RESUMO
BACKGROUND: Imbalance in hormonal levels, regulated by host genetic factors, are known to be a major cause of obesity. Therefore, we aimed to evaluate association of genetic polymorphisms of β2-adrenergic receptor (β2-AR) and insulin receptor substrate-1 (IRS-1) with hormonal levels in northern Indian obese. METHODS: A total of 111 obese and 89 age matched non-obese subjects were studied after taking detailed clinical profile. Hormonal assays in serum/plasma for different hormones were done using IRMA and RIA kits. Genetic analysis of β2-AR (-47 and -20, T to C) and IRS-1 (Arg972Gly) was done using PCR-RFLP. STATISTICAL ANALYSIS: Statistical analysis was performed by SPSS (version 11.5) software. All continuous variables were expressed as mean ± SD and tested by ANOVA test. Comparisons of categorical variables were assessed using X2 tests or Fisher's exact test. P-value <0.05 was considered as significant. RESULTS: Analysis showed that obese subjects had significantly higher value of blood pressure (systolic), WHR, leptin insulin and glucagon and lower value of GH. In β2-AR (-47) T/C and IRS-1 Gly972Arg gene polymorphisms we did not found significant differences in genotype or allele frequencies. Moreover, none of the studied hormonal or metabolic parameters showed any association with the gene polymorphisms. CONCLUSIONS: Study reveals no significant association of β2-AR (-47 and -20, T to C) and IRS-1 Gly 972 Arg polymorphisms with obesity in northern Indians.
RESUMO
Present study examined the effect of short-term cigarette smoking on insulin resistance and lipid profile in asymptomatic healthy adults. This case control study comprised of 44 healthy male subjects in the age group of 18-40 yrs having BMI 25+3 and WHR < 1.0. Of these 22 smokers were included in the study group and 22 non-smokers in the control group. Subject selection was done such that one smoker and one non-smoker sibling or first degree male relative were selected from the same family. We compared fasting plasma glucose, insulin, lipid profile, and homeostatic model assessment index (HOMA Index) as a measure of insulin resistance between both the groups. Our observation showed that significantly higher values of serum glucose (133.36 +/- 23.45 mg/dl; P < 0.001), serum insulin (32.04 +/- 6.0 2 microU/ml; P < 0.001) and HOMA index (3.62 +/- 0.21; P < 0.001) were found in smokers as compared to non-smokers (serum glucose 86.95 +/- 19.32 mg/dl, insulin 20.09 +/- 4.8 microU/ml, HOMA index 3.29 +/- 0.30). No significant difference was observed for number of subjects having insulin resistance (HI > 3.8) and lipid profile in both the groups. Thus it appears that smokers are prone to develop hyperinsulenemia, hyperglycemia and the metabolic syndrome.