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. Author manuscript; available in PMC: 2009 Apr 10.
Published in final edited form as: Front Biosci (Landmark Ed). 2009 Jan 1;14:19–44. doi: 10.2741/3229

Figure 7. Proposed model for the role of AMPK in the hypothalamic control of food intake.

Figure 7

The activation of AMPK in the hypothalamus during starvation and its inactivation upon refeeding are mediated by nutritional changes in circulating hormones and nutrients. Ghrelin and adiponectin, which stimulate food intake, activate hypothalamic AMPK, whereas glucose, insulin, leptin and presumably resistin, which are known to inhibit food intake, inhibit it. Once activated, AMPK phosphorylates and inactivates ACC. The expected consequences are elevated malonyl-CoA concentration, leading to subsequent inhibition of mitochondrial fatty acid oxidation, and increased level of LCFA-CoA. The hypothalamic integration of these signals results in opposite changes in orexigenic/anorexigenic neuropeptides expression and subsequent modification of food intake. The underlying mechanism(s) upstream and downstream AMPK remain to be identified. ACC, acetyl-CoA carboxylase; ACS, acyl-CoA synthetase; AMPK, AMP-activated protein kinase; CPT-1, carnitine palmitoyl transferase 1; FAS, fatty acid synthase; MCD, malonyl-CoA decarboxylase; mTOR, mammalian target of rapamycin.