• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Food intake reductions and increases in energetic responses by hindbrain leptin and melanotan II are enhanced in mice with POMC-specific PTP1B deficiency
【24h】

Food intake reductions and increases in energetic responses by hindbrain leptin and melanotan II are enhanced in mice with POMC-specific PTP1B deficiency

机译：患有POMC特异性PTP1B缺乏症的小鼠的食物摄入减少以及后脑瘦素和美拉坦（melanotan）II的能量反应增强

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

Leptin regulates energy balance through central circuits that control food intake and energy expenditure, including proopiomelanocortin (POMC) neurons. POMC neuron- specific deletion of protein tyrosine phosphatase 1B (PTP1B) (Ptpn1 loxP/loxP POMC-Cre), a negative regulator of CNS leptin signaling, results in resistance to diet-induced obesity and improved peripheral leptin sensitivity in mice, thus establishing PTP1B as an important component of POMC neuron regulation of energy balance. POMC neurons are expressed in the pituitary, the arcuate nucleus of the hypothalamus (ARH), and the nucleus of the solitary tract (NTS) in the hindbrain, and it is unknown how each population might contribute to the phenotype of POMC-Ptp1b -/- mice. It is also unknown whether improved leptin sensitivity in POMC-Ptp1b -/- mice involves altered melanocortin receptor signaling. Therefore, we examined the effects of hindbrain administration (4th ventricle) of leptin (1.5, 3, and 6 μg) or the melanocortin 3/4R agonist melanotan II (0.1 and 0.2 nmol) in POMC-Ptp1b -/- (KO) and control PTP1Bfl/fl (WT) mice on food intake, body weight, spontaneous physical activity (SPA), and core temperature (TC). The results show that KO mice were hypersensitive to hindbrain leptin- and MTII-induced food intake and body weight suppression and SPA compared with WT mice. Greater increases in leptin- but not MTII-induced TC were also observed in KO vs. WT animals. In addition, KO mice displayed elevated hindbrain and hypothalamic MC4R mRNA expression. These studies are the first to show that hindbrain administration of leptin or a melanocortin receptor agonist alters energy balance in mice likely via participation of hindbrain POMC neurons.
机译：瘦素通过控制食物摄取和能量消耗的中央回路（包括proopiomelanocortin（POMC）神经元）调节能量平衡。 POMC神经元特异性蛋白酪氨酸磷酸酶1B（PTP1B）（Ptpn1 loxP / loxP POMC-Cre）的缺失，CNS瘦素信号的负调节剂，可抵抗饮食引起的肥胖并改善小鼠外周瘦素敏感性，从而建立PTP1B作为POMC神经元调节能量平衡的重要组成部分。 POMC神经元在垂体，下丘脑的弓形核（ARH）和后脑的孤立道（NTS）的核中表达，尚不清楚每个种群如何对POMC-Ptp1b-/的表型做出贡献- 老鼠。同样未知的是，POMC-Ptp1b-/-小鼠瘦素敏感性的改善是否涉及改变的黑皮质素受体信号传导。因此，我们研究了在POMC-Ptp1b-/-（KO）中瘦素（1.5、3和6μg）或黑皮质素3 / 4R激动剂美拉坦坦II（0.1和0.2 nmol）后脑给药（第4心室）的作用。控制PTP1Bfl / fl（WT）小鼠的摄食量，体重，自发体力活动（SPA）和核心温度（TC）。结果表明，与野生型小鼠相比，KO小鼠对后脑瘦素和MTII诱导的食物摄入以及体重抑制和SPA过敏。在KO与WT动物中，还观察到瘦素诱导的TC增加更大，而MTII诱导的TC没有增加。此外，KO小鼠显示出高的后脑和下丘脑MC4R mRNA表达。这些研究首次表明瘦素或黑皮质素受体激动剂的后脑给药可能通过后脑POMC神经元的参与改变小鼠的能量平衡。

著录项

相似文献

  • 外文文献
  • 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