Table 1.
Characteristics of the five studies that met the inclusion criteria of this systematic review.
| Author, Year | Country, Age (Mean, SD) | n | Study Design | Exposure | Outcome | Results | Conclusion |
|---|---|---|---|---|---|---|---|
| Kim et al., 2011 [29] | Korea, 30–69 years (48.7, 9.3) | 576 | Cross-sectional study | FADS polymorphisms: rs174537, rs174575, rs1000778 | T2DM risk: fasting glucose (mg/dL), fasting insulin (µIU/mL) and HOMA–IR Fatty acid concentration: serum phospholipid FA composition (relative %): SFA, MUFA, PUFA (ALA, LA, AA, EPA, DGLA, DPA, DHA) Insulin Resistance (HOMA) |
HOMA-IR and serum FA composition or FA ratios were associated with the FADS SNPs (rs174575 minor allele carriers had higher HOMA-IR when they had higher concentrations of DGLA (≥1.4% in total FA, p for interaction = 0.009) or of AA (≥4.6%, p for interaction = 0.047)). No significant association was found between n-3 FA serum composition, FADS polymorphism and HOMA-IR. | FADS SNPs were associated with higher HOMA-IR, when individuals had higher serum LC n-6 PUFA. No significant association was found for serum n-3 FA. |
| Kroger et al., 2011 [30] | Germany, 35–65 years (Controls 50, 8.9 and cases 55.1, 7.4) |
Controls: 2114; cases: 673 | Prospective cohort, 7 year follow up | Dietary intake: SFA (% of total fat intake), MUFA (% of total fat intake), n-3 PUFA (% of total fat intake), n-6 PUFA (% of total fat intake), total PUFA (% of total fat intake) FADS polymorphism: rs174546 Desaturase activity Fatty acid concentration: erythrocyte membrane phospholipids FA (% of total FA), AA/DGLA (D5D) and ALA/LA (D6D) ratios |
T2DM risk: clinical diagnosis of T2DM | Risk of T2DM differed according to FA profile of erythrocyte membrane phospholipids. Higher proportions of LA were associated with lower risk of T2DM (RR for extreme quintiles = 0.76 (95% CI: 0.54, 1.08)); whereas higher proportions of GLA and DGLA predicted increased T2DM risk (RR for extreme quintiles = 2.00 (95% CI: 1.38, 2.88); RR = 1.72 (95% CI: 1.18, 2.53), respectively). Activity of desaturase enzymes was linked to incidence of T2DM. Lower activity of D6D predicted lower risk of T2DM in carriers of the minor allele compared to those without (RR CT genotype = 0.75 (95% CI: 0.59, 0.96); TT genotype = 0.64 (95% CI: 0.43, 0.94)). Dietary FA intake was not associated with T2DM. | T2DM incidence was higher in individuals with higher proportions of LC n-6 PUFA and lower D6D activity. No association was found with dietary n-3 FA intake. |
| Cormier et al., 2013 [31] | Canada, 18–50 years (30.8, 8.7) |
208 | Randomized controlled trial, 6 week duration | Dietary intake: 3–3.3 g/day of fish oil (1.9–2.2 g of EPA + 1.1 of DHA) FADS polymorphism: rs174556, rs174627, rs482548, rs2072114, rs12807005, rs174448, rs2845573, rs7394871, rs7942717, rs7482316, rs174602, rs498793, rs174546, rs174570, rs174579, rs174611, rs174616, rs968567 |
Fasting Glucose (mM), Fasting Insulin (ρ/L), HOMA-IR | SNPs involved in the FADS gene cluster were associated with glycemic control parameters (a supplementation * genotype interaction effect on FG levels was observed for rs482548 (p = 0.008)), mainly decreased HOMA-IR, in response to a high dose intervention with n-3 PUFA (supplementation * genotype interaction effect for rs174602 (p = 0.01); rs174570 (p = 0.03); rs7394871 (p = 0.03)) | FADS SNPs were associated with lower HOMA-IR and higher fasting glucose in response to a high dose n-3 PUFA supplementation. |
| Yao et al., 2015 [33] | China, (Controls: 51.38, 11.27 years; cases: 63.24, 10.43 years) |
Controls: 421; cases: 331 | Case-control study | Dietary intake: total fat (%E), SFA (%E), MUFA (%E), PUFA (%E) FADS polymorphism: rs174545, rs2072114, rs174602, rs174616 Desaturase activity Fatty acid concentration: serum PUFA composition (% of total FA), EPA/ALA (D5D) and AA/LA (D6D) ratios |
T2DM risk * | Minor allele carriers of the rs174616 are associated with a decreased risk of T2DM (p = 0.023). Desaturase activity of D5D was decreased (p = 0.009), while D6D was increased (p < 0.001) in T2DM individuals. Dietary saturated fatty acid (p < 0.0014) was significantly higher in T2DM cases, whilst PUFA intake was lower (p > 0.054) |
Higher PUFAs intake, desaturase activity and SNP rs174616 are associated with decreased risk of T2DM. |
| Takkunen et al., 2016 [32] | Finland, 40–65 years (55.4, 7.14) |
407 | Prospective cohort, 6 year follow up | Dietary intake: total fat (g/day), SFA (g/100 g of total fat), MUFA (g/100 g of total fat), PUFA (g/100 g of total fat) Desaturase activity: AA/DGLA (D5D) and ALA/LA (D6D) ratios using FADS polymorphism (rs174550) for validation Fatty acid concentration: 20 serum FA (mol%) |
T2DM incidence OGTT (mmol/L) |
Total serum LC n-3 PUFA (p = 0.001) and estimated D5D activity (p = 0.011) predicted lower incidence of T2DM. | Lower incidence of T2DM was associated with serum LC n-3 PUFA, proportions of marine n-3 FA and estimated D5D activity. |
FADS: fatty acid desaturase; HOMA: homeostasis model assessment; OGTT: oral glucose tolerance test; FG: fasting glucose; FA: fatty acids; SNP: single nucleotide polymorphism; T2DM: type 2 diabetes mellitus; AA: arachidonic acid; ALA: alpha-linolenic acid; LA: linoleic acid; DGLA: dihomo gamma-linolenic acid; E: energy intake; EPA: eicosapentaenoic acid; DHA: docosahexaenoic acid; GLA: gamma-linolenic acid; D5D: delta 5 desaturase; D6D: delta 6 desaturase; SFA: saturated fatty acid; MUFA: monounsaturated fatty acid; %E: percentage of total energy intake; PUFA: polyunsaturated fatty acid; LC-PUFA: long chain polyunsaturated fatty acid; RR: relative risk; CI: confidence interval. * This study looked at T2DM as an exposure and an outcome.