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Melatonin reduces endoplasmic reticulum stress and autophagy in liver of leptin‐deficient mice
Author(s) -
LuxánDelgado Beatriz,
Potes Yaiza,
RubioGonzález Adrian,
Caballero Beatriz,
Solano Juan José,
FernándezFernández María,
Bermúdez Manuel,
Rodrigues Moreira Guimarães Marcela,
VegaNaredo Ignacio,
Boga José Antonio,
CotoMontes Ana
Publication year - 2016
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/jpi.12333
Subject(s) - melatonin , endoplasmic reticulum , leptin , endocrinology , autophagy , medicine , obesity , unfolded protein response , oxidative stress , inflammation , biology , apoptosis , microbiology and biotechnology , biochemistry
The sedentary lifestyle of modern society along with the high intake of energetic food has made obesity a current worldwide health problem. Despite great efforts to study the obesity and its related diseases, the mechanisms underlying the development of these diseases are not well understood. Therefore, identifying novel strategies to slow the progression of these diseases is urgently needed. Experimental observations indicate that melatonin has an important role in energy metabolism and cell signalling; thus, the use of this molecule may counteract the pathologies of obesity. In this study, wild‐type and obese (ob/ob) mice received daily intraperitoneal injections of melatonin at a dose of 500 μ g/kg body weight for 4 weeks, and the livers of these mice were used to evaluate the oxidative stress status, proteolytic (autophagy and proteasome) activity, unfolded protein response, inflammation and insulin signalling. Our results show, for the first time, that melatonin could significantly reduce endoplasmic reticulum stress in leptin‐deficient obese animals and ameliorate several symptoms that characterize this disease. Our study supports the potential of melatonin as a therapeutic treatment for the most common type of obesity and its liver‐associated disorders.