Abstract:Background: Little is known about changes in thyroid function in obese children. An influence of leptin on thyroid hormone synthesis has been proposed. Aims: To examine thyroid function and leptin concentrations in obese children. Methods: Triiodothyronine (T3), thyroxine (T4), thyroid stimulating hormone (TSH), and leptin were measured in 118 obese children (aged 4.5-16 years); thyroid function was also determined in 107 healthy children of normal weight. T3, T4, and TSH were analysed in 55 obese children who… Show more
“…The observation of elevated plasma sOB-R levels concentrations in children (Kratzsch et al, 2002) and the increased BL fraction, here reported, may contribute to the temporary blockade of the reproductive axis in prepubertal children, which may be overcome, once an increase of FL occurs, in association with an increased adiposity and possibly other factors, giving rise to pubertal development. No relationship between thyroid function and leptin concentrations were found in DS children, as also shown in subjects with congenital hypothyroidism (Asami et al, 2000) and obesity (Reinehr & Andler, 2002), whereas an inverse correlation between leptin and TSH was found in normal children of short stature (Ghizzoni et al, 2001). These discrepancies are similar to those observed in adults with or without thyroid diseases (Corbetta et al, 1997;Valcavi et al, 1997;Korbonits, 1998).…”
Objective: To evaluate plasma total, free (FL) and protein-bound (BL) leptin in children with Down's syndrome (DS) and different degrees of adiposity and its relationship with thyroid stimulating hormone (TSH), free thyroxine (FT 4 ), and free triiodothyronine (FT 3 ). Subjects: A total of 24 prepubertal clinically euthyroid DS children. Methods: Plasma leptin, TSH, FT 4 , and FT 3 concentrations were determined by immunometric/radioimmunologic assays. FL and BL were evaluated by fast protein liquid chromatography. Results: In DS children, leptin circulates in two fractions, corresponding to BL and FL. The amount of BL and FL is negatively and positively correlated to body mass index (BMI), respectively. Plasma leptin concentrations correlate with BMI, but not with TSH, FT 4 , and FT 3 . Conclusions: In prepubertal DS children, leptin circulates as both BL and FL, correlates with adiposity and its concentration appears independent of thyroid function. Sponsorship: MIUR, Università degli Studi di Milano, Banca Popolare di Milano Foundation.
“…The observation of elevated plasma sOB-R levels concentrations in children (Kratzsch et al, 2002) and the increased BL fraction, here reported, may contribute to the temporary blockade of the reproductive axis in prepubertal children, which may be overcome, once an increase of FL occurs, in association with an increased adiposity and possibly other factors, giving rise to pubertal development. No relationship between thyroid function and leptin concentrations were found in DS children, as also shown in subjects with congenital hypothyroidism (Asami et al, 2000) and obesity (Reinehr & Andler, 2002), whereas an inverse correlation between leptin and TSH was found in normal children of short stature (Ghizzoni et al, 2001). These discrepancies are similar to those observed in adults with or without thyroid diseases (Corbetta et al, 1997;Valcavi et al, 1997;Korbonits, 1998).…”
Objective: To evaluate plasma total, free (FL) and protein-bound (BL) leptin in children with Down's syndrome (DS) and different degrees of adiposity and its relationship with thyroid stimulating hormone (TSH), free thyroxine (FT 4 ), and free triiodothyronine (FT 3 ). Subjects: A total of 24 prepubertal clinically euthyroid DS children. Methods: Plasma leptin, TSH, FT 4 , and FT 3 concentrations were determined by immunometric/radioimmunologic assays. FL and BL were evaluated by fast protein liquid chromatography. Results: In DS children, leptin circulates in two fractions, corresponding to BL and FL. The amount of BL and FL is negatively and positively correlated to body mass index (BMI), respectively. Plasma leptin concentrations correlate with BMI, but not with TSH, FT 4 , and FT 3 . Conclusions: In prepubertal DS children, leptin circulates as both BL and FL, correlates with adiposity and its concentration appears independent of thyroid function. Sponsorship: MIUR, Università degli Studi di Milano, Banca Popolare di Milano Foundation.
“…On the other hand, this study is one of the few investigations that have unequivocally shown that weight loss leads to a reduction in both TSH and FT 3 levels. 9,10,19,20 Several explanations have been proposed to account for the influence of obesity on thyroid hormones. One suggests that the increased TSH level could reflect pituitary adaptation to increased adiposity through adipokines.…”
Section: Discussionmentioning
confidence: 99%
“…Finally, it is possible that obesity leads to a state of TSH and thyroid hormone resistance in peripheral tissues. 20 However, information on the tissue expression of genes encoding for TSH and thyroid hormone receptors, and activity of the respective proteins in relation to body weight or diabetes is scarce. TSHRs have been found in rats and in human adipose tissues.…”
Objective: Increased thyroid-stimulating hormone (TSH) and FT 3 levels are often found in clinically euthyroid obese individuals. Information on thyroid gene expression in human adipose tissue is scarce. The objective of this study was to measure the expression of the TSH receptor (TSHR) and the thyroid hormone receptor (TRa1) genes in subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) in obese individuals and to test the effect of weight loss on these genes. Study Design and Participants: This study is a prospective study involving 107 obese (body mass index (BMI) ¼ 46±8 kg m À2 , 52 with type 2 diabetes or impaired glucose tolerance) and 12 lean nondiabetic participants. A total of 27 obese patients were restudied 1 year after gastric bypass surgery. Total RNA was extracted from SAT and VAT obtained at baseline from all participants, and from SAT in obese patients post surgery. Results: Circulating TSH and FT 3 levels were 170 and 36%, respectively, higher in obese patients than in controls. In SAT, TSHR and TRa1 were reduced in the obese by 67 and 33%, respectively, regardless of glucose tolerance. A similar trend was found in VAT. Post surgery, a BMI decrease of 33% was associated with a decrease in TSH and FT 3 levels and with a 150 and 70% increase in SAT of TSHR and TRa1, respectively. Conclusion: In both subcutaneous and visceral fat, the thyroid gene expression (especially TSHR) is reduced in obesity. The reversal of these changes with major weight loss and the reciprocal changes in plasma TSH and FT 3 levels suggest a role for adipocytes in the regulation of TSH and thyroid hormones.
“…A slight increase in TSH levels has been reported in adults with moderate obesity and in obese Pituitary hormones and bariatric surgery S Camastra et al children. 17,38,39 In rodents, leptin modulates thyroid hormone production in situations in which energy conservation through a reduction in metabolic rate is required. 40 Such effect appears to occur principally at the level of TRH neurons in the paraventricular hypothalamic nucleus (PVN).…”
Moderate obesity is known to be associated with multiple endocrine abnormalities. Less information is available on the hormonal status of patients with morbid obesity and on the effects of major weight loss. We studied 16 severely obese (BMI 40.6-69.9 kg/m 2 ) nondiabetic patients and 7 nonobese (BMI range 24.6-27.7 kg/m 2 ), sex-and age-matched healthy volunteers. During 24 h in a metabolic ward, four meals were administered and hourly blood samples were drawn from a central venous catheter for the measurement of glucose, insulin, leptin, thyrotropic hormone (TSH), growth hormone (GH) and prolactin. Insulin sensitivity was measured by a euglycaemic hyperinsulinaemic clamp. Studies were repeated 6 months after biliopancreatic diversion, a mainly malabsorptive surgical approach, which caused an average weight loss of 35±4 kg (or 26 ± 2% of initial weight). Compared with controls, patients were hyperinsulinaemic (290 ± 31 vs 88 ± 4 pmol l À1 , P ¼ 0.0002), insulin resistant (23.5±2.8 vs 52.9±4.9 mmol min À1 kg FFM À1 , P ¼ 0.0006) and hyperleptinaemic (52.5±5.8 vs 10.9±3 ng ml À1 , P ¼ 0.0002). Plasma TSH levels were increased throughout the day-night cycle (averaging 2.02 ± 0.18 vs 1.09 ± 0.19 mU ml À1 of controls, P ¼ 0.01), whereas serum GH levels were suppressed (0.46±0.10 vs 3.01±1.15, P ¼ 0.002). Following surgery, the hyperinsulinaemia and insulin resistance were fully normalized; in concomitance with a major drop in leptin levels (to 14.4±2.7 ng ml À1 , P ¼ 0.02), TSH decreased and GH increased to near-normal levels. In the whole dataset, mean 24-h leptin levels were directly related to mean 24-h TSH levels after controlling for confounders this relationship was lost only after adjusting for fat mass. We conclude that in morbid obesity leptin is a determinant of changes in pituitary function.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.