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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Citrate (si)-Synthase, Dietary Fats, Electron Transport Complex IV, Female, Glucose, Glucose Tolerance Test, Insulin Receptor Substrate Proteins, Kidney, Lipids, Mitochondria, NADPH Oxidases, Oxidative Stress, Rats, Reactive Oxygen Species.
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Do low aerobic capacity and high-fat diet contribute to oxidative stress and IRS-1 degradation in the kidney? Context: Insulin receptor (IR-alpha and IR-beta) is reduced in the kidney of insulin-resistant rodents. It is unknown if there are also reductions in insulin receptor substrate (IRS)-1 or if these effects are due to metabolic injury. Thereby, we hypothesized intrinsically high aerobic fitness would protect against high-fat diet (HFD)-induced reactive oxygen species (ROS) and IRS-1 degradation. We investigated the effects of HFD on triglyceride content, ROS production and IRS-1 degradation in the kidney of high-capacity (HCR)/low-capacity (LCR) rats, a model of intrinsic high and low aerobic capacity. Eighteen-week-old HCR and LCR rats were placed on a HFD or normal chow diet for 7 weeks. Intraperitoneal glucose tolerance, ROS, IR-beta, total IRS-1 and ubiquitination were measured. The HCR displayed greater insulin sensitivity and were resistant to HFD-induced insulin resistance. In the LCR kidney, HFD increased ROS potential, and reduced total IR-beta and IRS-1 without altering triacylglycerol content. IRS-1 ubiquitination was higher in the LCR than HCR kidney, increased after HFD.
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Our data support that HFD-mediated kidney ROS is associated with reductions in IRS-1 and systemic insulin resistance. Further, high intrinsic aerobic capacity protects against IRS-1 degradation in the kidney following exposure to HFD. Final Decision: yes