Effect of Thyroid Hormone on Body Composition in Myxedema and Obesity

Kyle, Laurence H.; Ball, Michael F.; Doolan, Paul D.

doi:10.1056/nejm196607072750103

Cited by 44 publications

(14 citation statements)

References 9 publications

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“…In the hyperthyroid animals this situation is not observed. However, their low plasma proteins, seem to indicate that the excess of thyroid hormones also affects protein turnover in agreement with data in the literature (Rupp, Paschkis and Cantarow 1949;Sokoloff and Kaufman 1959;Kyle, Ball and Doolan 1966;Menahan and Wieland 1969).…”

Section: Discussionsupporting

confidence: 91%

“…These results can be the direct consequence of both an impaired protein synthesis {Rupp, Paschkis and Cantarow 1949;Sokoloff and Kaufman 1959;Kyle, Ball and Doolan 1966) (thus affecting preferentially the concentrations of essential amino acids), combined with a higher proteolysis (Menahan and Wieland 1969) in the case of hyperthyroid animals, and other factors not yet known.…”

Section: Discussionmentioning

confidence: 99%

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Plasma Amino Acids in Hypothyroid and Hypertyroid Rats

Remesar¹,

Arola²,

Palou³

et al. 1981

Horm Metab Res

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Plasma amino acid concentrations, together with other metabolic parameters were determined in thyroidectomized rats treated with daily injections of saline (hypothyroid), and 250 M9/kg L-T 4 (hypothyroid). Data were compared with sham-operated controls. There is a general increase in plasma amino acid concentrations in hyperthyroidism, a limited increase only in several amino acid concentrations in hypothyroid rats as compared with controls, and a considerable difference between the plasma aminograms of both groups. Amino acid homeostasis seems to be subject to greater modification in hyperthyroidism than in hypothyroidism.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Plasma Amino Acids in Hypothyroid and Hypertyroid Rats

Remesar¹,

Arola²,

Palou³

et al. 1981

Horm Metab Res

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“…Yet, it was promptly recognized that a decrease in the fat free mass accounted for most of the body weight reduction (7). In line with this effect of thyroid hormones on body size, weight loss is historically reported among the main features of thyrotoxicosis (8).…”

Section: Introductionmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: The crosstalk between thyroid gland and adipose tissue: signal integration in health and disease

Santini

Marzullo

Rotondi

et al. 2014

European Journal of Endocrinology

200

185

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Obesity and thyroid diseases are common disorders in the general population and they frequently occur in single individuals. Alongside a chance association, a direct relationship between 'thyroid and obesity' has been hypothesized. Thyroid hormone is an important determinant of energy expenditure and contributes to appetite regulation, while hormones and cytokines from the adipose tissue act on the CNS to inform on the quantity of energy stores. A continuous interaction between the thyroid hormone and regulatory mechanisms localized in adipose tissue and brain is important for human body weight control and maintenance of optimal energy balance. Whether obesity has a pathogenic role in thyroid disease remains largely a matter of investigation. This review highlights the complexity in the identification of thyroid hormone deficiency in obese patients. Regardless of the importance of treating subclinical and overt hypothyroidism, at present there is no evidence to recommend pharmacological correction of the isolated hyperthyrotropinemia often encountered in obese patients. While thyroid hormones are not indicated as anti-obesity drugs, preclinical studies suggest that thyromimetic drugs, by targeting selected receptors, might be useful in the treatment of obesity and dyslipidemia.

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“…Conversely, thyroid hormones induce expression of several components of the respiratory chain (38). In obese humans known to show impaired mitochondrial substrate oxidation (35), reduced thyroid function was proposed to be a potential cause for increased body weight (17) and reduced oxidative capacity (39,40) potentially by induction of mitochondrial uncoupling (41). The latter, also named adaptive thermogenesis, was proposed to induce energy expenditure by dissipation of energy after a thermogenic proton leak reducing the mitochondrial membrane potential, ultimately leading to reduced long-term energy storage.…”

Section: Discussionmentioning

confidence: 99%

“…Because most nutritive energy is ultimately converted within the mitochondria, researchers have repeatedly addressed the question whether altered mitochondrial activity might influence body mass in mammals. For example, thyroid hormones have been shown to regulate body mass by altering mitochondrial metabolism (17). Furthermore, increased expression of mitochondrial uncoupling proteins (UCPs) or a transcriptional coactivator, PGC1, has been suggested to promote systemic energy expenditure because of thermogenic effects, i.e., generation of heat (18)(19)(20)(21) and a concurrent decrease in OXPHOS (22).…”

mentioning

confidence: 99%

Reduced expression of mitochondrial frataxin in mice exacerbates diet-induced obesity

Pomplun

Voigt²,

Schulz³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Published evidence suggests that adiposity in humans may be linked to impaired energy expenditure for reasons widely unresolved. We have generated mice with a systemic impairment of oxidative phosphorylation (OXPHOS) due to aP2 cre-mediated targeted disruption, and unexpectedly ubiquitous reduction of mitochondrial frataxin protein expression. Only when maintained on a high-calorie diet resembling Westernized eating habits, these animals accumulate additional body fat, leading to increased body mass, and develop diabetes mellitus, despite the fact that both calorie uptake and physical activity were identical to that in control animals. This phenotype is caused by a mild but significant reduction in total energy expenditure paralleled by increased expression of ATP citrate lyase, a rate-limiting step in de novo synthesis of fatty acids and triglycerides. Taken together, these findings indicate that a limited impairment in oxidative metabolism within the mitochondria directly predisposes mammals to excessive body weight gain.metabolism ͉ mitochondria ͉ oxidative phosphorylation

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Effect of Thyroid Hormone on Body Composition in Myxedema and Obesity

Cited by 44 publications

References 9 publications

Plasma Amino Acids in Hypothyroid and Hypertyroid Rats

Plasma Amino Acids in Hypothyroid and Hypertyroid Rats

MECHANISMS IN ENDOCRINOLOGY: The crosstalk between thyroid gland and adipose tissue: signal integration in health and disease

Reduced expression of mitochondrial frataxin in mice exacerbates diet-induced obesity

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