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Assessment of the Metabolic Effects of Isocaloric 2:1 Intermittent Fasting in Mice
Published on: November 27, 2019
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[Mibefradil improves skeletal muscle mass, function and structure in obese mice]
1Department of Geriatrics, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Summary
Mibefradil treatment helps obese mice by reducing weight gain and improving muscle mass and function. This occurs through activating the AKT/mTOR pathway, enhancing lipid metabolism, and modulating autophagy.
Area of Science:
- Metabolic disease research
- Skeletal muscle physiology
- Pharmacological interventions
Background:
- Obesity induced by high-fat diets (HFD) negatively impacts skeletal muscle mass and function.
- Understanding the molecular mechanisms underlying diet-induced muscle dysfunction is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the effects of mibefradil on skeletal muscle in obese mice.
- To explore the role of the Akt/mTOR signaling pathway in mibefradil's effects on muscle.
Main Methods:
- Mice were fed a normal diet, HFD, or HFD with mibefradil.
- Grip strength, hindlimb muscle mass (DXA), and muscle fiber cross-sectional area were assessed.
- Lipid profiles, autophagy markers (LC3, p62), and Akt/mTOR pathway activation were analyzed.
Main Results:
- HFD led to increased body weight, reduced grip strength, and smaller muscle fiber size.
- Mibefradil treatment reversed these effects, improving muscle mass, strength, and fiber size.
- Mibefradil modulated autophagy and increased Akt/mTOR pathway activation.
Conclusions:
- Mibefradil mitigates HFD-induced obesity and muscle deficits in mice.
- The AKT/mTOR pathway activation appears central to mibefradil's beneficial effects on lipid metabolism and muscle health.
- Mibefradil may offer a therapeutic strategy for obesity-related muscle dysfunction.
