Summary: The steady-state plasma glucose (SSPG) concentration was lower in major allele carriers, regardless of the diet consumed. Significant diet genotype interactions were found for SSPG and plasma nonesterified FFA (NEFA) concentrations.

Summary: Higher n-6 Polyunsaturated Fats intake increases plasma TGs and RLPs and decreases LDL particle size in carriers of the -1131C allele, contributing to a more atherogenic lipid profile for this subset of the population. Moreover, this interaction was not observed for n-3 Polyunsaturated Fats.

Summary: The study has detected moderately higher waist-to-hip ratio (WHR) changes for the carriers of the -11377C (P=0.03) allele.

Summary:

Summary: The study has detected moderately higher waist-to-hip ratio (WHR) changes for the carriers of the -1391A (P=0.02)

Summary: The study provided new data on ApoB and ApoA1 genotypes and MetS risk. The novel gene-nutrient interactions between SNPs of these genes and dietary fat suggest that genetic predisposition to MetS may be more evident in individuals with a high habitual dietary fat intake, in particular MUFA.

Summary: The study identified statistically significant interactions between the polymorphism and saturated fat regarding BMI in all three populations. A mean increase in BMI was observed between genotypes with high but not with low- saturated fat intake in all studies. Major allele was significantly associated with higher obesity prevalence in all populations only in the high-saturated fat stratum.

Summary: Total cholesterol (Chol) and triacylglycerols (TG) in plasma and TG-rich lipoproteins (TRL) (large TRL and small TRL) were measured,as well as HDL, Apo A-I, Apo B, Apo B-48, and Apo B-100. Postprandial responses were higher in the TT group than in carriers of the minor allele (CC/TC) for total TG in plasma (21.37% of change of area under curve, P=0.014), large TRLTG (24.75% change, P=0.017) and small TRL-Chol (26.63% change, P=0.003). The work shows that carriers of the minor allele for Apo A-II -265T/C (CC/TC) have a lower postprandial response compared with TT homozygotes

Summary: Postprandial responses were higher in the TT group than in carriers of the minor allele (CC/TC) for total TG in plasma, large TRLTG and small TRL-Chol. The work shows that carriers of the minor allele have a lower postprandial response compared with TT homozygotes.

Summary: Data of postprandial lipemia revealed that subjects with the −1131CT/CC genotype had a higher postprandial response of total plasma TG (p = 0.043), large triacylglycerol-rich lipoproteins-TG (TRL-TG) (p = 0.002), large TRL-Chol (p = 0.004), small TRL-Chol (p = 0.004) and small TRL-RP (p = 0.001) than subjects with the −1131TT genotype.

Summary: The dietary intervention prevented an age-related increase in triglyceride levels in individuals with IFG or new-onset Type 2 Diabetes Mellitus who possess the major allele in homozygous condition.

Summary: This interaction was dose-dependent, and no statistically significant heterogeneity by gender was detected. In subjects homozygous for the −1131T major allele, BMI increased as total fat intake increased. Conversely, this increase was not present in carriers of the −1131C minor allele.

Summary: In conclusion, the modifications observed in postprandial lipoprotein metabolism in subjects with apoA–V −1131 T / C polymorphism could be involved in the higher risk of coronary artery disease observed in carriers of the −1131C allele.

Summary: In subjects homozygous for the -1131T major allele, BMI increased as total fat intake increased. Conversely, this increase was not present in carriers of the -1131C minor allele. Accordingly, the study has found significant interactions in determining obesity and overweight risks. APOA5-1131C minor allele carriers had a lower obesity risk (OR, 0.61, 95%; CI, 0.39-0.98; P = 0.032) and overweight risk (OR, 0.63, 95%; CI, 0.41-0.96; P = 0.031) compared with TT subjects in the high fat intake group (/or=30% of energy ) but not when fat intake was low (OR, 1.16, 95%; CI, 0.77-1.74; P = 0.47 and OR = 1.15, 95%; CI, 0.77-1.71; P = 0.48) for obesity and overweight, respectively). When specific fatty acid groups were analyzed, monounsaturated fats showed the highest statistical significance for these interactions.

Summary: APOA5 56G carriers displayed significant decrease in TG (P=0.006), and increase in HDL-C (P 0.002) levels relative to their basal values in the fasting state when compared with noncarriers (a TG reduction of -35.8+/- 2.8% vs -27.9+/- 0.9% and a HDL-C increase of 11.8 +/- 1.3% vs 6.9 +/- 0.5%, respectively) after 3-week treatment. In the postprandial lipemia after a fat load, the 56G carriers showed a significant decrease in the area under curve for TG and increase for HDL-C than the noncarriers.

Summary: Interaction of the -1131T/C SNP with total fat energy intake was observed for plasma TG (P = 0.032) and total cholesterol (P = 0.034). This polymorphism was not associated with TG or other lipids.

Summary: APOA5-1131C minor allele frequency was significantly greater in hypertriglyceridemic patients than normotriglyceridemic controls. ApoA-V concentrations were not significantly different between controls and cases. Normotriglyceridemic controls with T/C and C/C showed lower apoA-V concentrations (14% and 27%, respectively), than did T/T controls. Similar genotypic effects on apoA-V were found in hypertriglyceridemic cases. In both groups, APOA5-1131T.C was associated with higher triglycerides, smaller LDL particle size, and lower HDL-cholesterol.

Summary: The study provided new data on ApoB and ApoA1 genotypes and MetS risk. The novel gene-nutrient interactions between SNPs of these genes and dietary fat suggest that genetic predisposition to MetS may be more evident in individuals with a high habitual dietary fat intake, in particular MUFA.

Summary: Compared with carriers of the G allele, TT subjects had a significantly (P 0.05) shorter lag time after the SFA diet. The replacement of the SFA diet by the CHO or MUFA diet induced a greater increase (P 0.05) in lag time in the TT subjects than in the GG or GT subjects. Carriers of the T allele had higher LDLcholesterol (P 0.05) and apolipoprotein B (P 0.05) plasma concentrations after the SFA diet than did GG subjects. Compared with GG subjects, carriers of the T allele had a significantly (P 0.05) greater decrease in LDL cholesterol and apolipoprotein B when they changed from the SFA to the CHO diet.

Summary: MAF: A-0.28; major allele homozygotes: 10.8+/-0.3; heterozygotes: 9.2+/-0.4; major allele homozygotes: 10.2+/-0.9; p-value: 0.0069

Summary: Associations were only observed among Caucasians, with no effects among African Americans, and were stronger among women than men, although numbers in stratified analyses were small. Differences in catalase activity by genotype were most pronounced among those in the highest tertiles of consumption of fruits and vegetables, with weaker relationships among those who were lower consumers. Among those with major allele carriers, there was no change in activity by consumption, but there were notable decreases in activity by tertiles of consumption for those with at least one T allele.

Summary: For blood lipids, there were significant results demonstrated in individual associations of dietary pattern, MRND and VEGFR2 gene SNPs rs2071559 for these biomarkers.

Summary: G allele carriers at the ADAM17_m1254A / G polymorphism exhibited significantly higher risk of obesity (P=0.003), were shorter (P=0.017), had higher insulin (P=0.016), and lower HDL-C concentrations(P=0.027) than AA subjects.

Summary: In the total participants and participants with hypertension, the study has observed significant and consistent interactions between rs16147 genotype and dietary fat intake on changes in multiple BP phenotypes at 2 years (all P for interactions <0.05). The risk allele (C allele) was associated with a greater reduction of BP phenotypes in response to low-fat diet, whereas an opposite genetic effect was observed in response to high-fat diet. In addition, the C allele was related to greater changes in 4 BP phenotypes in hypertensive compared with nonhypertensive participants.

Summary: The findings of the study support the functionality of both promoter SNPs and provide the association between -11391G/A SNPs and obesity-related traits and new insights into their modulations by MUFA intake.

Summary: Men homozygous for the C allele have a higher risk profile consisting of hypoadiponectinemia and higher Insulin resistance; however, they are hyper-responders to MUFA- and CHO rich-diets with induction of enhanced insulin sensitivity

Summary: The carriers of the AA genotype of rs3758953 in ABCC8 had a higher 2-h insulin level (624+/-410 vs. 550+/-386 pmol/l, P=0.002) and a higher 2-h glucose level (9.1+/-1.4 vs. 8.8+/-1.5 mmol/l, P=0.024) in an OGTT at baseline than the carriers of the G allele.

Summary: LTA rs915654 A allele carriers had higher MetS risk compared with the TT subjects [odds ratio (OR) 1.45 95% confidence interval [CI] 1.11–1.89, P = 0.006]. The combined effect of carrying both the LTA rs915654 A allele and the TNF-α rs1800629 GG genotype demonstrated further increased MetS risk (OR 1.54) compared with noncarriers. Possession of the IL-6 rs1800797 GG genotype by the TNF-α and LTA risk genotype carriers additively increased their MetS risk (OR 2.10). The combined LTA and TNF-α risk genotype carriers with the lowest Polyunsaturated Fatss (Polyunsaturated Fats)/SFA levels had even greater risk of the MetS (OR 2.13). Among carriers of the three risk genotypes with the lowest 50th percentile of Polyunsaturated Fats/SFA, MetS risk was increased more than 4-fold compared with noncarriers (OR 4.40). Similarly a low Polyunsaturated Fats/SFA exacerbated the risk of fasting hyperglycemia, high SBP, abdominal obesity, and high C3 levels in these individuals. risk was more than 5-fold higher in the risk genotype carriers with the highest SFA levels compared with noncarriers (OR 5.20).

Summary: EPO polymorphism influenced erythrogram and plateletgram results, suggesting an aerobic advantage for the TG genotype and a disadvantage for the GG genotype as regards possible microvascular complications. This polymorphism influenced the runners’ response to pequi oil:significant responses were observed for the EPO TT genotype in erythrocyte, hematocrit, mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration values, and for the TT and TG genotypes in red blood cell distribution width values. Significant differences were also observed in the plateletgram for the TT and TG genotypes.

Summary: An interaction between rs884164 and Polyunsaturated Fats n3 showed BMI, weight, waist, glucose and TAG levels are increased in carriers of the minor allele with elevated Polyunsaturated Fats n3 intake. Furthermore, rs884164 showed significant interaction with Polyunsaturated Fats n6 with HDL levels decreasing and TAG increasing among minor allele carriers with elevated Polyunsaturated Fats n6 intake. The minor allele subjects showed elevated levels for each trait, compared to non-carriers.

Summary: Analyzing the association of UCP2 and UCP3 polymorphisms, statistical analyses of changes of BMI and fat mass induced by VLCD among women who had finished a one-month weight control program (n = 301) revealed that two polymorphisms in UCP2-3 gene cluster were associated with the changes of BMI induced by VLCD, including UCP2 866G/A and UCP2-UCP3-ht1.

Summary: An interaction was studied between dietary fat intake and SNPs, with a high intake of saturated and monounsaturated fats being associated with active disease, mainly in patients carrying the variant alleles of the 857 TNFA _x005F_x0002_ polymorphism (OR = 6.0, 95 % CI = 1.4 – 26.2;OR = 5.17; 95 % CI = 1.4 – 19.2, respectively)

Summary: Subjects were grouped as having no minor A allele at the –238 position (0/0), or one minor A allele at the –238 (1/0) position. TNFA genotypes modified the association between dietary Polyunsaturated Fats and HDL-cholesterol concentrations (p = 0.04 for interaction). Among individuals with the 0/0 genotype, total polyunsaturated fats was positively associated with HDL-cholesterol in both men (p = 0.008) and women (p = 0.03), and for both n–6 (p = 0.004) and n–3 (p = 0.04) Polyunsaturated Fats.However, an inverse relationship was observed among men carrying the 1/0 genotype (p = 0.005).

Summary: Subjects were grouped as having no minor A allele at the –308 positions (0/0), or one minor A allele at –308 (0/1) position. TNF- genotypes modified the association between dietary Polyunsaturated Fats and HDL-cholesterol concentrations (p = 0.04 for interaction). Among individuals with the 0/0 genotype, total Polyunsaturated Fats was positively associated with HDL-cholesterol in both men (p = 0.008) and women (p = 0.03), and for both n–6 (p = 0.004) and n–3 (p = 0.04) polyunsaturated fats. However, an inverse relationship was observed among men carrying the 1/0 genotype (p = 0.005).

Summary: MAF: A-0.19; major allele homozygotes: 6.03+/-0.05; p-value: 0.0052

Summary: The TNF-α rs1800629 and IL-6 rs1800797 GG homozygotes tended to have greater, albeit nonsignificant, MetS risk [OR 1.21 (95% CI 0.90–1.63) and OR 1.10 (95% CI 0.85–1.44)], they both displayed increased risk of fasting hyperglycemia compared with their respective A allele carriers. The combined effect of carrying both the LTA rs915654 A allele and the TNF-α rs1800629 GG genotype demonstrated further increased MetS risk (OR 1.54) compared with noncarriers. Possession of the IL-6 rs1800797 GG genotype by the TNF-α and LTA risk genotype carriers additively increased their MetS risk (OR 2.10). The combined LTA and TNF-α risk genotype carriers with the lowest Polyunsaturated Fatss (Polyunsaturated Fats)/SFA levels had even greater risk of the MetS (OR 2.13). Among carriers of the three risk genotypes with the lowest 50th percentile of Polyunsaturated Fats/SFA, MetS risk was increased more than 4-fold compared with noncarriers (OR 4.40). Similarly a low Polyunsaturated Fats/SFA exacerbated the risk of fasting hyperglycemia, high SBP, abdominal obesity, and high C3 levels in these individuals. risk was more than 5-fold higher in the risk genotype carriers with the highest SFA levels compared with noncarriers (OR 5.20).

Summary: When dietary fat intake was 30% of total energy intake [percentage energy (%E)], the odds of being obese with the TNFA GA+AA genotype was only 12% of that with GG, but increasing intake of dietary fat (%E) was associated with a significantly faster rate of increase in obesity risk in women with the TNFA GA+AA genotype compared with those with the GG genotype (P = 0.036). There were significant diet-gene interactions between alpha-linolenic acid (%E) and the total cholesterol:HDL-cholesterol ratio (P = 0.036), and Polyunsaturated Fats (%E) and LDL cholesterol levels (P = 0.026), with participants with the A allele being more responsive to changes in relative fat intake.