Key result
High dietary insulin load linked to higher BMI and inflammation in PPAR-γ risk-allele carriers.
Why the study?
The effect of interaction between PPAR-γ Pro12Ala polymorphisms and dietary insulin load and insulin index on cardio-metabolic markers in diabetic patients was unclear.
Does the interaction between PPAR-γ Pro12Ala polymorphism and dietary insulin indices affect cardio-metabolic markers in diabetic patients?
Cross-Sectional (n=393)
Does the interaction between PPAR-γ Pro12Ala polymorphism and dietary insulin indices affect cardio-metabolic markers in diabetic patients?
p-value: p=0.006
The PPAR-γ Pro12Ala polymorphism intensifies the adverse effects of high dietary insulin load and index on cardiovascular risk factors in diabetic patients.
May heighten obesity and inflammatory risk in diabetic risk-allele carriers on high-DIL/DII diets; leaves open gene-diet personalization hypotheses.
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.
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Abaj et al. (2022) conducted a cross-sectional in Diabetes (n=393). High dietary insulin load and index (DIL and DII) in PPAR-γ Pro12Ala risk-allele carriers vs. CC homozygotes and lower DIL/DII was evaluated on Cardio-metabolic markers including obesity indices, lipids, and inflammatory markers (p=0.006). Diabetic risk-allele carriers of PPAR-γ Pro12Ala consuming diets with high insulin load had higher BMI (P_interaction=0.006) and inflammatory markers compared to CC homozygotes.
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