• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Chronic PYY3-36 treatment promotes fat oxidation and ameliorates insulin resistance in C57BL6 mice.
【24h】

Chronic PYY3-36 treatment promotes fat oxidation and ameliorates insulin resistance in C57BL6 mice.

机译：慢性PYY3-36治疗可促进C57BL6小鼠脂肪氧化并改善胰岛素抵抗。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

PYY(3-36) is a gut-derived hormone acting on hypothalamic nuclei to inhibit food intake. We recently showed that PYY(3-36) acutely reinforces insulin action on glucose disposal in mice. We aimed to evaluate effects of PYY(3-36) on energy metabolism and the impact of chronic PYY(3-36) treatment on insulin sensitivity. Mice received a single injection of PYY(3-36) or were injected once daily for 7 days, and energy metabolism was subsequently measured in a metabolic cage. Furthermore, the effects of chronic PYY(3-36) administration (continuous and intermittent) on glucose turnover were determined during a hyperinsulinemic-euglycemic clamp. PYY(3-36) inhibited cumulative food intake for 30 min of refeeding after an overnight fast (0.29 +/- 0.04 vs. 0.56 +/- 0.12 g, P = 0.036) in an acute setting, but not after 7 days of daily dosing. Body weight, total energy expenditure, and physical activity were not affected by PYY(3-36). However, it significantly decreased the respiratory quotient. Both continuous and intermittent PYY(3-36) treatment significantly enhanced insulin-mediated whole body glucose disposal compared with vehicle treatment (81.2 +/- 6.2 vs. 77.1 +/- 5.2 vs. 63.4 +/- 5.5 micromol.min(-1).kg(-1), respectively). In particular, PYY(3-36) treatment increased glucose uptake in adipose tissue, whereas its impact on glucose disposal in muscle did not attain statistical significance. PYY(3-36) treatment shifts the balance of fuel use in favor of fatty acids and enhances insulin sensitivity in mice, where it particularly promotes insulin-mediated glucose disposal. Notably, these metabolic effects of PYY(3-36) remain unabated after chronic administration, in contrast to its anorexic effects.
机译：PYY（3-36）是一种肠源激素，作用于下丘脑核，抑制食物摄入。我们最近显示，PYY（3-36）可以急性增强小鼠葡萄糖处置中的胰岛素作用。我们旨在评估PYY（3-36）对能量代谢的影响以及慢性PYY（3-36）治疗对胰岛素敏感性的影响。小鼠接受单次PYY（3-36）注射或每天注射一次，共7天，随后在代谢笼中测量能量代谢。此外，在高胰岛素-正常血糖钳夹期间确定了慢性PYY（3-36）给药（连续和间歇）对葡萄糖更新的影响。 PYY（3-36）在急性情况下禁食过夜（0.29 +/- 0.04对0.56 +/- 0.12 g，P = 0.036）后，在连续30分钟的进食中抑制了累积食物摄入，但每天7天后没有抑制加药。体重，总能量消耗和体育锻炼不受PYY（3-36）影响。但是，它大大降低了呼吸商。与溶媒治疗相比，连续和间歇性PYY（3-36）治疗均显着增强了胰岛素介导的全身葡萄糖处置（81.2 +/- 6.2 vs. 77.1 +/- 5.2 vs.63.4 +/- 5.5 micromol.min（-1 ）.kg（-1））。特别是，PYY（3-36）处理可增加脂肪组织中的葡萄糖摄取，而其对肌肉中葡萄糖处置的影响没有统计学意义。 PYY（3-36）处理可改变燃料使用的平衡，而有利于脂肪酸，并增强小鼠的胰岛素敏感性，在小鼠中特别促进胰岛素介导的葡萄糖处置。值得注意的是，与厌食症相比，PYY（3-36）的这些代谢作用在长期给药后仍未减弱。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号