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RESEARCH-ARTICLE

Oleic Acid Directly Regulates POMC Neuron Excitability in the Hypothalamus

Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine of Yeshiva University, Bronx, New York

Submitted 4 December 2008; accepted in final form 25 February 2009

ABSTRACT

The mammalian CNS relies on a constant supply of external glucose for its undisturbed operation. However, neurons can readily switch to using fatty acids and ketones as alternative fuels. Here, we show that oleic acid (OA) excites pro-opiomelanocortin (POMC) neurons by inhibition of ATP-activated potassium (K_ATP) channels. The involvement of K_ATP channels is further supported by experiments in SUR1 KO animals. Inhibition of β-oxidation using carnitine palmitoyltransferase-1 inhibitors blocks OA-induced depolarization. The depolarizing effect of OA is specific because it is not mimicked by octanoic acid. Furthermore, OA does not regulate the excitability of agouti-related peptide neurons. High-fat feeding alters POMC neuron excitability, but not its response to OA. Finally, the melanocortinergic system appears to be critical for the effects of OA on endogenous glucose production in mice. Thus β-oxidation in POMC neurons may mediate the appetite-suppressing (anorexigenic) effects of OA.

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