Relation of −55CT polymorphism of uncoupling protein 3 gene with fat mass and insulin resistance in morbidly obese patients

Abstract 

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/m²) 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/m², 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/m², 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.