Abstract Title:

Melatonin reduces endoplasmic reticulum stress and autophagy in liver of leptin-deficient mice.

Abstract Source:

J Pineal Res. 2016 Apr 19. Epub 2016 Apr 19. PMID: 27090356

Abstract Author(s):

Beatriz de Luxán-Delgado, Yaiza Potes, Adrian Rubio-González, Beatriz Caballero, Juan José Solano, María Fernández-Fernández, Manuel Bermúdez, Marcela Rodrigues Moreira Guimarães, Ignacio Vega-Naredo, José Antonio Boga, Ana Coto-Montes

Article Affiliation:

Beatriz de Luxán-Delgado


The sedentary lifestyle of modern society along with the high intake of energetic food have made obesity a current worldwide health problem. Despite great efforts to study 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 the present study, wild-type and obese (ob/ob) mice received daily intraperitoneal injections of melatonin at a dose of 500μg/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. This article is protected by copyright. All rights reserved.

Study Type : Animal Study
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