Adiponectin gene polymorphisms are associated with long-chain ω3 polyunsaturated fatty acids in serum phospholipids in non-diabetic Koreans

Abstract

Objective: Hypoadiponectinemia is caused by interactions between genetic and environmental factors, including the quality of dietary fats. We investigated the association of single-nucleotide polymorphisms (SNPs) in the adiponectin gene (ADIPOQ) with dietary fat intake or fatty acid (FA) composition in serum phospholipids, plasma adiponectin, and insulin resistance (IR). Methods: Non-diabetic subjects (n=1194) were genotyped for three ADIPOQ SNPs (-11377C>G;45T>G;276G>T) after screening of eight sites. Dietary fat intake, FA composition in serum phospholipids, adiponectin, and homeostasis model assessment of IR (HOMA-IR) were also measured. Results: 276G carriers (n=1082) showed lower HDL-cholesterol (P=0.024) and adiponectin (P<0.001) but higher glucose (P=0.015) and HOMA-IR (P=0.005) than 276T/T subjects (n=112). No associations were found in other SNPs. 276G carriers showed a higher proportion of myristic acid and lower proportions of total ω6FA, total ω3FA, 18:2ω6, 20:3ω6, 20:4ω6, 18:3ω3, 20:5ω3, 22:5ω3, and 22:6ω3 in serum phospholipids. After adjusted for age, sex, BMI, and the proportion of 18:2ω6 and 18:3ω3 (biomarkers of long-term essential FA intake), 276G>T was still associated with total ω3FA (P=0.026), 20:5ω3 (P=0.021), and 22:5ω3 (P=0.024). Among FAs in serum phospholipids, 18:2ω6 highly correlated with PUFA intake (r=0.260, P<0.001) and adiponectin (r=0.150, P<0.001). 276G carriers with higher proportion of 18:2ω6 (≥12.5%) exhibited more pronounced characteristics, i.e., lower adiponectin (P<0.001), HOMA-IR (P=0.013), and long-chain ω3PUFAs (20:5ω3, 22:5ω3, and 22:6ω3, P<0.05). Additionally, the effect of 276G>T on the relationship between adiponectin and HOMA-IR was modified by 18:2ω6 proportion. Conclusion: ADIPOQ 276G is associated with reduced proportion of long-chain ω3PUFAs in serum phospholipids in non-diabetic Koreans.