Table 1.
Gene-nutrient interactions which modulate metabolic syndrome risk.
| Gene Locus | Polymorphism | Dietary Factors | Odds Ratio | Conclusions | Reference Number |
|---|---|---|---|---|---|
| Acetyl-CoA carboxylase β (ACC2) | rs4766587 | n-6 PUFA | 1.82 | Risk conferred by the A allele was exacerbated among individuals with a high-fat intake (>35% energy) (OR 1.62), particularly a high intake (>5.5% energy) of n-6 PUFA (OR 1.82 for gene-nutrient interaction). | [83] |
| Apolipoprotein A-I (APOA1) | rs670 | MUFA | 1.57 | MetS risk was exacerbated among the habitual high-fat consumers (>35% energy, OR 1.58). In addition a high MUFA fat increased MetS risk (OR 1.57). | [84] |
| Apolipoprotein B (APOB) | rs512535 | MUFA | 1.89 | MetS risk was increased among the habitual high-fat consumers (>35% energy, OR 2.00). Moreover a high MUFA intake increased MetS risk (OR 1.89). | [84] |
| Complement component 3 ( C3) | rs2250656 rs11569562 | n-6 PUFA | 2.2 (rs2250656)
0.32 (rs11569562) |
AA genotype for rs2250656 had increased MetS risk relative to minor G subjects. GG genotype for rs11569562 had decreased MetS risk compared with minor A allele carriers. | [101] |
| Interleukin 1 beta (IL-1β) | 6054 G | n-3 PUFA | 3.29 (GG) 1.95 (GA) |
Low n-3-PUFA intake (below the median) among the 6054 G allele carriers was associated with increased MetS risk (OR 3.29, for GG and OR 1.95, for GA) compared with the AA genotype. | [88] |
| Long-chain acyl CoA synthetase 1 (ACSL1) | rs9997745 | Total PUFA | Risk abolished | GG genotype had increased MetS risk (OR 1.90) compared with the A allele. The risk conferred by GG homozygosity was abolished among those subjects consuming either a low-fat or a high-PUFA diet. | [82] |
| Leptin receptor (LEPR) | rs3790433 | n-3 and n-6 PUFA | 1.65 | LEPR rs3790433 GG homozygotes had increased MetS risk (OR 1.65) compared with the minor A allele carriers, which may be accounted for by their increased risk of elevated insulin concentrations (OR 2.40) and insulin resistance (OR 2.15). Low (less than median) plasma (n-3) and high (n-6) PUFA status exacerbated the genetic risk conferred by GG homozygosity to hyperinsulinemia (OR 2.92–2.94) and insulin resistance (OR 3.40–3.47). These associations were abolished against a high (n-3) or low (n-6) PUFA background. | [104] |
| Lymphotoxin-α (
LTA) Interleukin 6 (IL-6) Tumor necrosis factor-α (TNF-α) |
LTA rs915654 TNF-α rs1800629 IL-6 rs1800797 | Total PUFA/SFA | 4.4 | LTA rs915654 minor A allele carriers and TNF-α rs1800629 major G allele homozygotes had increased MetS risk (OR 1.37 and OR 1.35). Possession of the IL-6 rs1800797 GG genotype by the LTA and TNF-α “risk genotype” carriers further increased MetS risk (OR 2.10). Low total PUFA/SFA exacerbated MetS risk (OR 4.4). | [92] |
| Peroxisome proliferator-activated receptor-delta (PPAR-δ) | -87T>C | Total fat | 0.42 | Low dietary fat consumers (<34.4% of energy from fat (median of fat consumption)) carrying the -87C allele had reduced MetS risk (OR 0.42). | [111] |
| Transcription factor 7-like 2 (TCF7L2) | rs7903146 | Total SFA | 2.35 | High SFA intake (≥15.5% energy) exacerbated MetS risk (OR 2.35) and was associated with further impaired insulin sensitivity in the T allele carriers of rs7903146 compared to the CC homozygotes and particularly to the T allele carriers with the lowest SFA intake. | [60] |
Metabolic Syndrome (MetS); monounsaturated fatty acids (MUFA); polyunsaturated fatty acids (PUFA); saturated fatty acids (SFA) Adapted from Perez-Martinez et al. [31].