Expression of leptin and β3-adrenergic receptors in rat adipose tissue in altered thyroid states

Fain, John N.; Coronel, Elizabeth C.; Beauchamp, Michael J.; Bahouth, Suleiman W.

doi:10.1042/bj3220145

Cited by 63 publications

(57 citation statements)

References 53 publications

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“…In light of these results, alterations in thyroid status might lead to compensatory changes in circulating leptin. Thus, our findings are in agreement with some studies and support an inverse relationship between thyroid activity and leptin production within the adipose tissue [18,20,21].…”

Section: Discussionsupporting

confidence: 82%

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TSH Influences Serum Leptin Levels Independent of Thyroid Hormones in Hypothyroid and Hyperthyroid Patients

et al. 2005

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Abstract. Leptin is considered to play a role in maintenance of energy balance and body weight by neuroendocrine mechanisms. The physiological mechanisms for thyroid hormone-induced alteration in serum leptin are not well known. In the present study, the relationship between thyroid hormones and leptin levels was investigated in patients with overt hypothyroidism and hyperthyroidism before and after successful treatment. Leptin levels were determined by radioimmunoassay and body mass index (BMI) was calculated for each subject. Serum leptin levels of 26 hypothyroid and 22 hyperthyroid patients were compared with those of 20 healthy volunteers who comprised the controls. Serum leptin levels of hypothyroid patients (28.4 ± 4.1 ng/ml) were found to be significantly higher than the controls (19.1 ± 3.2 ng/ml) (p<0.01), whereas hyperthyroid patients had lower levels (10.7 ± 1.2 ng/ml) (p<0.01). In hypothyroid patients, serum leptin levels were decreased significantly to 20.6 ± 2.1 ng/ml with thyroxin treatment (p<0.05). However, in hyperthyroid group, serum leptin levels were increased to 12.4 ± 2.2 ng/ml by treatment (p>0.05). BMI was not changed with the treatment in either group. The serum leptin levels were correlated with BMI and thyrotropin (TSH) in both hypothyroid and hyperthyroid patients. Serum leptin levels are affected in thyroid disorders and the correlation of leptin with TSH is independent of thyroid hormones.

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Section: Discussionsupporting

confidence: 82%

“…Fain et al observed increased mRNA expression of leptin in adipocytes of hypothyroid rats, and a reduction in expression in response to T3 treatment [20]. A recent study showed that TSH releases leptin by a direct action at the adipocytes in human adipose tissue via the presence of TSH receptors in adipose tissue [21].…”

Section: Discussionmentioning

confidence: 99%

TSH Influences Serum Leptin Levels Independent of Thyroid Hormones in Hypothyroid and Hyperthyroid Patients

et al. 2005

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“…Theoretically, one would expect an inhibitory effect of thyroid hormones on leptin secretion, since thyroid hormones have a permissive role on the effects of catecholamines on betaadrenergic receptors, and since stimulation of these receptors suppresses leptin expression (231). This seems consistent with the inverse relation which is seen between leptin and thyroid hormone levels.…”

Section: Leptin and The Thyroid Axissupporting

confidence: 70%

Human leptin: from an adipocyte hormone to an endocrine mediator

2000

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Leptin is a mainly adipocyte-secreted protein that was discovered 5 years ago. Most of the research following this discovery focused on the role of leptin in body weight regulation, aiming to illuminate the pathophysiology of human obesity. However, more and more data are emerging that leptin is not only important in the regulation of food intake and energy balance, but that it also has a function as a metabolic and neuroendocrine hormone. It is now clear that it is especially involved in glucose metabolism, as well as in normal sexual maturation and reproduction. Besides this, interactions with the hypothalamic±pituitary±adrenal, thyroid and GH axes and even with haematopoiesis and the immune system have also been described. It has been shown that leptin secretion by the adipocyte is partly regulated by other hormones, such as insulin, cortisol, and sex steroids, mainly testosterone. Also, other hormones like thyroid hormone and GH are possibly involved in leptin synthesis. Leptin itself exerts effects on different endocrine axes, mainly on the hypothalamic±pituitary±gonadal axis and on insulin metabolism, but also on the hypothalamic±pituitary±adrenal, thyroid and GH axes.Leptin may thus be considered a new endocrine mediator, besides its obvious role in body weight regulation.

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“…However, none of the two hormones measured in our study because of their known circadian rhythm are likely to be involved. Tri-iodothyronine administration to hypothyroid rats actually resulted in a rapid decrease in ob mRNA (22). Glucocorticoids have been shown to potently stimulate ob gene expression and leptin secretion in rats and in man, both in vivo and in vitro (23)(24)(25).…”

Section: Figurementioning

confidence: 99%

Hypoleptinemia in patients with anorexia nervosa: loss of circadian rhythm and unresponsiveness to short-term refeeding

Balligand

Brichard

et al. 1998

European Journal of Endocrinology

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Leptin is a protein encoded by the ob gene that is expressed in adipocytes and regulates eating behavior via neuroendocrine mechanisms. Plasma leptin levels have been shown to correlate with weight and body fat in normal, obese and anorexic subjects. In the last of these populations, the dynamic profile of plasma leptin levels during short-term refeeding has never been assessed. We thus investigated basal plasma leptin levels in 29 female patients with anorexia nervosa (AN) (age 21.9 Ϯ 1.4 years, body mass index (BMI) 15.2 Ϯ 0.3 kg/m 2 ) and in 80 normal female controls (age 21.2 Ϯ 0.2 years, BMI 20.3 Ϯ 0.3 kg/m 2 , mean Ϯ S.E.M.). Basal plasma leptin levels in AN were decreased by 77% compared with controls (2.5 Ϯ 0.2 vs 11.1 Ϯ 0.7 ng/ml, P < 0.0001). In both AN subjects and controls, plasma leptin levels correlated significantly with BMI (r 2 ¼ 0.448, P < 0.0001 and r 2 ¼ 0.339, P < 0.0001 respectively). Five AN patients (four female, one male, age 22.0 Ϯ 4.7 years, BMI 14.2 Ϯ 0.4 kg/m 2 , body fat 4.3 Ϯ 0.9 kg or 11.0 Ϯ 1.9% of body weight, basal metabolic rate (BMR) 958 Ϯ 122 kcal/day) were studied during a 3-day refeeding period and compared with eight control subjects (two male, six female, age 25.7 Ϯ 1.2 years, BMI 21.3 Ϯ 0.8 kg/m 2 , body fat 15.1 Ϯ 0.9 kg or 24.6 Ϯ 1.7%, BMR 1455 Ϯ 78 kcal/day) submitted to 36-h fasting. The amount of calories administered was based on BMR þ 20% (carbohydrate 60%, protein 17%, fat 23%). In contrast to the rise in leptin levels that occurred during refeeding after a prolonged fast period in normal subjects, plasma leptin levels remained low and unchanged throughout the 3 days of renutrition in AN patients. The circadian rhythm of leptin was also completely abolished. This contrasted with the preserved circadian variations of cortisol, whose mean levels were increased. In conclusion, we confirmed that plasma leptin levels are low in AN and correlate with body weight. We further demonstrated that plasma leptin levels do not respond to short-term refeeding in anorexic patients in whom circadian variations are not restored, which suggests that the acute regulation of leptin by positive changes in energy balance is not preserved under a critical threshold of body fat. [415][416][417][418][419][420] European Journal of Endocrinology 138

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Expression of leptin and β3-adrenergic receptors in rat adipose tissue in altered thyroid states

Cited by 63 publications

References 53 publications

TSH Influences Serum Leptin Levels Independent of Thyroid Hormones in Hypothyroid and Hyperthyroid Patients

TSH Influences Serum Leptin Levels Independent of Thyroid Hormones in Hypothyroid and Hyperthyroid Patients

Human leptin: from an adipocyte hormone to an endocrine mediator

Hypoleptinemia in patients with anorexia nervosa: loss of circadian rhythm and unresponsiveness to short-term refeeding

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