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Published on: June 2, 2015
Melatonin administration decreases adipogenesis in the liver of ob/ob mice through autophagy modulation
Beatriz de Luxán-Delgado1, Beatriz Caballero, Yaiza Potes
1Department of Morphology and Cellular Biology, Faculty of Medicine, University of Oviedo, Oviedo, Spain.
Abstract:
Despite efforts to curb the incidence of obesity and its comorbidities, this condition remains the fifth leading cause of death worldwide. To identify ways to reduce this global effect, we investigated the actions of daily melatonin administration on oxidative stress parameters and autophagic processes as a possible treatment of obesity in ob/ob mice. The involvement of melatonin in many physiological functions, such as the regulation of seasonal body weight variation, glucose uptake, or adiposity, and the role of this indoleamine as an essential antioxidant, has become the focus of numerous anti-obesity studies. Here, we examined the oxidative status in the livers of obese melatonin-treated and untreated mice, observing a decrease in the oxidative stress levels through elevated catalase activity. ROS-mediated autophagy was downregulated in the liver of melatonin-treated animals and was accompanied by significant accumulation of p62. Autophagy is closely associated with adipogenesis; in this study, we report that melatonin-treated obese mice also showed reduced adiposity, as demonstrated by diminished body weight and reduced peroxisome proliferator-activated receptor gamma expression. Based on these factors, it is reasonable to assume that oxidative stress and autophagy play important roles in obesity, and therefore, melatonin could be an interesting target molecule for the development of a potential therapeutic agent to curb body weight.
Insights
Daily melatonin administration reduced oxidative stress and fat accumulation in obese mice. This suggests melatonin may be a potential therapeutic agent for obesity treatment and weight management.
Area of Science:
- Biochemistry
- Metabolism
- Endocrinology
Background:
- Obesity is a global health crisis and the fifth leading cause of death worldwide.
- Melatonin, an indoleamine, regulates physiological functions and acts as an antioxidant, making it a focus for anti-obesity research.
- Oxidative stress and autophagy are implicated in obesity pathogenesis.
Purpose of the Study:
- To investigate the effects of daily melatonin administration on oxidative stress and autophagy in obese mice (ob/ob).
- To evaluate melatonin's potential as a therapeutic agent for obesity.
Main Methods:
- Administration of daily melatonin to obese mice.
- Assessment of oxidative stress markers, including catalase activity, in liver tissue.
- Analysis of autophagic processes, p62 accumulation, and adipogenesis markers (body weight, peroxisome proliferator-activated receptor gamma expression).
Main Results:
- Melatonin treatment decreased oxidative stress in the liver, indicated by elevated catalase activity.
- ROS-mediated autophagy was downregulated in melatonin-treated mice, with significant p62 accumulation.
- Obese mice treated with melatonin exhibited reduced body weight and decreased peroxisome proliferator-activated receptor gamma expression, suggesting diminished adiposity.
Conclusions:
- Oxidative stress and autophagy play significant roles in obesity.
- Melatonin administration effectively reduced oxidative stress and adiposity in obese mice.
- Melatonin shows promise as a potential therapeutic target for managing obesity and curbing body weight.
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