A personalised diet approach study: Interaction between PPAR-γ Pro12Ala and dietary insulin indices on metabolic markers in diabetic patients.

BACKGROUND: The present study aimed to investigate the effect of the interaction between peroxisome proliferator-activated receptor gamma (PPAR-γ) Pro12Ala polymorphisms and dietary insulin load and insulin index (DIL and DII) on cardio-metabolic markers among diabetic patients. METHODS: This cross-sectional study was conducted on 393 diabetic patients. A food-frequency questionnaire was used for DIL and DII calculation. PPAR-γ Pro12Ala was genotyped by a polymerase chain reaction-restriction fragment length polymorphism method. Biochemical markers, including total cholesterol, low-density lipoprotein, high-density lipoprotein, triglyceride, superoxide dismutase, C-reactive protein, total antioxidant capacity, pentraxin-3, isoprostaneF2α, interleukin-18, leptin and ghrelin, were measured by a standard protocol. RESULTS: Risk-allele carriers (CG, GG) had higher obesity indices [body mass index (pinteraction = 0.006) and WC (pinteraction = 0.04)] compared to individuals with the CC genotype when they consumed a diet with higher DIL and DII respectively. Besides, carriers of the G-allele who were in the highest tertile of DIL had lower high-density lipoprotein (pinteraction = 0.04) and higher isoprostaneF2α (pinteraction = 0.03) and pentraxin-3 (pinteraction = 0.03). Moreover, the highest tertile of the DII, showed an increase in interleukin-18 (pinteraction = 0.01) and lower superoxide dismutase (pinteraction = 0.03) for risk-allele carriers compared to those with CC homozygotes. CONCLUSIONS: We revealed that the PPAR-γ Pro12Ala polymorphism was able to intensify the effect of DIL and DII on cardiovascular disease risk factors; risk-allele carriers who consumed a diet with high DIL and DII score were more likely to be obese and have higher inflammatory markers. Also, protective factors against cardiovascular disease risk factors were reduced significantly in this group compared to CC homozygotes.