Adiponectin Gene Polymorphisms Are Associated with Long-Chain ω3-Polyunsaturated Fatty Acids in Serum Phospholipids in Nondiabetic Koreans

Abstract

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. Nondiabetic 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 insulin resistance (HOMA-IR) were also measured. The 276G carriers (n = 1082) showed lower high-density lipoprotein 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. After adjusted for age, sex, body mass index, and the proportion of 18:2ω6 and 18:3ω3 (biomarkers of long term essential FA intake), the 276G carriers showed lower proportions of total ω3FA (P = 0.026), 20:5ω3 (P = 0.021), and 22:5ω3 (P = 0.024) in serum phospholipids. Among FAs in serum phospholipids, 18:2ω6 highly correlated with ω3-polyunsaturated FA (PUFA) intake (r = 0.260, P < 0.001) and adiponectin (r = 0.150, P < 0.001). The 276G carriers with a higher proportion of 18:2ω6 (≥12.5%) exhibited more pronounced characteristics, i.e. lower adiponectin (P < 0.001), lower high-density lipoprotein cholesterol (P = 0.004), higher HOMA-IR (P = 0.013), and lower long-chain ω3PUFAs (20:5ω3, 22:5ω3, and 22:6ω3, P < 0.001). Additionally, the effect of 276G>T on the relationship between adiponectin and HOMA-IR was modified by 18:2ω6 proportion. ADIPOQ 276G is associated with reduced proportion of long-chain ω3PUFAs in serum phospholipids in nondiabetic Koreans.