Serum leptin levels and bioelectrical impedance assessment of body composition in patients with Graves' disease and hypothyroidism.
We investigated whether thyroid status modulates serum leptin concentrations and body composition as determined by bioelectric impedance analysis (BIA). The percent body fat mass (%FM) in male Graves' disease was significantly lower than that in age- and sex- matched normal subjects, at the levels of 11.4+/-6.4% (mean+/-SD) vs 19.9+/-9.2% for men (n=12, P<0.05) but not for women (22.6+/-7.6% vs 24.9+/-13.1%, n=28). In contrast, in female hypothyroidism (n=11) %FM was significantly higher than that in normal subjects (32.9+/-11.5%, P<0.01). Among other body composition parameters, the percentage of body water (%BW), and lean body mass (LBM) were significantly lower in hypothyroid patients, and the ECM (extracellular mass)/BCM (body cell mass) ratio was significantly (P<0.0001) increased in Graves' disease which was the result of marked depletion of BCM with concomitant expansion of ECM. The serum leptin levels were significantly decreased in male Graves' patients (2.3+/-0.7 ng/ml, P<0.05), whereas in female Graves' patients (8.8+/-5.9 ng/ml) and patients with hypothyroidism (9.5+/-7.6 ng/ml), the levels were not different from those of normal controls matched for BMI or %FM. There was a positive correlation between serum leptin levels and %FM in female Graves' patients (r=0.635, P=0.001) and in hypothyroid patients (r=0.801, P=0.014) but not in male Graves patients. There was no significant relationship between serum leptin levels and thyroid hormones, TRAb, or TSAb. In euthyroid obese subjects there was a positive relationship between serum leptin levels and serum TSH levels (r=0.37, P<0.01). These results suggest that hyperthyroidism is characterized by the decreased fat mass and serum leptin levels in men, but female patients appear to be resistant to the effect of thyroid hormones. Together with previous reports, thyroid status has a minor role in the regulation of serum leptin levels.
Miyakawa
M
M
Department of Internal Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical University, Japan.
Tsushima
T
T
Murakami
H
H
Isozaki
O
O
Takano
K
K
D000328:Adult; D001323:Autoantibodies / Q000097:blood; D001823:Body Composition; D015992:Body Mass Index; D001834:Body Water; D017097:Electric Impedance; D005260:Female; D006111:Graves Disease / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D007037:Hypothyroidism / Q000188:drug therapy / Q000503:physiopathology*; D018828:Immunoglobulins, Thyroid-Stimulating / Q000097:blood; D020738:Leptin / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D054411:Receptors, Leptin; D011989:Receptors, Thyrotropin / Q000097:blood; D013963:Thyroid Hormones / Q000097:blood; D013972:Thyrotropin / Q000097:blood
D001323:Autoantibodies; D018828:Immunoglobulins, Thyroid-Stimulating; C515448:LEPR protein, human; D020738:Leptin; D054411:Receptors, Leptin; D011989:Receptors, Thyrotropin; D013963:Thyroid Hormones; C094372:thyrotropin-binding inhibitory immunoglobulin; D013972:Thyrotropin