Similar metabolic responses to calorie restriction in lean and obese Zucker rats
Similar metabolic responses to calorie restriction in lean and obese Zucker rats
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DOI：
10.1016/j.mce.2009.05.001
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发表时间：
2009-10-15
影响因子：
4.1
通讯作者：
Shimokawa, Isao
中科院分区：
文献类型：
--
作者：
Chiba, Takuya;Komatsu, Toshimitsu;Shimokawa, Isao
卡路里限制(CR)被认为在很大程度上依赖于由胰岛素/胰岛素样生长因子-1(IGF-1)和瘦素信号调节的神经内分泌系统，在许多生物中减少发病率和延长寿命。为了阐明胰岛素和瘦素敏感性是否在对CR的代谢适应中不可或缺，我们研究了CR对肥胖Zucker(FA/FA)大鼠和瘦对照组(+/+)大鼠的影响。CR不能完全改善(FA/FA)大鼠的胰岛素抵抗。然而，CR诱导了下丘脑弓状核神经肽Y(NPY)的表达，并改变了(FA/FA)和(+/+)大鼠肝脏代谢相关基因的表达。NPY的上调增加了血浆皮质酮水平，抑制了垂体生长激素(GH)的表达，从而调节脂肪细胞因子的产生，诱导组织特异性胰岛素敏感性。因此，中枢NPY通过外周信号的激活可能在CR的效果中发挥关键作用，即使在胰岛素抵抗和瘦素受体缺陷的情况下也是如此。(C)2009爱思唯尔爱尔兰有限公司。保留所有权利。
Calorie restriction (CR), which is thought to be largely dependent on the neuroendocrine system modulated by insulin/insulin-like growth factor-I (IGF-1) and leptin signaling, decreases morbidity and increases lifespan in many organisms. To elucidate whether insulin and leptin sensitivities are indispensable in the metabolic adaptation to CR, we investigated the effects of CR on obese Zucker (fa/fa) rats and lean control (+/+) rats. CR did not fully improve insulin resistance in (fa/fa) rats. Nonetheless, CR induced neuropeptide Y (NPY) expression in the hypothalamic arcuate nucleus and metabolism related gene expression changes in the liver in (fa/fa) rats and (+/+) rats. Up-regulation of NPY augmented plasma corticosterone levels and suppressed pituitary growth hormone (GH) expression, thereby modulating adipocytokine production to induce tissue-specific insulin sensitivity. Thus, central NPY activation via peripheral signaling might play a crucial role in the effects of CR, even in insulin resistant and leptin receptor deficient conditions. (C) 2009 Elsevier Ireland Ltd. All rights reserved.