Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance
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DOI:
10.1152/ajpendo.00500.2006
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发表时间:
2007-07-01
影响因子:
5.1
通讯作者:
Lust, Robert M.
Lust, Robert M.
中科院分区:
医学2区
文献类型:
--
作者:
Noland, Robert C.;Thyfault, John P.;Lust, Robert M.

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人们认为,通过耐力运动训练等方式提高氧化能力可以预防肥胖和糖尿病的发生。为低(LCR)和高(HCR)能力耐力跑而饲养的老鼠提供了一种在有氧能力方面具有固有差异的遗传模型,允许在没有训练刺激的混杂影响的情况下测试这种假设。本研究的目的是确定高脂饮食 (HFD) 对未经训练的 LCR 和 HCR 雄性大鼠的体重增加模式、胰岛素敏感性和脂肪酸氧化能力的影响。结果表明,与 HCR 大鼠相比,食物喂养的 LCR 大鼠体重较重,甘油三酯水平较高,胰岛素敏感性较低,且骨骼肌氧化能力较低。接触 HFD 后,LCR 大鼠的体重和脂肪量增加,并且胰岛素抵抗状况恶化,尽管其消耗的代谢能量与食物喂养的对照组相似。这些代谢变量在 HCR 大鼠中保持不变。 HFD 增加了两种品系大鼠的骨骼肌氧化能力,而肝脏氧化能力仅在 LCR 大鼠中降低。这些结果表明,LCR 大鼠容易肥胖,并且骨骼肌氧化能力的增强并不能防止 HFD 引起的体重过度增加或胰岛素抵抗的加剧。基础骨骼肌氧化能力的升高和保护肝脏氧化能力的能力可能会保护 HCR 大鼠免受 HFD 诱导的肥胖和胰岛素抵抗。
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 with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and 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 that 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 an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance.