Department of Biomedical and NeuroMotor Sciences, 40126 Bologna, Italy.
Department of Chemical Physiology and Biochemistry, Oregon Health & Science University, Portland, OR 97239, USA.
Int J Mol Sci. 2023 Jan 31;24(3):2684. doi: 10.3390/ijms24032684.
It is well established that decreases in plasma leptin levels, as with fasting, signal starvation and elicit appropriate physiological responses, such as increasing the drive to eat and decreasing energy expenditure. These responses are mediated largely by suppression of the actions of leptin in the hypothalamus, most notably on arcuate nucleus (ArcN) orexigenic neuropeptide Y neurons and anorexic pro-opiomelanocortin neurons. However, the question addressed in this review is whether the effects of increased leptin levels are also significant on the long-term control of energy balance, despite conventional wisdom to the contrary. We focus on leptin's actions (in both lean and obese individuals) to decrease food intake, increase sympathetic nerve activity, and support the hypothalamic-pituitary-thyroid axis, with particular attention to sex differences. We also elaborate on obesity-induced inflammation and its role in the altered actions of leptin during obesity.
众所周知,血浆瘦素水平下降,如禁食,会发出饥饿信号,并引发适当的生理反应,如增加进食欲望和减少能量消耗。这些反应主要通过抑制瘦素在下丘脑的作用来介导,尤其是对弓状核(ArcN)的食欲肽神经肽 Y 神经元和厌食性 pro-促黑激素神经元的作用。然而,本篇综述中要探讨的问题是,尽管与传统观点相反,升高的瘦素水平是否对长期能量平衡控制也有重要影响。我们重点关注瘦素的作用(在瘦人和肥胖个体中),包括降低食物摄入、增加交感神经活动和支持下丘脑-垂体-甲状腺轴,特别关注性别差异。我们还详细阐述了肥胖引起的炎症及其在肥胖期间瘦素作用改变中的作用。