The Role of Phospholipase C Beta in Fatty Acid Induced AMPK Signaling During Exercise
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Chronic exercise triggers muscle adaptation in response to energy demand by switching muscle types, increasing mitochondria contents, or changing gene expression patterns. Phospholipase C (PLC) is known to be involved in the metabolism, proliferation, and differentiation of muscle cells. However, its function during exercise has not been studied. In this study, 19 mice were divided into 2 groups, exercise and control groups. The mice in the exercise group were exercised on a treadmill for 4 weeks. We observed that both mRNA and protein expression levels of PLCβ2 increased in the skeletal muscles, particularly in the soleus muscle, of mice after 4 weeks of treadmill exercise. The expression of GPR40, a G-protein coupled receptor (GPCR) and a putative binding partner of PLCβ2, was also found to be increased in the mice belonging to the exercise group. To investigate the role of GPR40 in muscle adaptation, the mice were administered oleic acid, which activates AMPK and acetyl-CoA carboxylase (ACC). The results revealed that AMPK-target genes such as Cebp-β and Ppar-γ were upregulated upon oleic acid treatment. Furthermore, pre-treatment with STO-609, a PLC inhibitor, downregulated the expression of AMPK-target genes in differentiated muscle cell lines. Taken together, these results suggest a novel role for PLCβ2, that involves the regulation of fatty acid metabolism during exercise.
Abstract
Chronic exercise triggers muscle adaptation in response to energy demand by switching muscle types, increasing mitochondria contents, or changing gene expression patterns. Phospholipase C (PLC) is known to be involved in the metabolism, proliferation, and differentiation of muscle cells. However, its function during exercise has not been studied. In this study, 19 mice were divided into 2 groups, exercise and control groups. The mice in the exercise group were exercised on a treadmill for 4 weeks. We observed that both mRNA and protein expression levels of PLCβ2 increased in the skeletal muscles, particularly in the soleus muscle, of mice after 4 weeks of treadmill exercise. The expression of GPR40, a G-protein coupled receptor (GPCR) and a putative binding partner of PLCβ2, was also found to be increased in the mice belonging to the exercise group. To investigate the role of GPR40 in muscle adaptation, the mice were administered oleic acid, which activates AMPK and acetyl-CoA carboxylase (ACC). The results revealed that AMPK-target genes such as Cebp-β and Ppar-γ were upregulated upon oleic acid treatment. Furthermore, pre-treatment with STO-609, a PLC inhibitor, downregulated the expression of AMPK-target genes in differentiated muscle cell lines. Taken together, these results suggest a novel role for PLCβ2, that involves the regulation of fatty acid metabolism during exercise.
참고문헌 (18)
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