Interaction of dietary fat intake with APOA2, APOA5 and LEPR polymorphisms and its relationship with obesity and dyslipidemia in young subjects

Abstract

BackgroundDiet is an important environmental factor that interacts with genes to modulate the likelihood of developing disorders in lipid metabolism and the relationship between diet and genes in the presence of other chronic diseases such as obesity. The objective of this study was to analyze the interaction of a high fat diet with the APOA2 (rs3813627 and rs5082), APOA5 (rs662799 and rs3135506) and LEPR (rs8179183 and rs1137101) polymorphisms and its relationship with obesity and dyslipidemia in young subjects.MethodsThe study included 200 young subjects aged 18 to 25 years (100 normal-weight and 100 obese subjects). Dietary fat intake was measured using the frequency food consumption questionnaire. Genotyping of polymorphisms was performed by PCR-RFLP.ResultsIndividuals carrying the APOA5 56 G/G genotype with a high saturated fatty acid consumption (OR = 2.7, p = 0.006) and/or total fat (OR = 2.4, p = 0.018), associated with an increased risk of obesity. We also found that A/G + G/G genotypes of the 668 A/G polymorphism in the LEPR gene with an intake ≥12 g/d of saturated fatty acids, have 2.9 times higher risk of obesity (p = 0.002), 3.8 times higher risk of hypercholesterolemia (p = 0.002) and 2.4 times higher risk of hypertriglyceridemia (p = 0.02), than those with an intake <12 g/d of saturated fatty acids. Similarly, LEPR 668 A/G + G/G carriers with a high fat total intake had 3.0 times higher risk of obesity (p = 0.002) and 4.1 times higher risk of hypercholesterolemia (p = 0.001).ConclusionOur results suggest that dietary fat intake modifies the effect of APOA5 and LEPR polymorphisms on serum triglycerides, cholesterol levels and obesity in young subjects.

Dietary Fatty Acid Composition Modulates Obesity and Interacts with Obesity‐Related Genes

“…The deleterious association of the A allele with obesity was observed in subjects with a low n-6 PUFA intake [165] 200 Mexican normal-weight and obese men and women/ survey APOA5 t /rs662799 and rs3135506 Carriers of rs3135506 GG genotype with a high SFA consumption had an increased risk of obesity.…”

“…[179] 2280 non-Hispanic whites men and women/survey APOA5 t /rs662799 and rs3135506 Rs662799 C minor allele carriers with the high MUFA intake had a lower obesity risk compared with TT carriers [180] 3462 Whites and Hispanic men and women/follow-up survey APOA2 u /rs5082 CC genotype with a high SFA intake was associated with a higher obesity prevalence [181] 2071 Puerto Ricans origin and Northern European ancestry men and women/survey APOA2 u /rs5082 CC carriers who consumed a greater amount of SFA from a high-fat dairy foods had a greater BMI than those who consume less dairy fat [182] 737 Iranian diabetic patients men and women/survey APOA2 u /rs5082 Carriers of CC allele with a high SFA intake had higher BMI [165] 200 Mexican normal-weight and obese men and women/ survey APOA2 u /rs3813627 and rs5082 No interaction was found between SFA intake and APOA2 SNP [183] 1225 Spanish overweight and obese men and women/ survey APOA2 u /rs5082 A high SFA intake was associated with a greater WC in minor allele homozygotes CC compared with non-minor allele carriers [184] 4602 Asian and Mediterranean obese men and women/ survey…”

Relationship among porcine lncRNA TCONS_00010987, miR-323, and leptin receptor based on dual luciferase reporter gene assays and expression patterns

“…Adipocytes synthesize and secrete leptin, which in turn acts on the hypothalamus to maintain the stability of body fat [8]. At high levels, leptin inhibits food intake through the melanocortin receptor system, and at low levels, it promotes food intake through neuropeptide Y. Mutations in the LEPR gene result in leptin insensitivity, hyperphagia, morbid obesity, and metabolic and endocrine abnormalities [26]. In pigs, LEPR mRNA was expressed in adipose tissue, brain, muscle, fat, liver, hypothalamus, pituitary gland and reproductive tissues (endometrium and ovary) [27].…”

Misvisende om kosthold i ny nasjonal retningslinje for forebygging av hjerte- og karsykdommer

“…I løpet av det siste tiåret har et økende antall studier undersøkt interaksjoner mellom inntak av mettet fett og genvarianter som er forbundet med sykdomsrisiko. Tverrsnitts-og kohortstudier har eksempelvis antydet at et høyere inntak av mettet fett kan forsterke genetiske sårbarheter for blant annet høyt kolesterol 267 , koronarsykdom 268 , fedme [269][270][271] og insulinresistens 272,273 . Slike sammenhenger er imidlertid ikke helt konsekvente 274,275 og kan foreløpig anses som hypotesegenererende.…”