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J Neurophysiol (March 4, 2009). doi:10.1152/jn.91294.2008
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Submitted on December 4, 2008
Revised on February 25, 2009
Accepted on February 25, 2009

OLEIC ACID DIRECTLY REGULATES POMC NEURON EXCITABILITY IN THE HYPOTHALAMUS

Young-Hwan Jo1*, Ya Su, Roger Gutierrez-Juarez2, and Streamson C Chua, Jr2

1 albert Einstein college of medicine
2 Albert Einstein College of Medicine

* To whom correspondence should be addressed. E-mail: yjo{at}aecom.yu.edu.

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 excites pro-opiomelanocortin (POMC) neurons by inhibition of ATP-activated potassium (KATP) channels. The involvement of KATP channels is supported further by experiments in SUR1 KO animals. Inhibition of -oxidation using carnitine palmitoyltransferase-1 inhibitors blocks oleic acid-induced depolarization. The depolarizing effect of oleic acid is specific as it is not mimicked by octanoic acid. Furthermore, oleic acid does not regulate the excitability of agouti-related peptide neurons. High fat feeding alters POMC neuron excitability, but not its response to oleic acid. Finally, the melanocortinergic system appears to be critical for the effects of oleic acid on endogenous glucose production in mice. Thus, {beta}-oxidation in POMC neurons may mediate the metabolic and anorexigenic effects of oleic acid.




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