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A high normal TSH is associated with the metabolic syndrome. Clin Endocrinol 72 5 — Oh JY, Sung YA, Lee HJ.

Elevated thyroid stimulating hormone levels are associated with metabolic syndrome in euthyroid young women.

Korean J Internal Med 28 2 —6. Garduño-Garcia Jde J, Alvirde-Garcia U, López-Carrasco G, Padilla Mendoza ME, Mehta R, Arellano-Campos O, et al. TSH and free thyroxine concentrations are associated with differing metabolic markers in euthyroid subjects. Eur J Endocrinol 2 —8. Bakiner O, Bozkirli E, Cavlak G, Ozsahin K, Ertorer E.

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Citation: He J, Lai Y, Yang J, Yao Y, Li Y, Teng W and Shan Z The Relationship Between Thyroid Function and Metabolic Syndrome and Its Components: A Cross-Sectional Study in a Chinese Population. Received: 30 January ; Accepted: 15 March ; Published: 31 March Obesity is associated with increased serum TSH level, independent of thyroid function.

Swiss Med Wkly ;— v Marina A. Michalaki, Apostolos G. Vagenakis, Aggeliki S. Leonardou, Marianna N. Argentou, Ioannis G. Habeos, Maria G. Makri, Agathoklis I. Psyrogiannis, Fotis E.

Kalfarentzos, Venetsana E. January 1, , 16 1 : vi Rezzonico J, Rezzonico M, Pusiol E, Pitoia F, Niepomniszcze H. Introducing the thyroid gland as another victim of the insulin resistance syndrome.

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NEXT The Elusive Weight Maintenance. T4 has a long half-life and is converted to the active form, T3, within cells by the activating deiodinases D1 and D2 that catalyze outer ring deiodination. The third deiodinase, D3, terminates TH action by inactivating T3 and T4 by removing the iodine at the inner ring The local regulation of TH at intracellular level enables wide fluctuations of TH in local tissues and is a powerful tool with which to modulate TH action without perturbing systemic TH levels.

The correlation of a Thr92Ala polymorphism in the DIO2 gene, encoding protein D2, with altered glycemic control, obesity and type 2 diabetes mellitus T2DM 14 — 16 , as well as the association of genetic variants of the DIO1 gene, encoding protein D1, with insulin resistance 17 , reinforces the clinical relevance of the peripheral T4-to-T3 conversion in metabolic control.

In this review we summarize the role of the local control of TH by the deiodinases in the metabolic program of cells in the context of the tissue-specific impact of deiodination on energy metabolism, and discuss the effect of local alteration of TH on the metabolic functions of the body.

Although each cell of the body is virtually a TH target, the TH signal is differentially integrated in each tissue depending on the cell-autonomous machinery. Therefore, the action of TH on whole body metabolism is best evaluated by examining the specific contribution of TH and its modulating enzymes to energy metabolism in the context of each target tissue.

The relative roles of most components of the TH signaling pathways have been assessed in mouse models of inducible, tissue-specific activation or inactivation of deiodinases, receptors and transporters 1.

These studies revealed how different TH-induced processes contribute to regulating metabolic homeostasis in humans Figure 1. Figure 1. Metabolic effects of the intracellular regulation of thyroid hormone in different tissues.

A Liver: Lipid homeostasis is regulated by local T3 level thereby influencing susceptibility to obesity and liver steatosis. B Pancreas: The balance between the deiodinases controls the development and function of β-cells by enhancing Mafa transcription factor and inducing insulin secretion.

C Hypothalamus: Local availability of TH regulates feeding behavior and controls energy expenditure. D Skeletal Muscle: Increased T3 levels in skeletal muscle promote the shift from type I to type II fibers, influence regeneration and increase energy expenditure. E BAT: D2-mediated TH activation regulates UCP1 expression and thermogenesis, adipocyte proliferation and differentiation and body weight.

There is an intricate relationship between TH metabolism and liver 1 , 18 , Thyroid hormones regulate hepatic function by modulating the basal metabolic rate of hepatocytes; the liver in turn metabolizes the THs and regulates their systemic endocrine effects In the liver, TH regulates lipid metabolism mainly through the T3-TRβ TH receptor beta 1 , and the downstream regulation of cholesterol homeostasis synthesis and efflux , bile acid synthesis and fatty acid metabolism 1.

The local control of TH metabolism in liver is mediated by the expression of all three deiodinases. D1 is highly expressed in liver, where it contributes to plasmatic T3 homeostasis and mediates the clearance of rT3 from the circulation D1 expression is highly sensitive to T3 levels to such an extent that it is an indicator of the thyroid state of the liver Despite the high D1 levels in the liver, the intracellular T3 level in hepatocytes is not mediated by D1, but by the other TH-activating deiodinase, D2 The liver is the paradigm of spatio-temporal regulated expression of D2 that is transiently turned on in the neonatal mouse liver between the first and the fifth post-natal day.

During this short time, a peak of hepatic D2 expression occurs and rapidly declines to background levels This brief peak of D2 produces an excess of T3 that modifies the methylation and the expression pattern of thousands of hepatic genes thereby increasing future susceptibility to diet-induced obesity and liver steatosis Mouse models of hepatocyte-specific D2 inactivation Alb-D2KO do not undergo this physiological increase of liver T3 at birth, with a consequent delay in neonatal expression of lipid-related genes and a phenotype of resistance to obesity and liver steatosis These fundamental changes during perinatal life indicate that the thyroid state of specific tissue impacts on whole body metabolism thereby affecting the phenotype in adult life Finally, D3 is almost undetectable in the liver of healthy individuals, but robust re-activation of D3 has been found in regenerating liver tissue, in certain hepatic tumors and in sera and liver samples from critically ill humans, thus influencing the systemic thyroid status These results suggest that D3 plays a role in the tissue response to injury and in the imbalance of TH homeostasis commonly observed during critical illness.

Thyroid hormone plays a critical role in the development, maturation, and function of pancreatic cells, where T3 is required for the physiological maturation of pancreatic β-cells to glucose-stimulated insulin-secreting cells Pancreatic cells express both TRα and TRβ isoforms and the activated T3-TR complex directly bind to the promoter of islet transcription factor Mafa thereby resulting in its activation 27 , However, the exact physiological role of TH in glucose homeostasis remains controversial 29 , Although numerous in vitro and ex vivo studies have demonstrated that T3 mediates positive effects on β-cell function, exposure to high doses of TH results in a phenotype of glucose intolerance.

Indeed, hyperthyroidism is associated with glucose intolerance consequent to decreased insulin secretion 31 , 32 and to stimulation of hepatic gluconeogenesis Probably, in hyperthyroid conditions, impaired insulin secretion is not sufficient to suppress high hepatic glucose production.

Accordingly, the prevalence of diabetes mellitus in hyperthyroid patients is approximately double that of non-affected subjects In contrast, systemic hypothyroidism is associated with reduced hepatic gluconeogenesis and enhanced insulin sensitivity, as demonstrated by the onset of a hypoglycemic state after an insulin injection While during vertebrate development, reduced TH levels are important for normal function and for glucose homeostasis of pancreatic β-cells, exposure to high TH doses induces apoptosis of pancreatic β-cells In this context, the TH hormone-inactivating deiodinase D3 plays a fundamental role in lineage fate decisions and endocrine cell specification Indeed, studies in D3KO mice demonstrated that the reduction D3-mediated of TH action is critical for normal maturation and function of pancreatic β-cells D3KO mice exhibited a glucose intolerant phenotype due to impaired glucose-stimulated insulin secretion, reduced size, and absolute mass of pancreatic islet and β-cells, decreased insulin content, and reduced expression of key genes involved in glucose sensing, insulin synthesis, and exocytosis The pancreatic phenotype of the D3KO mice is proof that attenuation of TH-signaling via D3 activation is essential for normal development.

Peripheral TH signals are integrated within the hypothalamus and processed into coordinated responses to regulate energy balance. The center for regulation of food intake and of body weight is the melanocortin system, constituted by three neuronal populations: the pro-opiomelanocortin POMC -expressing neurons, the neuropeptide Y NPY and agouti-related peptide AgRP -co-expressing neurons and the melanocortin 4 receptor MC4R -expressing neurons 37 , The POMC neurons exert an anorexigenic function by activating MC4R neurons, which induce a reduction of food intake and increased energy expenditure.

All these neurons are sensitive to the TH signal that can either activate or inhibit melanocortin neurons, and thus, it is not surprising that local TH metabolism plays a critical role in appetite and feeding regulation.

Changes in central T3 levels occur in various metabolic conditions 39 , for example elevated T3 levels have been found in the hypothalamus during fasting Fasting induces alterations in the thyroid state, namely, a reduction in pituitary D2 levels and liver D1 levels correlated with low peripheral T3 levels in the presence of increased hypothalamic D2 activity.

The increase of T3 in the hypothalamus also causes TRH mRNA suppression 40 , Therefore, under food deprivation, despite a reduction in peripheral TH levels, there is a localized increase in T3 within the hypothalamus, which in turn increases orexigenic signals and decreases TRH production.

The hypothalamus probably maintains low TH levels to preserve energy stores, which would be dissipated in hyperthyroid condition. The fundamental role of deiodinases in the regulation of energy balance in brain has been demonstrated in mouse models of deiodinases depletion The enhanced TH levels alter the functioning of the hypothalamic circuitries, including the leptin-melanocortin system, thereby regulating energy balance and adiposity.

The hypothalamic D2-mediated T4 to T3 conversion is important for the photoperiodic response of the gonads 44 in which fine-tuned D2 and D3 expression tightly regulates LH stimulation TH influences skeletal muscle contraction, regeneration and metabolism All components of the TH signaling process, from TR to TH transporters MCT8 and MCT10 , and D2 and D3, are expressed in the skeletal muscle of rodents and humans During skeletal muscle development, D2 is up-regulated, particularly during the first postnatal days, and decreases at day 30, although its activity returns to high levels during differentiation of muscle stem cells 12 , 48 , In particular, during post-injury regeneration processes, D2 mRNA is up-regulated to enable correct myoblast differentiation D2 is a target of FOXO3, which is a protein involved in myocyte fusion and metabolism as well as in atrophy and autophagy Loss of D2 impairs stem cell differentiation and prevents up-regulation of myogenic transcription factor MyoD thereby increasing the proliferative potential of muscle stem cells.

D2-mediated TH in skeletal muscle influences also muscle fibers. D2-dependent T3 activation influences insulin response in skeletal muscle Indeed, D2KO mice are insulin-resistant, which demonstrates the relevance of D2 in glucose homeostasis. In humans, a common polymorphism of the Dio2 gene, the Thr92Ala substitution in protein D2, which partially impairs enzymatic activity, has been correlated with insulin resistance and diabetes 53 , Furthermore, muscle fibers respond to cold through TH-related mechanisms, namely increased glucose uptake, activation of oxidative pathways and increased mitochondria biogenesis 55 , Interestingly, D2 is up-regulated in muscle after 4 h of cold exposure Moreover, D2 is up-regulated in response to such metabolic signals as bile acids and insulin 1 , 58 and during exercise under β-adrenergic stimulus in order to amplify TH signaling and regulate PGC-1α expression 59 , Coordinated D2-D3 expression is required to fine-tune intracellular TH availability during muscle stem cell differentiation, and in vivo , during muscle regeneration While D2 is essential for a correct T3 surge and the subsequent differentiation of muscle stem cells, D3 fosters muscle stem cell proliferation by lowering TH availability during the early phases of the myogenic program This dual regulation is so critical that D3-depletion in vivo causes massive apoptosis of proliferating satellite cells and drastically impairs a full regeneration process.

These studies highlight the pivotal role of the intracellular TH coordination by the deiodinases in muscle physiology.

Brown adipose tissue is characterized by multilocular lipid droplets and numerous mitochondria, and governs heat production In fact, BAT is activated in response to a high fat diet or cold exposure in order to protect the organism from weight gain and hypothermia.

Thyroid hormone critically influences BAT activity The most obvious metabolic role of D2 is the regulation of energy expenditure in the BAT of small mammals, including human newborns. During cold exposure, the sympathetic nervous system induces D2 expression in brown adipocytes, thereby promoting local T4-to-T3 conversion, and activation of the transcription of target genes involved in the thermogenic program Loss of function of D2 reduces the level of UCP-1, which is normally up-regulated at RNA level by TH.

D2 is thus considered a marker of BAT activity 1 , Interestingly, global D2KO mice are resistant to diet-induced obesity, highly tolerant to glucose, and have a deficit in respiratory quotient at 22°C, while at 30°C they become more susceptible to obesity and develop intolerance to glucose 64 , T3 regulates the expression of several genes during adipogenic differentiation, among which GPD, ME, PEPCK, S14, FAS, and GLUT4 66 , While D2 activity is important during differentiation, D3 is considered a mitogenic marker in brown pre-adipocytes.

In fact, D3 mRNA and activity are induced by bFGF and aFGF in proliferating brown pre-adipocytes In BAT, T3 also accelerates fatty acid oxidation and lipogenesis through the action of the ACC and ME lipogenic enzymes.

Consequently, D2KO mice have reduced fatty acid oxidation and lipogenesis 4. The primary function of white adipose tissue WAT is to store energy in the form of single large lipid droplets, although it also secretes the leptin and adiponectin adipokines.

White adipocytes differ anatomically and physiologically from brown adipocytes. All TR isoforms and the TH transporter MCT8 are expressed in human subcutaneous adipose tissue Interestingly, D1 expression and activity are increased in the subcutaneous and visceral WAT of obese subjects A high-fat diet stimulates D1 and leptin expression, while caloric restriction decreases D1 activity as well as leptin levels, and increases levels of the leptin mediator SCD Leptin overexpression increases D1 activity and down-regulates SCD-1 expression Similar to brown adipocytes, in white adipocytes, D2 plays an important role in lipogenesis and in the regulation of the expression of genes related to adipocyte differentiation, while D3 sustains the proliferation of white adipocytes Interestingly, thyroidectomized mice have an increased level of both D1 and D2 Moreover, D2 is expressed also in human pre-adipocytes although its role is unclear Monodeiodination is quantitatively the most important pathway of TH activation.

Within peripheral tissue, multiple pathways modulate TH availability. These pathways govern the action and regulation of deiodinase expression, the action of TH transporters, and the expression and crosstalk of TH receptors with multiple partners.

This intricate network of TH modifiers increases the sensitivity and the speed of responses to changes induced in the internal and external environment by the thyroid signal. The price to be paid for this is an intricate regulation of each component in time and space.

Given the vast spectrum of metabolic body functions regulated by the TH signal, the deiodinases represent a powerful tool with which to modulate cellular metabolism in specific tissues without perturbing systemic levels of THs.

Consequently, the development of drugs that target deiodinase action is the next challenge in this field. Extensive work is still required to delineate the kinetics and regulation of the deiodinase enzymes in specific tissues to understand the full spectrum of their biological roles.

Thus, pharmacological research is poised to develop deiodinase modulators aimed at driving specific metabolic outcomes. Targeting tissue-specific TH actions may result in novel and safe therapeutic options for metabolic dysfunctions.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. and from AIRC to MD. IG We thank Jean Ann Gilder Scientific Communication srl.

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Rather than having a "faster" or "slower" metabolism, it's most accurate to describe your metabolism as efficient or functional versus inefficient or dysfunctional.

Metabolism is made up of several components. The winning formula for maintaining your weight is that what you take in in terms of calories should equal the calories you expend on a daily basis.

The following illustrates the calculation. To lose weight, you have to reduce the number of calories taken in from food, increase the number of calories expended, or both. Surprisingly, many overweight people and people with thyroid disease, in particular, do not take in any more calories than people of average weight and can sustain or even gain weight at far lower daily calorie levels.

If you fit into this category, this means that you are likely starting with a reduced basal metabolism, or resting metabolic rate, known as RMR. You may also be expending fewer calories from physical activity, and in some cases, the thermic effect of the food you eat may be blunted.

The end result: You aren't burning as many calories as someone of a similar weight with a more functional metabolism.

If you have undiagnosed hypothyroidism, or your condition is not adequately treated by your healthcare provider, almost anything you do to raise your metabolism on the output side may fail. So the first essential step is to get a thyroid test. And if you have been tested and are being treated, you need to make sure your thyroid treatment is optimized, and that you are taking the proper drug and dosage.

Metabolism is somewhat a function of genetics, but you can increase basal metabolism by building muscle. Muscle cells are up to eight times more metabolically active than fat cells, and muscle burns more calories than fat. Adding weight-bearing or resistance exercise, such as weightlifting, T-Tapp , or exercise bands, can help increase your basal metabolism.

Dehydration can also contribute to an inefficient metabolism by affecting body temperature. When you are dehydrated, your body temperature drops slightly and causes your body to store fat as a way to help raise or maintain the temperature.

Making sure you drink enough liquids, preferably at least 64 ounces eight glasses of water per day, to avoid this metabolic pitfall. Making the water cold can also add an additional metabolic boost. Aerobic exercise that increases the heart rate can raise metabolism while you're exercising.

Some experts believe that aerobic exercise also boosts resting metabolism for several hours, as muscles burn calories to recover and repair themselves. Resting metabolic rate typically increases as much as two to three times more after eating proteins versus carbohydrates and fats.

Digesting complex, high-fiber carbohydrates like high-fiber vegetables and cereals burn more calories than simple carbohydrates. You can increase the thermic effect of the foods you eat by focusing on quality protein, high-fiber fruits and vegetables, and an occasional high-fiber grain to meet your caloric needs.

If your metabolism is more of a challenge than you expected, you may want to explore measuring it precisely. RMR testing using devices such as DexaFit or BodySpec can evaluate your actual RMR, and the results can help you carefully determine the best way forward in crafting a successful weight loss plan.

Be sure to meet with your healthcare provider, as well—this way, you can formulate a unique, healthy "metabolic boosting," plan that is safe and right for you. Camps SG, Verhoef SP, Westerterp KR. Body Type Quiz Find a Doctor - EverydayHealth Care Hydration Calculator Menopause Age Calculator Symptom Checker Weight Loss Calculator.

See All. DailyOM Courses. About DailyOM Most Popular Courses New Releases Trending Courses See All. By Marie Suszynski. Medically Reviewed.

Elise M. Brett, MD. If you imagine that your metabolism is a revving engine, thyroid hormone would be the gas. A slower metabolism can make weight loss difficult, but it causes other symptoms too, such as fatigue and weakness. Try these tips: Take thyroid hormone.

Editorial Sources and Fact-Checking. Resources Can You Boost Your Metabolism? June 22, Cleveland Clinic. April 19, The Truth About Metabolism. Harvard Health Publishing. May 30, Boschmann M et al.

Water-Induced Thermogenesis. The Journal of Clinical Endocrinology and Metabolism. December Charrière N et al. PLOS ONE. Abdi H, Kazemian E, Gharibzadeh S, et al. Association between thyroid function and body mass index: a year follow-up. Ann Nutr Metab.

American Thyroid Association. Food and Drug Administration. LEVO-T®: highlights of prescribing information. Gruzdeva O, Borodkina D, Uchasova E, Dyleva Y, Barbarash O.

Leptin resistance: underlying mechanisms and diagnosis. Diabetes Metab Syndr Obes. Iwen KA, Schröder E, Brabant G. Thyroid hormones and the metabolic syndrome. Eur Thyroid J. Thyroid and weight FAQs. By Mary Shomon Mary Shomon is a writer and hormonal health and thyroid advocate.

She is the author of "The Thyroid Diet Revolution. Use limited data to select advertising. Create profiles for personalised advertising. Use profiles to select personalised advertising. Create profiles to personalise content. Use profiles to select personalised content.

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List of Partners vendors. Thyroid Disease. Weight Loss. By Mary Shomon. Medically reviewed by Do-Eun Lee, MD. Table of Contents View All. Table of Contents. Thyroid Hormones. How to Boost Metabolism: 12 Natural Ways. Are You Taking Too Much Levothyroxine?

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