Abstract

Background: Obesity and being overweight have been described as potential causes of neurological disorders. Leptin, a peptide expressed in fat tissue, importantly participates in energy homeostasis and storage and has recently been identified for its signaling receptors in neuronal circuits of the brain. Aim: To elucidate whether the endogenous modulation of leptin can be a protection against neuropsychiatric disorders. Method: A systematic review was performed in accordance with the PRISMA-P method, and reports of studies containing data of leptin concentrations in healthy individuals with or without obesity were retrieved from the PubMed database, using the combinations of Mesh terms for “Leptin” and “Metabolism”. Results: Forty-seven randomized and non-randomized controlled trials, dating from 2000 to 2021, were included in the qualitative synthesis. Discussion and conclusions: Leptin secretion displays a stabilizing pattern that is more sensitive to a negative energy intake imbalance. Leptin levels influence body weight and fat mass as a pro-homeostasis factor. However, long-term exposure to elevated leptin levels may lead to mental/behavioral disorders related to the feeding and reward systems.

Highlights

  • IntroductionPublisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations

  • Changes in leptin levels correlate with changes in total, subcutaneous, and visceral adipose tissue

  • It was found that leptin levels do not immediately return to their previous concentrations when individuals return to a eucaloric diet

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The implications of weight control for the development of metabolic disorders, such as cardiovascular diseases and diabetes, have been widely described in the scientific literature [1]. Genome-wide association studies have identified more than 100 genes involved in overweight and obesity phenotypes, and the complex polygenic gene-behavior interaction explains the relevance of exogenous factors in such processes [2,3,4,5,6,7]. The identification of genetic components involved in energy metabolism does not account for individual needs regarding diet and/or exercise in order to achieve weight control [8,9]

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