Gryllus bimaculatus Hydrolysate Ameliorates Obesity-Induced Muscle Atrophy by Activating Skeletal Muscle AMPK in Mice.

Background/

Objectives

Obesity-related metabolic complications contribute to musculoskeletal disorders and are often associated with muscular fat accumulation. The AMP-activated protein kinase (AMPK) is a therapeutic target that can mitigate these effects.

Methods

An in vivo study was conducted to understand the effects of Gryllus bimaculatus (GB), a potent AMPK activator, on metabolic and muscular homeostasis in diet-induced obesity (DIO). Six-week-old male C57BL/6J mice were fed either a normal diet or a high-fat diet (HFD) for eight weeks to induce DIO. Subsequently, HFD-fed mice were divided into four groups: HFD only, HFD with 100 mg/kg/day GB, HFD with 200 mg/kg/day GB, and HFD with 400 mg/kg/day GB for 16 weeks. To assess the effects of GB, we evaluated insulin resistance, muscle strength, muscular fat accumulation, and AMPK activation using an oral glucose tolerance test, grip strength test, histological assessments, serum lipid analyses, western blotting, and quantitative reverse transcription-polymerase chain reaction.

Results

The low- and mid-dose GB groups showed a trend toward improved insulin resistance. GB significantly reduced muscle fat accumulation and increased muscle strength. The mid- and high-dose GB groups showed a significantly upregulated expression of the molecular markers of mitochondrial biogenesis and fatty acid oxidation in muscle tissues. Additionally, the high-dose GB group activated AMPK and inhibited the activity of acetyl-CoA carboxylase in the skeletal muscle.

Conclusions

The results suggest that GB may serve as a nutraceutical candidate for the management of obesity-associated metabolic complications.