BackgroundDyslipidaemias result from the interaction between genetic and environmental factors, including diet disequilibrium and physical inactivity. Among the genetic factors associated with serum lipids, the Taq1B CETP polymorphism has been investigated. The B1 allele has been considered as a risk factor for dyslipidaemia because of its association with greater CETP levels and higher serum triglycerides. The present study aimed to determine the role of the Taq1B polymorphism with lipid and anthropometric variables and its interaction with diet and physical activity.MethodsIn total, 215 subjects were enrolled in this cross‐sectional study. Diet intake was evaluated using a 3‐day food consumption record and physical activity was determined in accordance with World Health Organization recommendations. The Taq1B CETP polymorphism was determined by allelic discrimination.ResultsSubjects with the B1B2/B2B2 genotype, who had a sucrose consumption ≥5% of the total kcal day−1, had higher levels of total cholesterol (TC) [165.55 (142.21–188.89) mg dL−1 versus 200.19 (184.79–215.60) mg dL−1; P for interaction = 0.034] and low‐density lipoprotein [99.29 (75.52–123.05) mg dL−1 versus 128.64 (113.59–143.69) mg dL−1; P for interaction = 0.037] than subjects with the B1B1 genotype. Subjects who did not perform physical activity and had the B1B2/B2B2 genotype showed significantly higher levels of TC [177.48 (161.36–193.60) mg dL−1 versus 194.49 (185.43–203.56) mg mL−1; P for interaction = 0.033] than subjects with the B1B1 genotype.ConclusionsWe provide evidence that subjects with inadequate environmental factors carriers of the polymorphic genotype had higher serum lipid levels than subjects with the B1B1 genotype.

Approximately 25–50% of the population worldwide exhibits serum triglycerides (TG) (≥150 mg/dL) which are associated with an increased level of highly atherogenic remnant-like particles, non-alcoholic fatty liver disease, and pancreatitis risk. High serum TG levels could be related to cardiovascular disease, which is the most prevalent cause of mortality in Western countries. The etiology of hypertriglyceridemia (HTG) is multifactorial and can be classified as primary and secondary causes. Among the primary causes are genetic disorders. On the other hand, secondary causes of HTG comprise lifestyle factors, medical conditions, and drugs. Among lifestyle changes, adequate diets and nutrition are the initial steps to treat and prevent serum lipid alterations. Dietary intervention for HTG is recommended in order to modify the amount of macronutrients. Macronutrient distribution changes such as fat or protein, low-carbohydrate diets, and caloric restriction seem to be effective strategies in reducing TG levels. Particularly, the Mediterranean diet is the dietary pattern with the most consistent evidence for efficacy in HTG while the use of omega-3 supplements consumption is the dietary component with the highest number of randomized clinical trials (RCT) carried out with effective results on reducing TG. The aim of this review was to provide a better comprehension between human nutrition and lipid metabolism.

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<b><i>Background:</i></b> Even though excessive adipose tissue is related to chronic metabolic disturbances, not all subjects with excess weight (EW) display metabolic alterations, and not all normal-weight (NW) subjects have a metabolically healthy (MH) phenotype, probably due to gene-environment interactions. The aim of this study was to investigate the interaction effects of <i>ADIPOQ</i> and <i>PPARG</i> genetic variants in NW and EW individuals with different metabolic phenotypes. <b><i>Methods:</i></b> Data on 345 adults from western Mexico were analyzed. The individuals were classified into NW and EW groups according to body mass index, and were categorized as MH or metabolically unhealthy (MUH), considering homeostatic model assessment insulin resistance (HOMA-IR) and National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) cut-off points for glucose, triglycerides, high-density lipoprotein cholesterol, and blood pressure. Subjects with ≤1 altered parameter were classified as MH. The single nucleotide polymorphisms (SNPs) –11377C&#x3e;G, –11391G&#x3e;A, +45T&#x3e;G, and +276G&#x3e;T for <i>ADIPOQ</i> and Pro12Ala for <i>PPARG</i> were analyzed by allelic discrimination. High-molecular-weight adiponectin isoform levels were measured by ELISA. <b><i>Results:</i></b> Lower serum adiponectin levels were associated with the MUH phenotype in EW subjects. NW subjects with the GG or TG genotype for the +45T&#x3e;G SNP had reduced odds of the MUH phenotype. Individuals who carried two copies of the GG haplotype at the –11391G&#x3e;A and –11377C&#x3e;G SNPs for <i>ADIPOQ</i> had lower serum adiponectin levels than those with zero copies. <b><i>Conclusion:</i></b> In this population, lower serum adiponectin levels were found in the EW-MUH phenotype, and no differences were observed between the NW-MH and the EW-MH phenotype. In addition, the +45T&#x3e;G SNP was associated with reduced odds of the MUH phenotype.