Gene-nutrient interactions and gender may modulate the association between ApoA1 and ApoB gene polymorphisms and metabolic syndrome risk

Abstract

Objective: Dyslipidemia is a key feature of the metabolic syndrome (MetS), which is determined by both genetic and dietary factors. Methods: We determined relationships between ApoA1 and ApoB polymorphisms and MetS risk, and whether dietary fat modulate this in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). Results: ApoB rs512535 and ApoA1 rs670 major G allele homozygotes had increased MetS risk (OR 1.65 [CI 1.24, 2.20] P = 0.0006, OR 1.42 [CI 1.08, 1.87] P = 0.013), which may be, partly, explained by their increased abdominal obesity and impaired insulin sensitivity (P < 0.05) but not dyslipidemia. Interestingly these associations derived primarily from the male GG homozygotes (ApoB rs512535 OR 1.92 [CI 1.31, 2.81] P = 0.0008, ApoA1 rs670 OR 1.50 [CI 1.05, 2.12] P = 0.024). MetS risk was exacerbated among the habitual high-fat consumers (> 35% energy) (ApoB rs512535 OR 2.00 [CI 1.14, 3.51] P = 0.015, OR 1.58 [CI 1.11, 2.25] P = 0.012 for ApoA1 rs670). In addition a high monounsaturated fat (MUFA) intake (> 14% energy) increased MetS risk (OR 1.89 [CI 1.08, 3.30] P = 0.026 and OR 1.57 [CI 1.10, 2.40] P = 0.014 for ApoB rs512535 and ApoA1 rs670, respectively). MetS risk was abolished among the habitual low-fat consumers (< 35% energy). Saturated and polyunsaturated fat intake did not modulate MetS risk. Conclusion: ApoB rs512535 and ApoA1 rs670 may influence MetS risk. Apparent modulation of these associations by gender and dietary fat composition suggest novel gene-gender-diet interactions.