Human resistin gene polymorphism is associated with visceral obesity and fasting and oral glucose stimulated C-peptide in the Québec Family Study

Abstract

Obesity and insulin resistance are common features of Type 2 Diabetes. A new protein called resistin has been shown to be secreted by adipocytes in mice and to influence insulin sensitivity. The goal of the present study was to investigate the associations between one polymorphism (g-420C>G) of the human resistin gene and phenotypes related to adiposity and glucose metabolism. We genotyped 725 (including 42 diabetics) adult subjects participating in the Quebec Family Study (QFS) by a minisequencing method. Forty-two were diabetic subjects. Phenotypes measured were: body mass index (BMI) and waist circumference (WC), % body fat (PFAT) and fat mass (FM) assessed by under water weighing, abdominal total, subcutaneous and visceral fat assessed by computed tomography and fasting plasma glucose, insulin and C-peptide and their responses to an oral glucose tolerance test (OGTT). Comparisons between genotypes were performed in non-diabetic men (no.=280) and women (no.=403) separately by analyses of covariance (ANCOVA). Among men, g-420 G homozygotes had less visceral fat (p < 0.05), lower levels of acute insulin responses to an OGTT and lower levels of C-peptide in a fasting state and in responses to an OGTT than carriers of the C allele (p < 0.01). These associations were independent of age and adiposity but were not observed in women. These results suggest that in men, the human resistin gene is associated with reduced amount of visceral obesity and lower insulin secretory responses to a glucose load.

Adipokines and the insulin resistance syndrome in familial partial lipodystrophy caused by a mutation in lamin A/C

“…However, reports of resistin in humans remain more controversial [53]. Thus, although some studies demonstrate that circulating resistin [54] or resistin gene polymorphism [55] have significant positive relationships with obesity and insulin resistance, in others findings have been discordant [56]. Despite the lack of correlation of resistin with most of the anthropometric and metabolic variables, in the FPLD group, those with total and HDL-cholesterol as well as triglycerides were significant.…”

Loss of Resistin Improves Glucose Homeostasis in Leptin Deficiency

“…These studies reveal that the actions of resistin depend on the presence or absence of leptin, as well as interaction with diet. In humans, where resistin appears to be primarily derived from macrophages rather than adipocytes, some studies have failed to demonstrate a significant association between resistin and adiposity and glucose (25,26), whereas others have shown increased resistin levels in obesity, inflammation, and type 2 diabetes (27)(28)(29). Although the connection between resistin and insulin sensitivity in humans has yet to be proven, our findings raise the possibility of cross talk between resistin and leptin in the regulation of energy and glucose homeostasis.…”

Variations in Inflammatory Biomarkers Following the Addition of Sitagliptin in Patients with Type 2 Diabetes not Controlled with Metformin

“…In the current study, we focused our attention on the effects of sitagliptin on various inflammatory biomarkers. Resistin is secreted by mononuclear cells and activated macrophages and has been reported to be elevated in adipose tissue and serum in patients with obesity and insulin resistance, although other studies have failed to establish such a relationship (24)(25)(26)(27)). Resistin appears to confer an increased risk of inflammation and atherosclerosis.…”