Adipocyte insulin resistance: effects of aging, obesity, exercise, and food restriction.
Adipocyte insulin resistance: effects of aging, obesity, exercise, and food restriction.
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脂肪细胞胰岛素抵抗：衰老、肥胖、运动和食物限制的影响。
DOI：
10.1152/jappl.1987.62.1.95
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Holloszy,JO
中科院分区：
文献类型：
--
作者：
Craig,BW;Garthwaite,SM;Holloszy,JO
本研究探讨了衰老、运动训练和食物限制对大鼠附睾脂肪细胞大小和胰岛素抵抗的影响。运动组在6个月大时获得自愿跑步轮。在12和28月龄时对大鼠进行研究。久坐不动的自由进食（SFE）大鼠肥胖，他们的脂肪细胞是极端的胰岛素抵抗，葡萄糖氧化和2-脱氧-D-葡萄糖（2-DOG）的摄取增加最小的响应高胰岛素浓度。与SFE大鼠相比，跑步者的脂肪细胞更小，对胰岛素的反应性更高（2-DOG摄取约为9倍，葡萄糖氧化约为30倍）。与SFE大鼠和跑步者相比，限制食物以保持体重的久坐大鼠的脂肪细胞在大小和胰岛素反应性方面都处于中间水平。脂肪细胞大小与2-DOG摄取和葡萄糖氧化对胰岛素的反应性之间存在密切的相关性，与年龄无关。在相同的治疗组中，成年（12个月）和老年（28个月）大鼠之间的脂肪细胞大小、胰岛素敏感性或胰岛素反应性无显著差异。我们的结论是，单独的衰老对脂肪细胞中葡萄糖代谢的胰岛素反应性几乎没有影响，肥胖老年大鼠脂肪细胞的胰岛素抵抗是由于脂肪细胞肥大，而不是衰老。运动可以有效地防止脂肪细胞肥大和胰岛素抵抗的发展。
This study examined the effects of aging, exercise training, and food restriction on epididymal fat cell size and resistance to insulin in rats. The exercise group was given access to voluntary running wheels at age 6 mo. The rats were studied at ages 12 and 28 mo. Sedentary free-eating (SFE) rats were obese and their fat cells were extremely insulin resistant, showing minimal increases in glucose oxidation and 2-deoxy-D-glucose (2-DOG) uptake in response to high insulin concentrations. The runners' adipocytes were smaller and had a greater responsiveness to insulin (approximately 9-fold for 2-DOG uptake and approximately 30-fold for glucose oxidation) than those of the SFE rats. Sedentary rats that were food restricted to keep their body weights the same as those of the runners had fat cells that were intermediate both in size and insulin responsiveness relative to those of the SFE rats and runners. There was a close correlation between fat cell size and responsiveness to insulin of 2-DOG uptake and glucose oxidation independent of age. There were no significant differences in fat cell size, insulin sensitivity, or insulin responsiveness between the adult (12 mo) and old (28 mo) rats in the same treatment groups. We conclude that aging alone has little or no effect on the responsiveness to insulin of glucose metabolism in fat cells and that the insulin resistance of adipocytes from obese older rats is due to fat cell hypertrophy, not aging. Exercise is effective in protecting against development of fat cell hypertrophy and insulin resistance.