Abstract

Sarcopenic obesity is a progressive loss of skeletal muscle mass and strength with increases in adiposity. The aim of this study was to investigate the effects of resveratrol on obesity and sarcopenia to potential therapy risk for skeletal muscle decline in physical function. C57BL/6J male mice fed either a high‐fat diet for 4 weeks and resveratrol (low‐, middle‐, and high‐dose) for 8 weeks to express the obesity effect. SAMP8 mice sarcopenic skeletal muscle functional deterioration expressed an age‐associated decline. Resveratrol (150 mg/kgBW) was administered by oral gavage two times a week one month of the experimental period. Exercise training based on adaptations in the muscle is training twice a week for 4 weeks. The skeletal muscles from mice in each group were analyzed by H&E staining, TUNEL and western blot analysis to determine mitochondrial function expression, apoptosis and relative fibrosis signaling. Results of the present study indicate that resveratrol in obesity skeletal muscle is linked to an increase in the expression of mitochondrial function involved in Bcl‐2 and PI3K/AKT. On the other hand, resveratrol attenuates sarcopenic SAMP8 mice, the age‐related loss of skeletal muscle mass and mitochondrial function involved Bad, caspase 3 and IL‐6/ERK1. However, exercise training did not find a significant difference in sarcopenic skeletal muscles SAMP8 mice. Exercise training did not induce sarcopenic skeletal muscle hypertrophy in SAMP8 mice. Therefore, we suggest that resveratrol as a therapeutic potential in the combination of sarcopenia and obesity, the state called sarcopenic obesity.Support or Funding InformationFunding of this study was provided by the Ministry of science and technology (MOST 104‐2811‐B‐009‐007, MOST 105‐2811‐B‐039‐008, and MOST 106‐2811‐B‐650‐003)Schematic representation of the inhibition effects of resveratrol on obesity and aging sarcopenia. The mechanisms underlying the pathophysiology of sarcopenic obesity. In obesity skeletal muscle, adipocytes undergo hypertrophy activation resulted in skeletal muscle atrophy due to accumulation of pro‐inflammation as well as mitochondrial dysfunction together with senescent muscle cells. Skeletal muscle inflammation trigger and support sarcopenic obesity development.Figure 7

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