No abstract

The mechanisms that regulate disease progression during hepatitis C virus (HCV) infection and the response to treatment are not clearly identified. Numerous studies have demonstrated that a strong host immune response against HCV favors HCV clearance. In addition, genetic factors and metabolic machinery, particularly cholesterol modulation, are involved in HCV infection. It is likely that the interplay between all of these factors contributes to the outcome of HCV infection. In recent years, the world has experienced its largest epidemic of obesity. Mexico and the United States are the leading sufferers from this epidemic at the global level. Obesity is associated with the development of numerous pathologies including hypercholesterolemia which is one of the eight most important risk factors for mortality in Mexico. This may be related to the course of HCV infection in this population. Here, we focus on the urgent need to study the progression of HCV infection in relation to ethnic characteristics. Discoveries are discussed that hold promise in identifying immune, metabolic and genetic factors that, in conjunction, could be therapeutic targets or predictors of the progression of HCV infection.

This study aimed to screen relevant interactions between DRD2/ANKK1 TaqIA polymorphism and dietary intakes with reference to phenotypical features in patients with T2D from western Mexico. In this cross-sectional study, a total of 175 T2D patients were enrolled. Dietary intake was evaluated using 3-day food records and appropriate software. Glycemic and blood lipid profiles were measured by standardized methods. Genotyping of the DRD2/ANKK1 TaqIA polymorphism was performed by the RFLP method. Gene-diet interactions regarding anthropometric and metabolic phenotypes were screened by adjusted multiple linear regression analyses. Genotype frequencies of the DRD2/ANKK1 TaqIA polymorphism were A1A1 (16.0%), A1A2 (52.6%), and A2A2 (31.4%). Statistically significant interactions between the DRD2/ANKK1 TaqIA genotypes and dietary factors in relation to blood triglyceride (TG) levels were found. Carriers of the A1 allele (A1A1 homozygotes plus A1A2 heterozygotes) were protected from TG increases by maltose intake (P int. = 0.023). Instead, A2A2 homozygotes were susceptible to TG rises through consumptions of total fat (P int. = 0.041), monounsaturated fatty acids (P int. = 0.001), and dietary cholesterol (P int. = 0.019). This study suggests that the interactions between DRD2/ANKK1 TaqIA polymorphism and dietary factors (sugar and fats) influence TG levels in diabetic patients.

Purpose To analyze clinically relevant interactions between the apolipoprotein E ( APOE ) ε2, ε3 and ε4 alleles and nutritional factors on glycemic control and lipid levels in a cohort of type 2 diabetes (T2D) patients from western Mexico. Patients and Methods In this cross-sectional study of the cohort of T2D patients, a total of 224 individuals were selected for interaction studies. Clinical and anthropometric data were obtained from pre-designed medical records. Dietary intake was assessed by validated three-day food consumption records. Biochemical measurements were determined by automated methods. APOE genotyping was performed by a real-time allelic discrimination assay. Gene–diet interactions were tested by corrected multiple linear regression analyses, which were adjusted by potential confounding factors such as age, sex, energy intake, BMI and anti-hyperglycemic therapy (Metformin, Glibenclamide or Insulin), and years with T2D. Results Seventy-six percent of patients with T2D were on Metformin therapy. The frequencies of the APOE alleles were ε2 (5.8%), ε3 (74.1%) and ε4 (20.1%). After statistical settings, significant APOE alleles-by-diet interactions in relation to the metabolic profile were found. Interestingly, higher blood levels of total cholesterol (p int. = 0.016), non-HDL-c (p int. = 0.024), and LDL-c (p int. = 0.030) were found only in carriers of the APOE ε2 allele with a low consumption of MUFA. In contrast, carriers of the APOE ε4 allele with a high ω-6:ω-3 PUFA ratio in the diet had higher %HbA1c blood concentrations (p int. = 0.035). Conclusion This study suggests a differential metabolic impact of APOE alleles on lipid/glycemic phenotypes depending on the dietary intake, with important potential implications in the personalized medicine and nutritional management of patients with type 2 diabetes mellitus.