Oleic acid directly regulates POMC neuron excitability in the hypothalamus

Young Hwan Jo, Ya Su, Roger Gutierrez-Juarez, Streamson Chua

Research output: Contribution to journalArticlepeer-review

87 Scopus citations


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 (KATP) channels. The involvement of KATP 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. Thus β-oxidation in POMC neurons may mediate the appetite-suppressing (anorexigenic) effects of OA.

Original languageEnglish (US)
Pages (from-to)2305-2316
Number of pages12
JournalJournal of neurophysiology
Issue number5
StatePublished - May 2009

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology


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