Some studies have pointed to a role of uncoupling protein 3 (UCP3) in the regulation of whole-body energy homoeostasis and regulation of fat distribution. The aim of our study was to investigate the influence of -55CT polymorphism of UCP3 gene on fat mass and insulin resistance in morbidly obese patients. A population of 47 obese subjects (body mass index [BMI] >40 kg/m(2)) was selected randomly in a prospective way. A nutritional evaluation was performed. Dietary intake and exercise were recorded. The mean age was 48.2 +/- 15.4 years; and the BMI was 44.7 +/- 4.7 kg/m(2), with 10 men (21.3%) and 37 women (78.7%). Thirty-two (68.1%) had the genotype -55CC (wild-type group), and 15 patients (31.9%) had -55CT (mutant-type group). In the mutant-type group, insulin (20.6+/-10.8 vs 31.2 +/- 17.4 mIU/L, P < .05), homeostasis model assessment (5.3 +/- 2.7 vs 8.7 6.6, P < .05), weight (114.1 +/- 17.3 vs 122.8+/-19.1 kg, P < .05), BMI (44.1 +/- 4.6 vs 45.7 +/- 6.3 kg/m(2), P < .05), fat mass (56.3 +/- 11.4 vs 61.4 +/- 15.1 kg, P < .05), and waist circumference (124.8 +/- 12.5 vs 128.3 +/- 9.1 cm, P < .05) were higher than those in the wild-type group. Adiponectin levels were higher in wild-type group than mutant-type group (70.3 +/- 26.1 vs 30.5 +/- 32.5 ng/mL, P < .05). In conclusion, mutant-type group of -55CC UCP3 gene patients had higher weight, fat mass, and insulin resistance than wild-type group.
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