Nutrition
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For almost 50 y, the US National Health and Nutrition Examination Survey (NHANES) has measured the caloric consumption, and body heights and weights of Americans. The aim of this study was to determine, based on that data, how macronutrient consumption patterns and the weight and body mass index in the US adult population have evolved since the 1960s. ⋯ Since 1971, the shift in macronutrient share from fat to carbohydrate is primarily due to an increase in absolute consumption of carbohydrate as opposed to a change in total fat consumption. General adherence to recommendations to reduce fat consumption has coincided with a substantial increase in obesity.
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The apolipoprotein B (APOB) gene has been reported to be a candidate gene for individual susceptibility to dyslipidemia and obesity. The aim of this study was to investigate the effect of the APOB rs1469513 polymorphism on plasma lipid profiles and obesity-related phenotypes, together with their modulation by dietary intake in Korean individuals. ⋯ Our findings support a significant association between the APOB rs1469513 variant, plasma lipid profiles, and obesity-related phenotypes. This association has the potential to be modified by dietary fat intake. These results may offer proof that the differences between normal weight and overweight/obese individuals might partly result from different SNPs.
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The gut-associated lymphoid tissue is continuously exposed to antigens in the gut lumen and becomes the first line of defense against enteric bacteria and associated toxin. The aim of this study was to investigate the effects of parenteral glutamine (GLN) supplementation in combination with enteral nutrition (EN) on intestinal mucosal immunity in septic rats by cecal ligation and puncture (CLP). ⋯ The results of this study show that parenteral glutamine supplementation in combination with enteral nutrition may attenuate PP apoptosis, increase PP cell yield and intestinal lamina propria IgA plasma cells, and subsequently improve intestinal mucosal immunity. Clinically, these results suggest therapeutic efforts at improving intestinal immunity may contribute to the prevention and treatment of sepsis.
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Previous studies have shown duodenal-jejunal exclusion (DJE) results in the rapid resolution of type 2 diabetes; however, the underlying mechanism is unknown. This study aimed to measure the hepatic expression of insulin receptor substrate-2 (IRS-2) and glucose transporter-2 (GLUT-2) in type 2 diabetic rats post-DJE, and to investigate their roles in improved hepatic insulin resistance and glucose intolerance. ⋯ DJE led to upregulated hepatic IRS-2 and GLUT-2 expression in the hepatic insulin signaling pathway and improved insulin sensitivity in type 2 diabetic rats.