Abstract
Development of obesity is primarily the result of imbalance between energy intake and energy expenditure. Thyroid hormones influence energy expenditure by regulating cellular respiration and thermogenesis and by determining resting metabolic rate. Triiodothyronine influences lipid turnover in adipocytes and impacts appetite regulation through the central nervous system, mainly the hypothalamus. Thyroid-stimulating hormone may also influence thermogenesis, suppress appetite and regulate lipid storage through lipolysis and lipogenesis control. Subclinical hypothyroidism may induce changes in basal metabolic rate with subsequent increase in BMI, but obesity can also affect thyroid function via several mechanisms such as lipotoxicity and changes in adipokines and inflammatory cytokine secretion. The present study investigated the complex and mutual relationships between the thyroid axis and adiposity.
Highlights
Thyroid hormonal tests are routinely ordered when seeking obesity origins [1]
In the arcuate nucleus (ARC), the critical place of the hypothalamus regulating feeding and metabolism, leptin increases the synthesis of anorexic peptides, POMC, α-melanocyte-stimulating hormone (α-MSH) and cocaine- and amphetamineregulated transcript (CART) that are projected from the ARC to the PVN and activate pro-thyrotropin-releasing hormone (TRH) gene expression
It was documented that downregulation of the leptin pathway and decreased expression of DIO2, DIO3 and genes regulated by Thyroid hormones (THs) in the liver may cause fat accumulation that leads to nonalcoholic fatty liver disease (NAFLD) [80]
Summary
Thyroid hormonal tests are routinely ordered when seeking obesity origins [1]. Often higher levels of serum thyrotropin (thyroid-stimulating hormone, TSH) within the reference range or slightly elevated levels are found in the obese state [2,3,4]. Thyroid hormones (THs) and TSH independently regulate the mass and function of adipose tissue; adipose tissue, through the production of adipokines (adipocytokines), affects the activity of the HPT system. TSHR protein expression in the human subcutaneous adipose tissue was determined in 120 patients with different BMIs by Lu et al [15]. TSH β (TSHB) gene mRNA and protein expression in both visceral and subcutaneous human adipose tissue were described; TSH alpha subunit mRNA and protein were not demonstrated [22,23]. Treatment of human mature adipocytes with recombinant TSH enhanced mitochondrial respiratory capacity and ATP production and led to increased adipogenesis-related genes, but no effects were observed in human preadipocytes with low expression of TSHR [23]. Central administration of TRH and TSH in experimental animals caused a reduction in food intake, and similar effects were seen following peripheral administration of TRH (Table 1) [24]
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