...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Experimental Biology and Medicine: Journal of the Society for Experimental Biology and Medicine >Peripheral signals conveying metabolic information to the brain: short-term and long-term regulation of food intake and energy homeostasis.
【24h】

Peripheral signals conveying metabolic information to the brain: short-term and long-term regulation of food intake and energy homeostasis.

机译：周围的信号将代谢信息传递到大脑：食物摄入量和能量稳态的短期和长期调节。

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

Numerous peripheral signals contribute to the regulation of food intake and energy homeostasis. Mechano- and chemoreceptors signaling the presence and energy density of food in the gastrointestinal (GI) tract contribute to satiety in the immediate postprandial period. Changes in circulating glucose concentrations appear to elicit meal initiation and termination by regulating activity of specific hypothalamic neurons that respond to glucose. Other nutrients (e.g., amino acids and fatty acids) and GI peptide hormones, most notably cholecystokinin, are also involved in short-term regulation of food intake. However, the energy density of food and short-term hormonal signals by themselves are insufficient to produce sustained changes in energy balance and body adiposity. Rather, these signals interact with long-term regulators (i.e., insulin, leptin, and possibly the orexigenic gastric peptide, ghrelin) to maintain energy homeostasis. Insulin and leptin are transported into the brain where they modulate expression of hypothalamic neuropeptides known to regulate feeding behavior and body weight. Circulating insulin and leptin concentrations are proportional to body fat content; however, their secretion and circulating levels are also influenced by recent energy intake and dietary macronutrient content. Insulin and leptin concentrations decrease during fasting and energy-restricted diets, independent of body fat changes, ensuring that feeding is triggered before body energy stores become depleted. Dietary fat and fructose do not stimulate insulin secretion and leptin production. Therefore, attenuated production of insulin and leptin could lead to increased energy intake and contribute to weight gain and obesity during long-term consumption of diets high in fat and/or fructose. Transcription of the leptin gene and leptin secretion are regulated by insulin-mediated increases of glucose utilization and appear to require aerobic metabolism of glucose beyond pyruvate. Other adipocyte-derived hormones and proteins that regulate adipocyte metabolism, including acylation stimulating protein, adiponectin, diacylglycerol acyltransferase, and perilipin, are likely to have significant roles in energy homeostasis.
机译：许多外围信号有助于调节食物摄入和能量稳态。机械和化学感受器信号表明食物在胃肠道中的存在和能量密度有助于在餐后立即产生饱腹感。循环葡萄糖浓度的变化似乎通过调节对葡萄糖有反应的特定下丘脑神经元的活性来引起进餐开始和终止。其他营养素（例如氨基酸和脂肪酸）和GI肽激素，尤其是胆囊收缩素，也与短期食物摄入量有关。但是，食物本身的能量密度和短期激素信号不足以使能量平衡和身体肥胖持续发生变化。而是，这些信号与长期的调节剂（即胰岛素，瘦素以及可能的致食性胃肽生长素释放肽）相互作用，以维持能量稳态。胰岛素和瘦素被转运到大脑，在大脑中它们调节下丘脑神经肽的表达，该肽可调节进食行为和体重。循环中的胰岛素和瘦素浓度与体内脂肪含量成正比。然而，它们的分泌和循环水平也受近期能量摄入和饮食中大量营养素含量的影响。禁食和能量受限的饮食中，胰岛素和瘦素的浓度会降低，而与体脂的变化无关，从而确保在人体能量存储耗尽之前就开始进食。饮食中的脂肪和果糖不会刺激胰岛素分泌和瘦素产生。因此，在长期摄入高脂肪和/或果糖饮食的过程中，胰岛素和瘦素的生产减少可能导致能量摄入增加，并导致体重增加和肥胖。瘦素基因的转录和瘦素分泌受胰岛素介导的葡萄糖利用增加的调节，并且似乎需要除丙酮酸以外的葡萄糖的有氧代谢。其他调节脂肪细胞代谢的脂肪细胞源激素和蛋白质，包括酰化刺激蛋白，脂联素，二酰基甘油酰基转移酶和周脂素，可能在能量稳态中起重要作用。

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