Adiposity mediates the association between whole grain consumption, glucose homeostasis and insulin resistance: findings from the US NHANES

Mohsen Mazidi, Niki Katsiki, Andre Pascal Kengne, Dimitri P. Mikhailidis, Maciej Banach

Growing evidence suggests an inverse association between whole grain (WG) consumption and insulin resistance (IR) or inflammation. However, it is still unclear whether adiposity plays a role in this relationship. We investigated whether the associations between WG intake with IR, glucose homeostasis and inflammation are mediated by adiposity in US adults. The 2005-2010 National Health and Nutrition Examination Surveys participants were included. WG intake was assessed and markers of IR and glucose homeostasis, inflammation, general and central adiposity. Analysis of co-variance and mediation analysis were applied, while accounting for survey design. Overall 16,621 participants were included in this analysis (mean age = 47.1 years, 48.3% men). After adjustment for age, gender, and race, mean C-reactive protein (CRP), apolipoprotein B (apo-B), fasting blood glucose (FBG), insulin, homeostatic model assessment of IR (HOMA-IR) and β cell function (HOMA-β), hemoglobin A1c (HbA1c), and 2 h glucose after an oral glucose tolerance test decreased with increasing quarters of WG (all p < 0.001). Body mass index (BMI) had significant mediation effects on the associations between WG intake and CRP, apo-B, fasting glucose, insulin, HOMA-IR, HOMA-B, HbA1c, triglyceride to high density lipoprotein-cholesterol (TG:HDL-C) ratio and triglyceride-glucose (TyG) index (all p < 0.05) after adjustment for age, gender, race/ethnicity, educational status, smoking and level of physical activity. Both waist circumference (WC) and anthropometrically predicted visceral adipose tissue (apVAT) mediated the association between WG intakes with CRP, FBG, HbA1c, TG:HDL-C ratio and TyG index, i.e. WC and apVAT had indirect effect (all p < 0.05). Our findings provide insights into the favourable impact of WG consumption on IR and inflammation, which may be affected by both central and visceral adiposity, i.e. the link between WG with IR and inflammation is more mediated in overweight/obese compared with lean individuals.