Influence of Dietary Starches Differing in Glycemic Index on Pro-oxidant and Anti-Oxidant Gene Expression and Insulin Sensitivity in a Mouse Model
Type of DegreeThesis
Nutrition and Food Science
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The prevalence of obesity and diabetes has reached pandemic proportions worldwide. In the U.S., increased intakes of refined carbohydrates have been reported to parallel this trend. In general, refined carbohydrates (e.g. highly processed grains, sweeteners, and sugar-sweetened beverages) cause more rapid and larger increases in postprandial glycemia and insulinemia than do complex carbohydrates (e.g. whole-grains, fiber-containing products, legumes, fruits and vegetables). Thus, the concept of glycemic index (GI) was developed as a way of ranking carbohydrates according to how they affect postprandial glycemia. In human and animal studies, high-GI diets have been correlated with an increased risk of obesity, insulin resistance, type 2 diabetes, and coronary heart disease; however, the exact molecular mechanism(s) by which high-GI diets elicit adverse effects is unknown. Oxidative stress has been implicated in the pathogenesis of coronary heart disease, insulin resistance, and type 2 diabetes through an overproduction of reactive oxygen species. Thus, the objectives of this study were to assess the chronic effects of a high-GI diet on 1) pro-oxidant and anti-oxidant gene expression in the adipose tissue, and 2) insulin sensitivity in male, C57Bl/6J mice. Mice were fed either a high fat (HF) or a low fat (LF) diet, ad libitum, containing either a high-GI starch (100% amylopectin, Amioca®) or a low-GI starch (60% amylose/40% amylopectin, Hi-Maize® or 55% amylose/ 45% amylopectin, HylonV®) for 15 weeks. The expression levels of the pro-oxidant gene, NADPH oxidase, and the anti-oxidant genes, superoxide dismutase-2 (SOD-2), glutathione peroxidase-1 (GPx-1), and catalase were quantified in the epididymal adipose tissue by real-time, reverse transcriptase polymerase chain reaction (RT-PCR) methods. In addition, plasma glucose, insulin, total triacylglycerol, adiponectin, and leptin concentrations were assayed in plasma samples collected at the time of sacrifice. The main treatment effects, the interaction between fat and starch, and differences among the means between groups were assessed using one-way and two-way ANOVA, MANOVA with repeated measures tests, unpaired Student’s t tests, and orthogonal contrast procedures. The results are reported as LSmeans ± SE, and were considered significant when P < 0.05. In comparison to the LF groups, the high dietary fat resulted in increased weight gain, absolute and relative adipose and liver weight, fasting plasma glucose and insulin, insulin resistance, and NADPH oxidase gene expression. Conversely, increased dietary fat decreased plasma adiponectin concentration, and GPx-1 and catalase gene expression. The high-GI diet, compared to both low-GI diets, increased the post-prandial glycemic response during a meal tolerance test, as well as non-fasting blood glucose concentrations at 4 and 8 weeks. However, the type of dietary starch consumed (whether high-GI or low-GI) did not influence the expression of pro-oxidant (NADPH oxidase) or antioxidant (Catalase, GPx-1, SOD-2) genes in the adipose tissue of male, C57Bl/6 mice. Similarly, with the exception of the HF/HylonV® group, the type of dietary starch consumed had no influence on insulin sensitivity. Thus, generation of oxidative stress in the adipose tissue of male, C57Bl/6 mice does not appear to be a mechanism by which high-GI diets elicit adverse effects.