Background

In response to energy abundant or deprived conditions, nutrients and hormones activate hypothalamic pathways to maintain energy and glucose homeostasis. The underlying CNS mechanisms, however, remain elusive in rodents and humans.

Scope of review

Here, we first discuss brain glucose sensing mechanisms in the presence of a rise or fall of plasma glucose levels, and highlight defects in hypothalamic glucose sensing disrupt in vivo glucose homeostasis in high-fat fed, obese, and/or diabetic conditions. Second, we discuss brain leptin signalling pathways that impact glucose homeostasis in glucose-deprived and excessed conditions, and propose that leptin enhances hypothalamic glucose sensing and restores glucose homeostasis in short-term high-fat fed and/or uncontrolled diabetic conditions.

Major conclusions

In conclusion, we believe basic studies that investigate the interaction of glucose sensing and leptin action in the brain will address the translational impact of hypothalamic glucose sensing in diabetes and obesity.

中文翻译：

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大脑中葡萄糖感测和瘦素作用的相互作用。

背景

为了应对能量丰富或缺乏的状况，营养物质和激素会激活下丘脑途径，以维持能量和葡萄糖的体内稳态。然而，潜在的CNS机制在啮齿动物和人类中仍然难以捉摸。

审查范围

在这里，我们首先讨论血浆葡萄糖水平升高或降低时的脑葡萄糖传感机制，并着重于高脂喂养，肥胖和/或糖尿病情况下丘脑葡萄糖传感的缺陷破坏体内葡萄糖体内稳态。其次，我们讨论了脑瘦素信号转导途径，该机制在缺糖和过量的葡萄糖条件下影响葡萄糖稳态，并提出在短期高脂喂养和/或糖尿病不受控制的情况下，瘦素增强下丘脑葡萄糖的感觉并恢复葡萄糖稳态。

主要结论

总之，我们相信研究葡萄糖传感和瘦素在大脑中相互作用的基础研究将解决下丘脑葡萄糖传感在糖尿病和肥胖症中的转化作用。