Abstract
In this study, we demonstrated effects of acetyl-l-carnitine (ALC) on insulin resistance induced by tumor necrosis factor-α (TNF-α) in rat L6 cells. TNF-α downregulated insulin-stimulated glucose uptake and increased Serine 307 phosphorylation of insulin receptor substrate-1 (IRS-1). However, the treatment of ALC improved insulin-stimulated glucose uptake via AMP-activated protein kinase (AMPK) activation in a dose-dependent manner. Together, our data suggest that ALC inhibits TNF-α-induced insulin resistance through AMPK pathway in skeletal muscle cells.
Original language | English (US) |
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Pages (from-to) | 470-474 |
Number of pages | 5 |
Journal | FEBS Letters |
Volume | 583 |
Issue number | 2 |
DOIs | |
State | Published - Jan 22 2009 |
Externally published | Yes |
Bibliographical note
Funding Information:This work was supported by the foundation (No. 2006BAD27B01) from the Ministry of Science and Technology of the People’s Republic of China.
Keywords
- AMP-activated protein kinase
- Acetyl-l-carnitine
- Insulin resistance
- Tumor necrosis factor-α