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Am J Physiol Endocrinol Metab (March 6, 2007). doi:10.1152/ajpendo.00500.2006
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Submitted on September 14, 2006
Accepted on February 21, 2007

Artificial Selection for High Capacity Endurance Running is Protective Against High Fat Diet-Induced Insulin Resistance

Robert C. Noland1, John P. Thyfault2, Sarah T. Henes3, Brian R Whitfield3, tracey L. Woodlief3, Jasper R Evans3, Jennifer A. Lust1, Steven L Britton4, Lauren G Koch4, Ronald W Dudek5, G. Lynis Dohm1, Ronald N Cortright6, and Robert M Lust1*

1 Physiology, East Carolina University, Greenville, North Carolina, United States
2 Nutritional Sciences and Internal Medicine, University of Missouri, Columbia, Missouri, United States; Research, Harry S. Truman VA Hospital, 800 Hospital Drive, Columbia, 65211, United States
3 Exercise and Sport Science, East Carolina University, Greenville, North Carolina, United States
4 Physical Medicine and Rehabilitation, University of Michigan Medical School, Ann Arbor, Michigan, United States
5 Anatomy and Cell Biology, East Carolina University, Greenville, North Carolina, United States
6 Exercise and Sport Science, East Carolina University, Greenville, North Carolina, United States; Physiology, East Carolina University, Greenville, North Carolina, United States

* To whom correspondence should be addressed. E-mail: lustr{at}ecu.edu.

Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR) and high (HCR) capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared to HCR rats. Upon exposure to a HFD, LCR rats gained more weight, fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on a HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from high fat diet-induced obesity and insulin resistance.




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