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瘦素作为肥胖信号和奖赏系统调节剂对能量平衡的调节。

Regulation of energy balance by leptin as an adiposity signal and modulator of the reward system.

作者信息

Asgari Roshanak, Caceres-Valdiviezo Maria, Wu Sally, Hamel Laurie, Humber Bailey E, Agarwal Sri Mahavir, Fletcher Paul J, Fulton Stephanie, Hahn Margaret K, Pereira Sandra

机构信息

Centre for Addiction and Mental Health, Toronto, ON, Canada.

Centre for Addiction and Mental Health, Toronto, ON, Canada; Laboratory of Omic Sciences, School of Medicine, Universidad de Especialidades Espíritu Santo, Samborondón, Ecuador.

出版信息

Mol Metab. 2025 Jan;91:102078. doi: 10.1016/j.molmet.2024.102078. Epub 2024 Nov 29.

Abstract

BACKGROUND

Leptin is an adipose tissue-derived hormone that plays a crucial role in body weight, appetite, and behaviour regulation. Leptin controls energy balance as an indicator of adiposity levels and as a modulator of the reward system, which is associated with liking palatable foods. Obesity is characterized by expanded adipose tissue mass and consequently, elevated concentrations of leptin in blood. Leptin's therapeutic potential for most forms of obesity is hampered by leptin resistance and a narrow dose-response window.

SCOPE OF REVIEW

This review describes the current knowledge of the brain regions and intracellular pathways through which leptin promotes negative energy balance and restrains neural circuits affecting food reward. We also describe mechanisms that hinder these biological responses in obesity and highlight potential therapeutic interventions.

MAJOR CONCLUSIONS

Additional research is necessary to understand how pathways engaged by leptin in different brain regions are interconnected in the control of energy balance.

摘要

背景

瘦素是一种源自脂肪组织的激素,在体重、食欲和行为调节中起关键作用。瘦素作为肥胖水平的指标和奖励系统的调节剂来控制能量平衡,而奖励系统与喜欢美味食物有关。肥胖的特征是脂肪组织量增加,因此血液中瘦素浓度升高。瘦素对大多数形式肥胖的治疗潜力受到瘦素抵抗和狭窄剂量反应窗口的阻碍。

综述范围

本综述描述了瘦素促进负能量平衡并抑制影响食物奖励的神经回路所通过的脑区和细胞内途径的现有知识。我们还描述了在肥胖中阻碍这些生物学反应的机制,并强调了潜在的治疗干预措施。

主要结论

有必要进行更多研究以了解瘦素在不同脑区所涉及的途径在能量平衡控制中是如何相互连接的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b8b/11696864/0a767006c576/gr1.jpg

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