Clinical evidences reported subclinical alterations of thyroid function in obesity, although the relationship between thyroid status and obesity remains unclear. We cross-sectionally investigated the influence of metabolic features on hypothalamic-pituitary- thyroid axis in obesity. We enrolled 60 euthyroid subjects with no history of type 2 diabetes mellitus and assessed the relationship of thyroid function with insulin-resistance, measured using euglycemic clamp, and abdominal fat volume, quantified by CT-Scan. TSH correlated with BMI (r=0.46;p=0.02), both visceral (r=0.58;p=0.02) and subcutaneous adipose tissue volumes (r=0.43;p=0.03) and insulin-resistance (inverse relationship with insulin-sensitivity - glucose uptake: r=-0.40 p=0.04). After performing multivariate regression, visceral adipose tissue volume was found to be the most powerful predictor of TSH (β=3.05;p=0.01), whereas glucose uptake, HDL cholesterol, LDL cholesterol, subcutaneous adipose tissue volume and triglycerides were not. To further confirm the hypothesis that high-normal TSH values could be dependent on adipose tissue, and not on insulin-resistance, we restricted our analyses to moderately obese subjects BMI ranging 30-35 kg/ m2. This subgroup was then divided in insulin-resistant and insulinsensitive according to the glucose uptake (≤ or > 5 mg·kg-1·min-1, respectively). We did not find any statistical difference in TSH (insulin-resistant: 1.62±0.65 μU/mL vs. insulin-sensitive:1.46 ± 0.48;p=NS) and BMI (insulin-resistant: 32.2 ± 1.6 kg/m2 vs. insulin-sensitive:32.4 ± 1.4;p=NS), thus confirming absence of correlation between thyroid function and insulin-sensitivity per se. Our study suggests that the increase in visceral adipose tissue is the best predictor of subclinical thyroid dysfunction in obesity, independently from the eventual concurrent presence of insulin resistance.
|Publication status||Published - 2012|
- abdominal obesity
- insulin resistance
- subcutaneous adipose tissue
- visceral fat