Journal
AMERICAN JOURNAL OF NEPHROLOGY
Volume 30, Issue 2, Pages 112-119Publisher
KARGER
DOI: 10.1159/000204362
Keywords
IRS-1; Reactive oxygen species; Aerobic capacity; Insulin resistance
Categories
Funding
- NIH [R01 HL73101-01A1]
- Veterans Affairs Merit System [0018]
- National Center for Research Resources of NIH [R24 RR17718]
- NATIONAL CENTER FOR RESEARCH RESOURCES [R24RR017718] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL073101] Funding Source: NIH RePORTER
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Background/Aims: 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. Methods: 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. Results: 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-alpha and IRS-1 without altering triacylglycerol content. IRS-1 ubiquitination was higher in the LCR than HCR kidney, increased after HFD. Conclusions: 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. Copyright (C) 2009 S. Karger AG, Basel
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