Interaction between CETP polymorphism and dietary insulin index and load in relation to cardiovascular risk factors in diabetic adults

Abstract

AbstractGene–diet interactions may play an important role in the inter individual diversity observed in on cardiovascular disease (CVD) risk factors. Therefore, in the current study, we examined the interaction of CETP TaqB1 polymorphism with dietary insulin index and load (DII and DIL), in altering on CVD risk factors among type 2 diabetes mellitus (T2DM). In this cross-sectional study, blood samples were collected from 220 type 2 diabetic patients (134 females and 86 male) with a mean age of 52.24 years in Tehran, Iran. DIL and DII were obtained via validated food-frequency questionnaire (FFQ). Taq1B polymorphism was genotyped by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Biochemical markers including total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride (TG), superoxide dismutase (SOD), C-reactive protein (CRP), total antioxidant capacity (TAC), pentraxin-3 (PTX3), isoprostaneF2α (PGF2α). interleukin 18 (IL18), leptin and ghrelin were measured by standard protocol. Patients with B1B1 genotype had lower lipid profiles include LDL/HDL (P < 0.001) and TG (P = 0.04) when they consumed diets higher on the DIL and DII index. Moreover, carriers of B2B2 genotype who were in the last tertile of DIL had higher antioxidant and inflammatory markers include SOD (P = 0.01), PGF2α (P = 0.04) and CRP (P = 0.02). Further, a significant interaction between CETP TaqB1 and DII was shown in terms of WC (P = 0.01), where the highest WC were observed in B2B2 genotype carriers following a DII score. However, the highest inflammatory and antioxidant markers include CRP (P = 0.04), TAC (P = 0.01), SOD (P = 0.02), and PGF2α (P = 0.02) were observed in B2B2 genotype carriers when they consumed diets higher on the DII index. Based on the current study, it could be proposed that CETP polymorphism may be associated with CVD risk factors in T2DM patients with high following insulin indices, including DII and DIL. It seems that CETP Taq1B polymorphism can invert the result produced by insulin. This conclusion illustrates that the CETP Taq1B B1 allele could counteract the CVD risk induced by high DII and DIL.