Zigman Jeffrey M, Elmquist Joel K
Department of Medicine and Division of Endocrinology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.
Endocrinology. 2003 Sep;144(9):3749-56. doi: 10.1210/en.2003-0241.
Over the past decade, there has been a tremendous increase in the understanding of the molecular and neural mechanisms that control food intake and body weight. Yet eating disorders and cachexia are still common, and obesity cases are rising at alarming rates. Thus, despite recent progress, an increased understanding of the molecular and neural substrates that control body weight homeostasis is a major public health goal. In this review, we discuss the mechanisms by which metabolic signals interact with key behavioral, neuroendocrine, and autonomic regulatory regions of the central nervous system. Additionally, we offer a model in which hormones such as leptin and ghrelin interact with similar central nervous system circuits and engage them in such a way as to maintain an appropriate and tight regulation of body weight and food intake. Our model predicts that overstimulation or understimulation of these central pathways can result in obesity, anorexia, or cachexia.
在过去十年中，我们对控制食物摄入和体重的分子及神经机制的理解有了巨大的提升。然而，饮食失调和恶病质仍然很常见，肥胖病例正以惊人的速度上升。因此，尽管最近取得了进展，但进一步了解控制体重稳态的分子和神经基础仍是一个主要的公共卫生目标。在这篇综述中，我们讨论了代谢信号与中枢神经系统关键行为、神经内分泌和自主调节区域相互作用的机制。此外，我们提出了一个模型，其中瘦素和胃饥饿素等激素与类似的中枢神经系统回路相互作用，并以维持对体重和食物摄入进行适当且严格调节的方式激活这些回路。我们的模型预测，这些中枢通路的过度刺激或刺激不足会导致肥胖、厌食或恶病质。
