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

IF 7 2区医学 Q1 ENDOCRINOLOGY & METABOLISM Molecular Metabolism Pub Date : 2025-01-01 DOI:10.1016/j.molmet.2024.102078

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

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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.

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瘦素作为肥胖信号和奖励系统调节剂调节能量平衡。

瘦素是一种脂肪组织衍生的激素，在体重、食欲和行为调节中起着至关重要的作用。瘦素控制能量平衡，作为肥胖水平的一个指标，并作为奖励系统的调节剂，这与喜欢美味的食物有关。肥胖的特点是脂肪组织体积增大，从而导致血液中瘦素浓度升高。瘦素对大多数形式的肥胖的治疗潜力受到瘦素抵抗和窄剂量反应窗口的阻碍。这篇综述描述了目前对瘦素促进负能量平衡和抑制影响食物奖励的神经回路的大脑区域和细胞内通路的了解。我们还描述了肥胖中阻碍这些生物反应的机制，并强调了潜在的治疗干预措施。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Molecular Metabolism ENDOCRINOLOGY & METABOLISM-

CiteScore

14.50

自引率

2.50%

发文量

219

审稿时长

43 days

期刊介绍： Molecular Metabolism is a leading journal dedicated to sharing groundbreaking discoveries in the field of energy homeostasis and the underlying factors of metabolic disorders. These disorders include obesity, diabetes, cardiovascular disease, and cancer. Our journal focuses on publishing research driven by hypotheses and conducted to the highest standards, aiming to provide a mechanistic understanding of energy homeostasis-related behavior, physiology, and dysfunction. We promote interdisciplinary science, covering a broad range of approaches from molecules to humans throughout the lifespan. Our goal is to contribute to transformative research in metabolism, which has the potential to revolutionize the field. By enabling progress in the prognosis, prevention, and ultimately the cure of metabolic disorders and their long-term complications, our journal seeks to better the future of health and well-being.