(Downloading may take up to 30 seconds.
If the slide opens in your browser, select File -> Save As to save it.)
Click on image to view larger version.
FIG. 3. Model for regulation of adenosine monophosphate-activated protein kinase (AMPK) and fatty acid oxidation by leptin in skeletal muscle. Leptin activates AMPK via two distinct mechanisms. One is rapid and occurs directly through leptin receptors expressed on muscle cells. The other occurs with slower kinetics and is mediated via actions in the central nervous system (CNS), leading to stimulation of the sympathetic nervous system (SNS) and activation of G-coupled 
-adrenergic receptors expressed on muscle cells. Activation of muscle ObRb also increases AMP content, which may be the mechanism for the direct effect of leptin to activate AMPK. AMPK phosphorylates acetyl-CoA carboxylase (ACC), leading to inhibition of its activity and thus to reduced formation of malonyl-CoA. This, in turn, disinhibits the activity of carnitine palmitoyltransferase 1 (CPT-1), a required step for translocation of fatty acids into mitochondria (Minokoshi and Kahn, 2003). Underlining indicates a decrease in cellular contents (malonyl-CoA) or in enzyme activities (ACC). ATP, adenosine triphosphate. [Modified from Minokoshi Y, Kahn BB 2003 Role of AMP-activated protein kinase in leptin-induced fatty acid oxidation in muscle. Biochem Soc Trans 31:196–201.]
