Abstract

Increased consumption of processed foods is suspected to be contributing to obesity and chronic disease. We hypothesized that long‐term consumption of more processed food (mimicked with high (HGR) or low glycemic response (LGR) starches) would lead to oxidation of the circulating redox state, increased fat accumulation, and reduced insulin sensitivity. Mice consumed HGR or LGR food for 16 weeks. Body mass increased at a faster rate for those consuming the HGR diet (p < 0.05 for weeks 8‐16). Percentage body fat was greater and percentage lean mass was lower in the HGR group starting at 12 weeks (p < 0.05; MRI). However, insulin sensitivity at week 14 (OGTT; AUC, p = 0.14) and metabolic parameters (RER, heat production, activity) at weeks 4 or 15 were not significantly different between groups. At the termination of the study, redox pairs (L/P, B/A) suggested a more oxidized redox state in blood of mice on the LGR diet. TrxR activity in blood and TBARS of blood and liver tissues were similar between groups (p > 0.05). These data illustrate that the mechanism by which processed carbohydrates contributes to obesity is not via oxidation of the circulating redox state.Grant Funding Source: United States Department of Agriculture

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