Influence of Pro12Ala peroxisome proliferator-activated receptor γ2 polymorphism on glucose response to exercise training in type 2 diabetes

Abstract

Aims/hypothesis: Exercise training improves glycaemic control in some but not all individuals and little research has been done regarding genetic impact on the exercise training response in type 2 diabetes. The purpose of this study was to investigate the influence of the Pro12Ala variant of the peroxisome proliferator-activated receptor (PPAR) γ2 gene on changes in fasting plasma glucose in response to exercise training. Methods: The study population comprised 139 sedentary type 2 diabetic patients (age: 54.4±7.2; HbA1c: 7.7±0.9%) who completed 3 months of supervised exercise training. The primary outcome variable in our analysis was the post-intervention change in blood glucose. Other assessments included measures of body composition, insulin sensitivity indices and maximal oxygen uptake (VO2max). Results: The frequency of the Ala allele was 8.3% and the genotypes were in Hardy-Weinberg equilibrium. At baseline, neither body composition variables (weight, BMI, waist circumference), glucose homeostasis variables (glucose, insulin, HbA1c, homeostasis model assessment method) nor VO2max were different between genotypes (wild-type: Pro12Pro n=117, Ala carriers: X12Ala n=22). The exercise-training intervention led to similar improvements in body composition and glucose homeostasis variables in both genotype groups (p<0.05). The change in fasting plasma glucose was significantly different between PPARγ2 genotypes (-1.66 mmol/l vs -0.54 mmol/l, Ala carriers and wild-type, respectively) (p=0.034 unadjusted and p=0.089 including baseline glucose) and the significant association between genotype and glucose response remained after adjusting for statistically significant predictors (age, changes in insulin and BMI [p=0.015]) and including baseline glucose, insulin and BMI (p=0.031). Conclusions/interpretation: These data suggest that the Pro 12Ala polymorphism may influence the glycaemic response to exercise in type 2 diabetes. © Springer-Verlag 2005.