Adipose tissue redistribution caused by an early consumption of a high sucrose diet in a rat model / Redistribución del tejido adiposo en un modelo de rata debido al alto consumo de sacarosa desde edad temprana

Introduction: obesity is a major public health problem worldwide. The quantity and site of accumulation of adipose tissue is of great importance for the physiopathology of this disease. Objectives: the aim of this study was to assess the effect of a high carbohydrate diet on adipose tissue distribution. Methods: male Wistar rats, control (CONT) and high sucrose diet (HSD; 30% sucrose in their drinking water), were monitored during 24 weeks and total energy and macronutrient intake were estimated by measuring daily average consumption. A bioelectrical impedance procedure was performed at 22 weeks of treatment to assess body compartments and systolic arterial blood pressure was measured. Serum was obtained and retroperitoneal adipose tissue was collected and weighed. Results: HSD ingested less pellets and beverage, consuming less lipids and proteins than CONT, but the same amount of carbohydrates. Retroperitoneal adipose tissue was more abundant in HSD. Both groups were normoglycemic; triglycerides, adiponectin and leptin levels were higher, while total cholesterol and HDLcholesterol were lower in HSD; insulin, HOMA index and systolic blood pressure had a tendency of being higher in HSD. Discussion: this model presents dyslipidemia and a strong tendency for insulin resistance and hypertension. Even though there was no difference in body compartments between groups, retroperitoneal adipose tissue was significantly increased in HSD. This suggests that a rearrangement of adipose tissue distribution towards the abdominal cavity takes place as a result of chronic high sucrose consumption, which contributes to a higher risk of suffering from metabolic and chronic degenerative diseases (AU)

Introducción: la obesidad es uno de los mayores problemas de salud pública en todo el mundo. El momento en que se establece, la distribución y cantidad de tejido adiposo son de gran importancia para comprender su fisiopatología. Objetivos: observar la distribución de tejido adiposo en una dieta alta en sacarosa desde una edad temprana en un modelo animal. Métodos: se utilizaron ratas Wistar recién destetadas, animales control (CONT; agua ad libitum) y animales con dieta alta en sacarosa (HSD; 30% de sacarosa en el agua) durante 24 semanas. Se calcularon las kilocalorías y macronutrientes ingeridos diariamente; se evaluaron por impedancia bioeléctrica los compartimientos corporales, se midió la presión sistólica, se obtuvo el tejido adiposo retroperitoneal y el suero para medir parámetros bioquímicos. Resultados: los animales HSD comieron y bebieron menos, obteniendo menos proteínas y lípidos, sin diferencia en los hidratos de carbono. El tejido adiposo fue más abundante en HSD. Ambos grupos CONT Y HSD fueron normoglucémicos; HSD tuvieron triglicéridos, adiponectina y leptina altos, y el colesterol y las HDL más bajos; la insulina, el HOMA y la presión sistólica tuvieron tendencia a ser mayores en HSD. Discusión: este modelo presenta dislipidemia y una tendencia a tener resistencia a la insulina e hipertensión. A pesar de no haber una diferencia en los compartimentos corporales entre grupos, el tejido adiposo tuvo una localización específica en la espalda y fue más abundante en HSD. En conclusión, la distribución de grasa en el abdomen es consecuencia de una ingestión crónica alta en sacarosa, lo que predispone a padecer enfermedades crónico-degenerativas (AU)

A genetic variant of the CAPN10 gene in Mexican subjects with dyslipidemia is associated with increased HDL-cholesterol concentrations after the consumption of a soy protein and soluble fiber dietary portfolio / Una variante genética del gen capn10 en sujetos mexicanos con dislipidemia se asocia con un aumento de las concentraciones de colesterol hdl después del consumo de un portafolio dietario de soya y fibra soluble

Dyslipidemia is a major public health problem, and therefore, it is important to develop dietary strategies to diminish the prevalence of this disorder. It was recently reported that diet may play an important role in triggering insulin resistance by interacting with genetic variants at the CAPN10 gene locus in patients with metabolic syndrome. Nonetheless, it remains unknown whether genetic variants of genes involved in the development of type 2 diabetes are associated with variations in high-density lipoprotein cholesterol (HDL-C). The study used a single-center, prospective, cohort design. Here, we assessed the effect of four variants of the CAPN10 gene on HDL-C levels in response to a soy protein and soluble fiber dietary portfolio in subjects with dyslipidemia. In 31 Mexican dyslipidemic individuals, we analyzed four CAPN10 gene variants (rs5030952, rs2975762, rs3792267, and rs2975760) associated with type 2 diabetes. Subjects with the GG genotype of the rs2975762 variant of the CAPN10 gene were better responders to dietary intervention, showing increased HDL-C concentrations from the first month of treatment. HDL-C concentrations in participants with the wild type genotype increased by 17.0%, whereas the HDL-C concentration in subjects with the variant genotypes increased by only 3.22% (p = 0.03); the low-density lipoprotein cholesterol levels of GG carriers tended to decrease (-12.6%). These results indicate that Mexican dyslipidemic carriers of the rs2975762-GG genotype are better responders to this dietary intervention (AU)

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Association of the calpain-10 gene with type 2 diabetes in Europeans: results of pooled and meta-analyses.

We conducted pooled and meta-analyses of the association of the calpain-10 gene (CAPN10) polymorphisms SNP-43, Indel-19 and SNP-63 individually and as haplotypes with type 2 diabetes (T2D) in 3237 patients and 2935 controls of European ancestry. In the pooled analyses, the common SNP-43*G allele was associated with modest but statistically significant increased risk of T2D (odds ratio (OR)=1.11 (95% confidence interval (CI), 1.02-1.20), P=0.01). Two haplotype combinations were associated with increased risk of T2D (1-2-1/1-2-1, OR=1.20 (1.03-1.41), P=0.02; and 1-1-2/1-2-1, OR=1.26 (1.01-1.59), P=0.04) and one with decreased risk (1-1-1/2-2-1, OR=0.86 (0.75-0.99), P=0.03). The meta-analysis also showed a significant effect of the 1-2-1/1-2-1 haplogenotype on risk (OR=1.25 (1.05-1.50), P=0.01). However, there was evidence for heterogeneity with respect to this effect (P=0.06). The heterogeneity appeared to be due to data sets in which the cases were selected from samples used in linkage studies of T2D. Using only the population-based case-control samples removed the heterogeneity (P=0.89) and strengthened the evidence for association with T2D in both the pooled (SNP-43*G, OR=1.19 (1.07-1.32), P=0.001; 1-2-1/1-2-1 haplogenotype, OR=1.46 (1.19-1.78), P=0.0003; 1-1-2/1-2-1 haplogenotype, OR=1.52 (1.12-2.06), P=0.007; and 1-1-1/2-2-1 haplogenotype, OR=0.83 (0.70-0.99), P=0.03) and the meta-analysis (SNP-43*G, OR=1.18 (1.05-1.32), P=0.005; 1-2-1/1-2-1 haplogenotype, OR=1.68 (1.33-2.11), P=0.00001). The pooled and meta-analyses as well as the linkage disequilibrium and haplotype diversity studies suggest a role for genetic variation in CAPN10 affecting risk of T2D in Europeans.