Diabetes Center and.
Annu Rev Physiol. 2015;77:131-60. doi: 10.1146/annurev-physiol-021014-071656.
Diet-induced obesity leads to devastating and common chronic diseases, fueling ongoing interest in determining new mechanisms underlying both obesity and its consequences. It is now well known that chronic overnutrition produces a unique form of inflammation in peripheral insulin target tissues, and efforts to limit this inflammation have met with some success in preserving insulin sensitivity in obese individuals. Recently, the activation of inflammatory pathways by dietary excess has also been observed among cells located in the mediobasal hypothalamus, a brain area that exerts central control over peripheral glucose, fat, and energy metabolism. Here we review progress in the field of diet-induced hypothalamic inflammation, drawing key distinctions between metabolic inflammation in the hypothalamus and that occurring in peripheral tissues. We focus on specific stimuli of the inflammatory response, the roles of individual hypothalamic cell types, and the links between hypothalamic inflammation and metabolic function under normal and pathophysiological circumstances. Finally, we explore the concept of controlling hypothalamic inflammation to mitigate metabolic disease.
饮食诱导的肥胖会导致严重且常见的慢性疾病，这激发了人们对于确定肥胖及其后果相关新机制的持续兴趣。目前已经明确，慢性营养过剩会导致外周胰岛素靶组织发生独特形式的炎症，而限制这种炎症的努力在肥胖个体中维持胰岛素敏感性方面取得了一定的成功。最近，人们还观察到膳食过量会激活中脑腹侧基底部（mediobasal hypothalamus）细胞中的炎症通路，而该脑区对外周葡萄糖、脂肪和能量代谢具有中枢控制作用。在这里，我们回顾了饮食诱导的下丘脑炎症领域的进展，重点区分了下丘脑代谢性炎症和外周组织炎症之间的关键区别。我们特别关注炎症反应的特定刺激因素、特定下丘脑细胞类型的作用，以及在正常和病理生理情况下下丘脑炎症与代谢功能之间的联系。最后，我们探讨了控制下丘脑炎症以减轻代谢性疾病的概念。
