatocyte derived factors. Gut: Hormones in the gut are released in response to the ingestion of nutrients. These hormones are involved in appetite, glucose production, gastric emptying, and glucose removal.

Adipocytes: Adipose tissue secretes adipokines, which regulate insulin release through their involvement in glucose metabolism, control of food intake, and insulin gene expression. Function Glucose metabolism involves multiple processes, including glycolysis, gluconeogenesis, glycogenolysis, and glycogenesis.

Mechanism Glycolysis is the most crucial process in releasing energy from glucose, the end product of which is two molecules of pyruvic acid. Related Testing HbA1c. Since the HbA1C value summarizes long-term glycemic control, it is frequently used to evaluate patients with long-standing hyperglycemia, as seen in patients with diabetes, and to forecast the risk of diabetic complications.

Fasting Plasma Glucose. Plasma blood glucose level is measured after a period of fasting, typically at least 8 hours. Random Plasma Glucose.

A random plasma glucose measurement is sampled sometime after dietary intake was last ingested. Oral Glucose Tolerance Test.

All pregnant women should receive gestational diabetes mellitus GDM screening through an orally consumed glucose challenge and subsequent plasma blood glucose measurement. Measured via urine or serum samples, a C-peptide value aids in the evaluation and management of diabetes.

The presence of autoantibodies, including islet autoantibody, insulin autoantibody, insulinoma-associated antigen-2 autoantibodies, and anti-glutamic acid decarboxylase GAD autoantibodies, among others, are suggestive of auto-immune response as is seen in type 1 diabetes.

Pathophysiology Although not completely understood, Type 1 and Type 2 diabetes differ in their pathophysiology. Clinical Significance Poor glucose metabolism leads to diabetes mellitus. Diabetes is classified into two types- Type 1 DM- due to deficient insulin secretion.

Circulating insulin is virtually absent, leading to a catabolic state with exogenous insulin required for treatment.

This condition occurs predominantly in adults but is now increasingly present in children and adolescents. Review Questions Access free multiple choice questions on this topic.

Comment on this article. Figure Diagram of the relationship between the processes of carbohydrate metabolism, including glycolysis, gluconeogenesis, glycogenesis, glycogenolysis, fructose metabolism, and galactose metabolism Contributed by Wikimedia User: Eschopp, CC BY-SA 4. References 1. Jaiswal N, Gavin MG, Quinn WJ, Luongo TS, Gelfer RG, Baur JA, Titchenell PM.

The role of skeletal muscle Akt in the regulation of muscle mass and glucose homeostasis. Mol Metab. Chen Y, Zhao X, Wu H. Metabolic Stress and Cardiovascular Disease in Diabetes Mellitus: The Role of Protein O -GlcNAc Modification.

Arterioscler Thromb Vasc Biol. Taneera J, Dhaiban S, Mohammed AK, Mukhopadhyay D, Aljaibeji H, Sulaiman N, Fadista J, Salehi A. GNAS gene is an important regulator of insulin secretory capacity in pancreatic β-cells. Hay WW. Placental-fetal glucose exchange and fetal glucose metabolism.

Trans Am Clin Climatol Assoc. Schaefer-Graf U, Napoli A, Nolan CJ. Diabetes in pregnancy: a new decade of challenges ahead. Röder PV, Wu B, Liu Y, Han W. Pancreatic regulation of glucose homeostasis. Exp Mol Med. Han HS, Kang G, Kim JS, Choi BH, Koo SH. Knowing how the pancreatic, digestive, and intestinal hormones are involved in food metabolism can help you understand normal physiology and how problems develop with diabetes.

Throughout the body, cells use glucose as a source of immediate energy. During exercise or stress the body needs a higher concentration because muscles require glucose for energy Basu et al. Of the three fuels for the body, glucose is preferred because it produces both energy and water through the Krebs cycle and aerobic metabolism.

The body can also use protein and fat; however, their breakdown creates ketoacids, making the body acidic, which is not its optimal state. Excess of ketoacids can produce metabolic acidosis. Functioning body tissues continuously absorb glucose from the bloodstream.

For people who do not have diabetes, a meal of carbohydrates replenishes the circulating blood glucose about 10 minutes after eating and continues until about 2 hours after eating.

A first-phase release of insulin occurs about 5 minutes after a meal and a second phase begins at about 20 minutes. The food is broken down into small components including glucose and is then absorbed through the intestines into the bloodstream.

Glucose potential energy that is not immediately used is stored by the body as glycogen in the muscles, liver, and fat. Your body is designed to survive and so it stores energy efficiently, as fat. Most Americans have excess fat because they replenish the glucose stores by eating before any fat needs to be broken down.

When blood glucose levels fall after 2 hours, the liver replenishes the circulating blood glucose by releasing glycogen stored glucose. Glycogen is a polysaccharide, made and stored primarily in the cells of the liver. Glycogen provides an energy reserve that can be quickly mobilized to meet a sudden need for glucose.

Regulation of blood glucose is largely done through the endocrine hormones of the pancreas, a beautiful balance of hormones achieved through a negative feedback loop. The main hormones of the pancreas that affect blood glucose include insulin, glucagon, somatostatin, and amylin.

Insulin formed in pancreatic beta cells lowers BG levels, whereas glucagon from pancreatic alpha cells elevates BG levels. It helps the pancreas alternate in turning on or turning off each opposing hormone.

Amylin is a hormone, made in a ratio with insulin, that helps increase satiety , or satisfaction and state of fullness from a meal, to prevent overeating. It also helps slow the stomach contents from emptying too quickly, to avoid a quick spike in BG levels. As a meal containing carbohydrates is eaten and digested, BG levels rise, and the pancreas turns on insulin production and turns off glucagon production.

Glucose from the bloodstream enters liver cells, stimulating the action of several enzymes that convert the glucose to chains of glycogen—so long as both insulin and glucose remain plentiful. After a meal has been digested and BG levels begin to fall, insulin secretion drops and glycogen synthesis stops.

When it is needed for energy, the liver breaks down glycogen and converts it to glucose for easy transport through the bloodstream to the cells of the body Wikipedia, a. The liver converts glycogen back to glucose when it is needed for energy and regulates the amount of glucose circulating between meals.

Your liver is amazing in that it knows how much to store and keep, or break down and release, to maintain ideal plasma glucose levels. Imitation of this process is the goal of insulin therapy when glucose levels are managed externally. Basal—bolus dosing is used as clinicians attempt to replicate this normal cycle.

The concentration of glucose in the blood is determined by the balance between the rate of glucose entering and the rate of glucose leaving the circulation. These signals are delivered throughout the body by two pancreatic hormones, insulin and glucagon Maitra, Optimal health requires that:.

If you want to lose weight, what fuel would you decrease in your diet and what fuels would you increase? Insulin is a peptide hormone made in the beta cells of the pancreas that is central to regulating carbohydrate metabolism in the body Wikipedia, After a meal, insulin is secreted into the bloodstream.

When it reaches insulin-sensitive cells—liver cells, fat cells, and striated muscle—insulin stimulates them to take up and metabolize glucose. Insulin synthesis and release from beta cells is stimulated by rising concentrations of blood glucose.

Insulin has a range of effects that can be categorized as anabolic , or growth-promoting. Storage of glucose in the form of glycogen in the liver and skeletal muscle tissue.

Storage of fat. How would you explain the function of insulin to your patient with diabetes? What does it turn on and what does it turn off? Glucagon , a peptide hormone secreted by the pancreas, raises blood glucose levels. Its effect is opposite to insulin, which lowers blood glucose levels. When it reaches the liver, glucagon stimulates glycolysis , the breakdown of glycogen, and the export of glucose into the circulation.

The pancreas releases glucagon when glucose levels fall too low. Glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream. High BG levels stimulate the release of insulin. Insulin allows glucose to be taken up and used by insulin-dependent tissues, such as muscle cells.

Glucagon and insulin work together automatically as a negative feedback system to keeps BG levels stable. Glucagon is a powerful regulator of BG levels, and glucagon injections can be used to correct severe hypoglycemia. Glucose taken orally or parenterally can elevate plasma glucose levels within minutes, but exogenous glucagon injections are not glucose; a glucagon injection takes approximately 10 to 20 minutes to be absorbed by muscle cells into the bloodstream and circulated to the liver, there to trigger the breakdown of stored glycogen.

People with type 2 diabetes have excess glucagon secretion, which is a contributor to the chronic hyperglycemia of type 2 diabetes. The amazing balance of these two opposing hormones of glucagon and insulin is maintained by another pancreatic hormone called somatostatin , created in the delta cells.

It truly is the great pancreatic policeman as it works to keep them balanced. When it goes too high the pancreas releases insulin into the bloodstream. This insulin stimulates the liver to convert the blood glucose into glycogen for storage.

If the blood sugar goes too low, the pancreas release glucagon, which causes the liver to turn stored glycogen back into glucose and release it into the blood. Analyses of 6-month changes in primary and secondary outcomes were conducted based on intention-to-treat principle, with the missing data assumed to be missing at random.

Missing values were imputed using multiple imputation with chained equations Imputation was based on all collected measurements at 0, 3, and 6 months , and participant-specific characteristics, including sex, age, and baseline BMI.

The treatment arm was not taken into account when doing imputations. For month follow-up, we conducted a per-protocol analysis using the data collected from participants who retu-rned for follow-up.

CIs for change differences between treatments in primary and secondary outcomes 6-month changes were assessed by using two-sample Welsh unequal variance t test, where the outcome distribution was assumed to be normal. For the ratio of total cholesterol to HDL cholesterol and HOMA-IR, which did not distribute normally, we used the Mann-Whitney nonparametric test.

The comparison between treatments in continuous variables over time in multiple time points was done using repeated-measures mixed ANOVA test to evaluate the interaction between time within-subject factor and diet treatment between-subject factor , with the Greenhouse-Geisser correction used.

The simple main effects of differences between the two diet groups at each time point were assessed using t test. SPSS software was used to perform multiple imputations. A total of candidates were eligible according to the screening results and were invited to a profiling visit, which served as the start point of a run-in period of 2—4 weeks before the start of intervention Fig.

A total of participants completed the run-in period and were randomly assigned to the MED or PPT diet arm. These participants were included in the intention-to-treat population and in the primary analysis.

During the intervention, 25 participants 12 in MED and 13 in PPT withdrew from the study for various reasons as detailed in Fig. In total, A total of participants Notably, the difference in loss rates between groups at 12 months 6 participants in MED vs. Baseline characteristics of the cohort are described in Table 1.

No significant differences were noted between the groups Table 1. Self-reported adherence to the diet regimens was high and similar in both groups as assessed by dietary records and electronic follow-up questionnaires Supplementary Fig. In terms of diet composition, the 6-month mean carbohydrate intake per day was The mean ± SD intake of dietary fiber per day was Overall, these dietary intakes represent a dec-rease in fat intake mainly saturated fat versus an increase in carbohydrates including dietary fiber and protein in the MED group compared with base line.

In the PPT group, there was an overall decrease in carbohydrate intake including dietary fiber and an increase in protein and fat intake including saturated fat compared with baseline Supplementary Table 2. In accordance with the recommended foods on the MED diet, the most common foods consumed by MED participants included whole-wheat bread, rice, tahini, hummus, vegetables, and plain yogurt.

Commonly consumed foods by PPT participants included tahini, eggs, nuts, high-fat cheese, vegetables, chicken, beef, and fish Supplementary Fig. As expected, the PPT diet resulted in a relatively low average carbohydrate content since dietary carbohydrates are considered a major factor of PPGR prediction.

Furthermore, for each person, meals with a similar amount of carbohydrates but different food components yielded different PPGR predictions and thus promoted different recommendations, such that two meals with the same amount of carbohydrates could generate different scores and result in distinct actual PPGR in the same participant Supplementary Fig.

Consistent with this notion, changes in dietary carbohydrate intake during the intervention only modestly correlated with changes in primary outcomes Supplementary Fig. As designed, there was no significant difference in physical activity level between the groups mean ± SD 1.

Among the participants included in the primary analysis, there was a significant decrease in both time above and HbA 1c at the end of the intervention. In a sensitivity analysis of six imputation methods, the results remained statistically significant for time above and HbA 1c Supplementary Fig.

We also performed post hoc subgroup analyses for the difference between treatments in subgroups by age, BMI, sex, and compliance.

CIs for between-group change difference in primary and secondary outcomes. A : Primary outcomes. B : Secondary outcomes. BP dia, diastolic blood pressure; BP sys, systolic blood pressure; US, ultrasound.

The changes in primary outcomes over time are shown in Fig. Changes in primary and selected secondary outcomes during the intervention phase. A : Changes in primary outcomes over time in the MED diet and PPT diet.

Analysis was done based on intention-to-treat principle. To statistically evaluate the changes in outcomes over time, the repeated-measures ANOVA test was used, and the difference between groups at each time point was assessed by t test. B : Changes in three selected secondary outcomes over time in the MED diet and PPT diet.

To evaluate the differences between groups at each time point, a t test was used for weight and triglycerides, and a Mann-Whitney nonparametric test was used for total cholesterol-to-HDL cholesterol ratio. Chol, cholesterol. Changes in secondary outcomes at the end of the intervention 6 months are shown in Figs.

For other glycemic measurements, including FPG, insulin, and HOMA-IR, no significant differences were noted between the groups Fig. Additional secondary outcomes, including total cholesterol, blood pressure, liver enzymes ALT, AST , hepatic ultrasound, and anthropometric measurements weight, BMI, fat percentage demonstrated significant reductions in each group compared with its own baseline, but these did not reach significant differences between groups Fig.

At the end of the intervention, the average weight loss observed was 2. The changes in all secondary outcomes over time are shown in Fig. For other secondary outcomes, there was no significant interaction between diet group and time.

In other secondary outcomes, there was no significant difference between the groups at 12 months Supplementary Fig. During the monthly individual dietary follow-up meetings, dietitians asked participants about tolerance and side effects related to the diet, including bloating, fullness, indigestion, or any other diet-related symptoms.

Only temporary complaints were reported, and these were solved satisfactorily by standard dietary advice on eating patterns.

In some cases, the symptoms were resolved by the use of barrier products e. In these cases, we used the CGM data collected up to that time point and continued to collect other trial measures as usual, including dietary records, blood tests, and all other measurements.

Other glycemic and metabolic measures also improved significantly more with the PPT diet, including 5-h PPGR excursions, mean CGM glucose, blood fructosamine, FLI, blood triglycerides, HDL cholesterol, and total cholesterol-to-HDL cholesterol ratio, demonstrating another potential benefit of the PPT approach in reducing cardiometabolic risks in prediabetes 1.

These findings suggest that a dietary strategy focused on PPGR reductions is safe and effective for helping to improve glycemic control in prediabetes. At month follow-up, the significant difference in glycemic control between the groups was maintained, suggesting that personalized PPGR-targeting diets may have long-term efficacy in improving blood glucose levels.

Our findings support the general importance and beneficial effects of lifestyle modifications for diabetes prevention in prediabetes, as previously demonstrated in the DPP 4. While glycemia improved as measured by both time above and HbA 1c , the results of a single OGTT at 6 months were not significantly different between the groups.

This may be due to significant variability in the postprandial response to a single standard carbohydrate challenge compared with multiple other real-world meals over time. Alternatively, other biological mechanisms or study methodological aspects may explain this result, which requires further investigation in future studies.

Advantages of this trial design include the use of CGM throughout the entire intervention period, which allowed us to directly measure the effects of every meal on glucose levels while evaluating the importance of long-term reductions in PPGRs to metabolic health.

As such, and in contrast to blood tests, which provide a single point-of-care measure that may be sensitive to test errors, long-term CGM data may provide a more accurate reflection of the glycemic state.

Indeed, the use of CGM in the research setting and clinical practice for diabetes management is becoming more common Additionally, full dietary records logged by the study participants using a designated smartphone app allowed us to closely monitor compliance and diet adherence by participants in both arms while de facto assessing the distinction between the two dietary treatments.

The fact that the two groups had a similar number of calories reported on average during the intervention, along with similar modest weight loss rates observed in both groups, suggests that the dietary records were indeed reliable. We find that this approach enables a major advantage.

Typical dietary intake assessment in clinical trials is done by using food frequency questionnaires or occasional h recalls and food diaries, which inaccurately assess actual dietary consumption throughout the intervention period, thereby limiting the ability to draw precise conclusions about health outcomes of different dietary approaches.

Our study also has several limitations. We compared only two dietary approaches: a MED diet and our algorithm-based PPT diet. Since carbohydrate content of the meal constitutes an important component in the PPGR prediction algorithm, the PPT diet resulted in lower carbohydrate content on average compared with the MED diet.

Thus, it is possible that the beneficial effects observed in the PPT diet are mainly driven by the lower carbohydrate content. However, we speculate that this is not the case because the change in dietary carbohydrate intake during the intervention was not highly correlated with primary clinical outcomes e.

Furthermore, other studies demonstrated that low-carbohydrate diets are not superior to high-carbohydrate diets in terms of long-term glycemic control or weight management 14 , In a systematic review and meta-analysis of dietary carbohydrate restriction in patients with type 2 diabetes, Snorgaard et al.

Gardner et al. Finally, beyond the overall macronutrient composition of the diet, the PPT diet enabled an individualized set of recommendations at the level of meals, regardless of their carbohydrate content, such that identical meals yielded different recommendation levels for different people Supplementary Fig.

Nevertheless, differences between our algorithmbased PPT diet and other low-carbohydrate diets should be further explored. These limitations notwithstanding, in this randomized clinical trial in prediabetes, a personalized PPT diet improved glycemic control significantly more than a MED diet.

These findings may have implications for prediabetes dietary advice in clinical practice and potentially for other metabolic disorders, including type 2 diabetes, metabolic syndrome, and nonalcoholic fatty liver disease, pending rigorous clinical testing to generate evidence of benefit in these clinical conditions.

Clinical trial reg. NCT, clinicaltrials. The authors thank the Segal group members for fruitful discussions; Dr. David Zeevi Center for Studies in Physics and Biology, The Rockefeller University, New York, NY and Dr. Tal Korem Program for Mathematical Genomics, Department of Systems Biology, Columbia University Irving Medical Center, New York, NY , former laboratory members, for fruitful discussions and critical insights to the trial design and manuscript; Dr.

Relly Abel from Clalit Health Services and Billy Cohen from Maccabi Healthcare Services for help with recruitment of participants; Ofra Lavi from AMC Medical Center Laboratory for operating all processes of blood tests at the central laboratory of the trial; Rachel Segall for coordinating collaboration with AMC Medical Center Laboratory; and Anat Schneider, Maya Ahimas, and Shikma Shor The Robert H.

Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem for help with phone calls to candidates during registration and enrollment procedures. Duality of Interest. The funding for the study was provided jointly by the companies Janssen Pharmaceuticals, Inc.

Janssen is one of the investors of DayTwo. and E. are regular paid consultants for DayTwo. No other potential conflicts of interest relevant to this article were reported. No pharmaceutical manufacturers or other companies from the industry, including the sponsors mentioned above, contributed to the planning, design, or conduct of the trial.

The analyses presented here were performed by Weizmann scientists independent of the sponsors. The scientists have the right to publish regardless of the outcome. Author Contributions. was the clinical trial lead, oversaw the conduct of the study, and wrote the manuscript. and A.

designed and directed the project and data collection and analyses, interpreted the results, and contributed equally to the study. conceived the study and designed the intervention.

provided dietary recommendations and personal dietetic support throughout the intervention to all study participants. directed all computational aspects of the study, with support from D.

was the medical lead of the study with support from N. and N. coordinated participant recruitment and management throughout the intervention and follow-up. conceived and directed the project and analyses, designed the analyses, interpreted the results, and wrote the manuscript.

All authors reviewed and approved the manuscript and vouch for the accuracy and completeness of the data.

By pinpointing factors that influence glucose levels and adopting effective management techniques, you can work towards achieving better health outcomes and improved metabolic fitness.

As always, consult a healthcare professional if you have concerns about your glucose levels or require personalised guidance. Vively is a metabolic health app that shows you your glucose responses in real-time, using continuous glucose monitors CGMs. It combines your personal health data with education and support to help you achieve optimal metabolic health.

Sign up here. Dr Michelle Woolhouse is an integrative GP, with over 20 years experience treating chronic conditions through lifestyle medicine. Discover how controlling your glucose levels can aid in ageing gracefully. Learn about the latest research that links glucose levels and ageing, and how Vively, a metabolic health app, can help you manage your glucose and age well.

Delve into the concept of mindful eating and discover its benefits, including improved glucose control and healthier food choices. Learn about practical strategies to implement mindful eating in your daily life. Understand the nuances of polycystic ovary syndrome PCOS testing in Australia, the importance of early diagnosis, and the tests used to effectively diagnose the condition.

Also, find out when these diagnostic procedures should be considered. We acknowledge the Traditional Custodians of the lands where we live and work, the Gadigal of the Eora Nation. We pay our respects to their Elders past and present. CGM Program. For Organisations. Button Text. Your Cart.

Product is not available in this quantity. Glucose management. Key takeaways Monophasic glucose response indicates reduced insulin sensitivity and increased risk of metabolic dysfunction and impaired glucose metabolism. Biphasic glucose response indicates enhanced health outcomes, decreased glucose levels, and increased insulin sensitivity.

Incessant increase response indicates even poorer pancreatic beta cell function, insulin resistance, and increased risk of type 2 diabetes. Understanding the causes of different glucose curves can help identify factors that influence glucose levels and inform effective management techniques.

What are the three types of glucose spikes? Monophasic glucose response: characterised by a single glucose peak followed by a consistent decline, this curve might suggest a diminished and compromised first phase of insulin release. Biphasic glucose response: features an initial peak minutes post-meal, a drop in glucose levels, and then a secondary increase between minutes.

This curve is indicative of superior insulin release during the first phase and heightened insulin sensitivity. Incessant increase: a continuous gradual rise in blood sugar in the minutes post-meal without a drop of at least 4. May 2, Dr Michelle Woolhouse Integrative GP and Vively Medical Director Dr Michelle Woolhouse is an integrative GP, with over 20 years experience treating chronic conditions through lifestyle medicine.

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