(-)-Epicatechin improves body composition of male rats descendant of obese mothers postnatally fed with a high-fat diet.

A combination of maternal obesity and high-fat diet (HFD) in offspring postnatal life has deleterious effects, and (-)-epicatechin (Epi) treatment can reverse these adverse effects. To investigate whether Epi administration can modify fat mass, muscle mass, and bone mass in male rats descended from obese mothers, fed postnatally on an HFD. Male offspring of mothers fed with control diet formed the control group (C), control group with high-fat diet (CHF), and control group with high-fat diet + epicatechin (CHF + Epi). Male offspring of maternal obesity formed the group with control diet (MO), maternal obesity group with high-fat diet (MOHF), and maternal obesity group with high-fat diet + epicatechin (MOHF + Epi). We measured total fat and weight of visceral adipose tissue by dissection and by dual-energy x-ray absorptiometry scanning body composition. Epicatechin diminished total and visceral pads fat of male offspring of CHF + Epi and MOHF + Epi groups versus to male offspring of CHF and MOHF groups. Besides, epicatechin increased lean mass in CHF + Epi and MOHF + Epi groups, but these changes were not significant. Total body mineral density of the male offspring of CHF, MOHF, and MOHF + Epi groups was significantly higher versus male offspring of C and MO groups. Obesity programming model plus a high-fat postnatal diet presents higher visceral adipose tissue, decreased lean mass, and modified body mineral density when compared with a direct obesity model and its controls. Epicatechin treatment improved body composition; however, it was not able to induce similar values as presented by the controls.

Association of the T130I Variant of the HNF4A Gene with Metabolic Syndrome and Its Components in Mexican Children.

Background: Metabolic syndrome (MetS), a cluster of risk factors, leads to cardiovascular disease (CVD) and type 2 diabetes (T2D). The second leading cause of mortality in Mexico is T2D. Genetic factors participate in the pathogenesis of MetS. The HNFA gene encodes a transcription factor that plays a crucial role in energy homeostasis by regulating the metabolism of glucose and lipids. This study aimed to investigate the association of the T130I variant of the HNF4A gene in Mexican children with MetS and its constituent components. Methods: The study was performed in 477 children from elementary schools. MetS was classified according to the de Ferranti definition. Biochemical parameters were measured and genotyping was performed. Logistic regression under a dominant genetic model was used to analyze the association of the T130I variant of the HNF4A gene with MetS and with its components separately. Results: The prevalence of MetS was 25.4%, and 18.9% in children who presented insulin resistance. Interestingly, this is the first time that a significant association between the T130I variant of the HNF4A gene and MetS has been reported [odds ratios (OR) = 2.31; 95% confidence interval (CI) 1.10-4.83; P = 0.026]. Moreover, carriers of the risk allele show higher abdominal obesity (OR = 1.20; 95% CI 1.09-4.50; P = 0.029). These findings highlight the active role of genetic variants in the pathogenesis of MetS in Mexican children. Conclusions: The high prevalence of children with MetS and insulin resistance places this population at an elevated risk of early CVD and T2D. The Clinical Trial Registration Number is HJM2315/14C.

Pharmacogenetic Evaluation of Metformin and Sulphonylurea Response in Mexican Mestizos with Type 2 Diabetes.

BACKGROUND: In Mexico, approximately 25% of patients with type 2 diabetes (T2D) have adequate glycemic control. Polymorphisms in pharmacogenetic genes have been shown to have clinical consequences resulting in drug toxicity or therapeutic inefficacy. OBJECTIVE: The study aimed to evaluate the impact of variants in genes known to be involved in response to oral hypoglycemic drugs, such as CYP2C9, OCT, MATE, ABCA1 and C11orf65, in the Mexican Mestizo population of T2D patients. METHODS: In this study, 265 patients with T2D were enrolled from the Hospital Juárez de México, Mexico City. Genotyping was performed by TaqMan® assays. SNP-SNP interactions were analyzed using the multifactor dimensionality reduction (MDR) method. RESULTS: Carriers of the del allele of rs72552763 could achieve better glycemic control than noncarriers. There was a significant difference in plasma glucose and HbA1c levels among rs622342 genotypes. The results suggested an SNP-SNP interaction between rs72552763 and rs622342 OCT1 and rs12943590 MATE2. CONCLUSION: The interaction between rs72552763 and rs622342 in OCT1, and rs12943590 in MATE2 suggested an important role of these polymorphisms in metformin response in T2D Mexican Mestizo population.

Whole-exome sequencing in maya indigenous families: variant in PPP1R3A is associated with type 2 diabetes.

It has been presumed that increased susceptibility in Mexicans to type 2 diabetes (T2D) is attributed to the Native American genetic ancestry. Nonetheless, it is not known if there are private genetic variants that confer susceptibility to develop T2D in our population. The Maya indigenous group has the highest proportion of Native American ancestry (98%) which makes it a representative group of the original peoples of Mexico. Thus, the aim of the present study is to identify new genetic variants associated with T2D in Maya families. Whole-exome sequencing was performed on DNA samples from Maya families with a third-generation family history of T2D only in one parental line. Four variants were identified for APOB, PPP1R3A, TPPP2, and GPR1 genes, and were further tested for association with T2D in 600 unrelated Maya in a case-control study. For the first time, rs1799999 in PPP1R3A was associated with risk of T2D in Mayan Mexican individuals (OR = 1.625, P = 0.014). Interestingly, carriers of rs1799999 presented increased values of HOMA-IR. In addition, rs1801702 in APOB was associated with total cholesterol and LDL-C (P = 0.019 and P = 0.020, respectively) in normoglycemic individuals; rs3732083 in GPR1 with HOMA-IR (P = 0.016) and rs9624 in TPPP2 with total cholesterol and triglycerides (P = 0.002 and P = 0.005, respectively) in T2D subjects. Overall, these findings support the idea that there are other genetic variants yet to be described, involved in T2D development in Maya population, being insulin resistance and lipid metabolism the main mechanisms implicated. Thus, these results can contribute to the understanding of diabetes genetic background in Mexican population.