Abstract

Aim. To investigate the role of AMPK activation and autophagy in mediating the beneficial effects of exercise and caloric restriction in obesity. Methods. Dietary-induced obesity mice were made and divided into 5 groups; one additional group of normal mice serves as control. Mice in each group received different combinations of interventions including low fat diet, caloric restriction, and exercise. Then their metabolic conditions were assessed by measuring serum glucose and insulin, serum lipids, and liver function. AMPK phosphorylation and autophagy activity were detected by western blotting. Results. Obese mice models were successfully induced by high fat diet. Caloric restriction consistently improved the metabolic conditions of the obese mice, and the effects are more prominent than the mice that received only exercise. Also, caloric restriction, exercise, and low fat diet showed a synergistic effect in the improvement of metabolic conditions. Western blotting results showed that this improvement was not related with the activation of AMPK in liver, skeletal muscle, or heart but correlates well with the autophagy activity. Conclusion. Caloric restriction has more prominent beneficial effects than exercise in dietary-induced obese mice. These effects are correlated with the autophagy activity and may be independent of AMPK activation.

Highlights

  • Caloric restriction (CR) and exercise have been considered to have beneficial effects on human health, including reducing the risks for the development of diabetes, cardiovascular disease, and cancer [1, 2]

  • To study the relationship between the chronic CR, exercise, and autophagy and whether AMPK activation is involved in this process, we used high fat diet to induce the obese mice models, and we investigated the effects of different intervention on the improvement of mice metabolic conditions

  • The results showed that there was no significant difference in AMPK phosphorylation among groups in any of these tissues (Figure 7), implying the AMPK activation does not contribute to the long-term benefits of caloric restriction

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Summary

Introduction

Caloric restriction (CR) and exercise have been considered to have beneficial effects on human health, including reducing the risks for the development of diabetes, cardiovascular disease, and cancer [1, 2]. Studies have shown that CR and exercise can improve the metabolic conditions in obesity, but the underlying mechanism is still unclear. AMPK activation plays important roles in adjusting the metabolic pathways to restore the ATP level in both short-term and long-term manner [4]. Because of this activity, it has been considered as a potential mediator of the effects of CR and exercise. Whether AMPK activation is induced in chronic CR or exercise is still an unresolved issue due to distinct observations on the AMPK activity after long-term CR or exercise in mouse [5]

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