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Am J Physiol Regul Integr Comp Physiol 292: R268-R273, 2007. First published September 21, 2006; doi:10.1152/ajpregu.00334.2006
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APPETITE, OBESITY, DIGESTION, AND METABOLISM

Mechanism of the induction of brain c-Fos-positive neurons by lipid absorption

Chun-Min Lo,1 Liyun Ma,2 Dian Ming Zhang,1 Rachel Lee,1 Abby Qin,1 Min Liu,1 Stephen C Woods,2 Randall R. Sakai,2 Helen E. Raybould,3 and Patrick Tso1

Departments of 1Pathology and 2Psychiatry, University of Cincinnati, Cincinnati, Ohio; and 3Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, University of California, Davis, California

Submitted 17 May 2006 ; accepted in final form 30 August 2006

Many gastrointestinal meal-related signals are transmitted to the central nervous system via the vagus nerve and thereby control changes in meal size. The c-Fos-positive neuron has been used as a marker of neuronal activation after lipid meals to examine the contribution of a selective macronutrient on brain neurocircuit activity. In rats fed Intralipid, the c-Fos-positive neurons were highly stimulated in the nucleus of the solitary tract (NTS) and in the hypothalamus, including the paraventricular nucleus (PVN), arcuate nucleus of the hypothalamus (ARC), and ventromedial hypothalamus at 4 h lipid feeding. However, c-Fos-like immunoreactivity was markedly attenuated in these brain regions when chylomicron formation/secretion was blocked by Pluronic L-81. After lymph was diverted from the lymph cannulated animals, the rats had a lower number of c-Fos-positive cells in the NTS and ARC. In contrast, the rats had higher c-Fos-positive neurons in PVN. The present study also revealed that c-Fos-positive neurons induced by feeding of Intalipid were abolished by CCK type 1 receptor antagonist, Lorglumide. We conclude that the formation and/or secretion of chylomicron are critical steps for initiating neuronal activation in the brain.

cholecystokinin type 1 receptor antagonist; chylomicron; hindbrain; hypothalamus



Address for reprint requests and other correspondence: P. Tso, Dept. of Pathology and Laboratory Medicine, Univ. of Cincinnati, 2120 E. Galbraith Rd., Bldg. A, ML 0507, Cincinnati, OH 45237 (e-mail: tsopp{at}email.uc.edu)







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