Abstract
Chronic exposure to saturated fatty acids can cause insulin resistance. However, the acute effects of fatty acids are not clear and need to be elucidated because plasma fatty acid concentrations fluctuate postprandially. Here, we present the acute effects of palmitate (PA) on skeletal muscle cells and their underlying molecular mechanisms. Immuno-fluorescence results showed that PA rapidly induced GLUT4 translocation and stimulated glucose uptake in rat skeletal muscle cell line L6. Phosphorylation of AMP-activated protein kinase (AMPK), Akt, and extracellular signal-related kinase1/2 (ERK1/2) was enhanced by PA in a time-dependent manner. Cell surface-bound PA was sufficient to stimulate Akt phosphorylation. The inhibitors of PI3 kinase (PI3K), AMPK, Akt, and ERK1/2 could decrease PA-induced glucose uptake, and PI3K inhibitor decreased AMPK, Akt, and ERK1/2 phosphorylation. Weakening AMPK activity reduced phosphorylation of Akt but not ERK1/2, and Akt inhibitor could not affect ERK1/2 activation either. Meanwhile, ERK1/2 inhibitors had no effect on Akt phosphorylation. Taken together, our data suggest that PA-mediated glucose uptake in skeletal muscle cells may be stimulated by the binding of PA to cell surface and followed by PI3K/AMPK/Akt and PI3K/ERK1/2 pathways independently.
Highlights
Chronic exposure to saturated fatty acids can cause insulin resistance
To elucidate the mechanism underlying the response of skeletal muscle to acute increases in fatty acids, we examined the acute effects of PA on glucose uptake and on phosphorylation of AMP-activated protein kinase (AMPK), Akt, and extracellular signal-related kinase (ERK) 1/2 in skeletal cell lines
To determine the acute effect of PA on glucose uptake in skeletal muscle, a rat skeletal muscle cell line that stably expresses GLUT4 with a myc tag located in its first exofacial loop, L6-GLUT4myc (L6), was treated with 300 M PA or 100 nM insulin
Summary
Chronic exposure to saturated fatty acids can cause insulin resistance. the acute effects of fatty acids are not clear and need to be elucidated because plasma fatty acid concentrations fluctuate postprandially. Liu. Palmitic acid acutely stimulates glucose uptake via activation of Akt and ERK1/2 in skeletal muscle cells. Manco et al [8] have suggested that, in addition to IMTG concentration, the IMTG fatty acid fraction pattern, i.e., whether palmitic acid is present rather than oleic acid, is significantly correlated to glucose uptake in muscle tissue This is consistent with other reports suggesting that saturated fatty acids suppress body insulin sensitivity. To elucidate the mechanism underlying the response of skeletal muscle to acute increases in fatty acids, we examined the acute effects of PA on glucose uptake and on phosphorylation of AMP-activated protein kinase (AMPK), Akt, and extracellular signal-related kinase (ERK) 1/2 in skeletal cell lines. Our data suggest that PI3 kinase (PI3K), AMPK, Akt, and ERK1/2 play critical roles in PAinduced glucose uptake and that cell surface-bound PA is sufficient to trigger the signal transduction
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