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炎症状态下食欲与胰岛素信号传导的调节

Regulation of appetite and insulin signaling in inflammatory states.

作者信息

Teli Thalia, Xanthaki Despina, Karalis Katia P

机构信息

Developmental Biology Section, Foundation for Biomedical Research of the Academy of Athens, Athens, 11527 Greece.

出版信息

Ann N Y Acad Sci. 2006 Nov;1083:319-28. doi: 10.1196/annals.1367.022.

Abstract

Inflammatory states are characterized by decreased food intake, hyperglycemia, and insulin resistance. The contribution of cytokines in this phenotype is important and is exerted through activation of SOCS proteins and inhibition of insulin signaling, as well as through direct stimulation of the ob gene. Obesity, a condition that has reached epidemic rates, is characterized by hyperglycemia, hyperlipidemia, insulin resistance and increased food intake, and body weight. In the following article we summarize the current views of the mechanisms underlying insulin resistance in obesity and the other inflammatory states. We also discuss the regulation of appetite in inflammatory states, and we provide evidence on the cytokine-independent induction of anorexia following immune activation in mice. Understanding of the exact mechanisms regulating these processes may provide important insights for the control of this group of diseases that compromise to a great extent the quality of life and are associated with high mortality.

摘要

炎症状态的特征是食物摄入量减少、高血糖和胰岛素抵抗。细胞因子在这种表型中的作用很重要,它通过激活SOCS蛋白和抑制胰岛素信号传导,以及直接刺激ob基因来发挥作用。肥胖,一种已达到流行率的疾病,其特征是高血糖、高血脂、胰岛素抵抗、食物摄入量增加和体重增加。在接下来的文章中,我们总结了目前关于肥胖和其他炎症状态下胰岛素抵抗潜在机制的观点。我们还讨论了炎症状态下的食欲调节,并提供了小鼠免疫激活后非细胞因子依赖性厌食诱导的证据。了解调节这些过程的确切机制可能为控制这组严重影响生活质量并与高死亡率相关的疾病提供重要见解。

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