Abstract
The effects of malnutrition on skeletal muscle result in not only the loss of muscle mass but also fatigue intolerance. It remains unknown whether the metabolic capacity is related to the fiber type composition of skeletal muscle under malnourished condition although malnutrition resulted in preferential atrophy in fast muscle. The purpose of the present study was to investigate the effects of metabolic capacity in fast and slow muscles via the energy‐sensing of AMPK and SIRT1 in malnutrition. Wistar rats were randomly divided into control and malnutrition groups. The rats in the malnutrition group were provided with a low‐protein diet, and daily food intake was limited to 50% for 12 weeks. Malnutrition with hypoalbuminemia decreased the body weight and induced the loss of plantaris muscle mass, but there was little change in the soleus muscle. An increase in the superoxide level in the plasma and a decrease in SOD‐2 protein expression in both muscles were observed in the malnutrition group. In addition, the expression level of AMPK in the malnutrition group increased in both muscles. Conversely, the expression level of SIRT1 decreased in both muscles of the malnutrition group. In addition, malnutrition resulted in a decrease in the expression levels of PGC‐1α and PINK protein, and induced a decrease in the levels of two key mitochondrial enzymes (succinate dehydrogenase and citrate synthase) and COX IV protein expression in both muscles. These results indicate that malnutrition impaired the metabolic capacity in both fast and slow muscles via AMPK‐independent SIRT1 inhibition induced by increased oxidative stress.
Highlights
Regardless of this, both muscles had metabolic disorders, (2) an increase in oxidative stress was observed in the plasma and both muscles under malnourished condition, (3) the energy-sensing response was observed as AMP-activated protein kinase (AMPK)-independent silent information regulator of transcription 1 (SIRT1) inhibition in both muscles, and (4) malnutrition decreased the expression of PGC-1α and PINK1 in both muscles
The response to ROS differs between AMPK and SIRT1. These results suggest that the energy-sensing response of skeletal muscle in malnutrition was characterized by AMPK-independent
This study demonstrated that malnutrition impaired the metabolic capacity of both fast and slow muscles
Summary
The novel findings of the present study are listed as follows:. (1) malnutrition resulted in the muscle loss of fast muscle, but no atrophy was observed in slow muscle. (1) malnutrition resulted in the muscle loss of fast muscle, but no atrophy was observed in slow muscle Regardless of this, both muscles had metabolic disorders, (2) an increase in oxidative stress was observed in the plasma and both muscles under malnourished condition, (3) the energy-sensing response was observed as AMPK-independent SIRT1 inhibition in both muscles, and (4) malnutrition decreased the expression of PGC-1α and PINK1 in both muscles. Together our results indicate that malnutrition-induced downregulation of SIRT1 impairs mitochondrial homeostasis and metabolic capacity in skeletal muscle through decreased PGC-1α and PINK1. These results were suggested that changes in oxidative stress and SIRT1 were reduced metabolic capacity even under malnourished condition without the atrophy of slow muscles. Future studies should be performed to determine the downstream factors of PGC-1α and PINK1 or other pathways of mitochondrial homeostasis in malnutrition
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