title: Mechanism of the induction of brain c-Fos-positive neurons by lipid absorption.
abstract: 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.
authors.affiliation: Department of Pathology, University of Cincinnati, Cincinnati, OH 45237, USA.
authors.forename: Chun-Min
authors.initials: CM
authors.lastname: Lo
authors.forename: Liyun
authors.initials: L
authors.lastname: Ma
authors.forename: Dian Ming
authors.initials: DM
authors.lastname: Zhang
authors.forename: Rachel
authors.initials: R
authors.lastname: Lee
authors.forename: Abby
authors.initials: A
authors.lastname: Qin
authors.forename: Min
authors.initials: M
authors.lastname: Liu
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Woods
authors.forename: Randall R
authors.initials: RR
authors.lastname: Sakai
authors.forename: Helen E
authors.initials: HE
authors.lastname: Raybould
authors.forename: Patrick
authors.initials: P
authors.lastname: Tso
mesh_terms: D000818:Animals; D001111:Arcuate Nucleus of Hypothalamus / Q000187:drug effects / Q000378:metabolism; D001921:Brain / Q000166:cytology / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects*; D002914:Chylomicrons / Q000096:biosynthesis; D005217:Fat Emulsions, Intravenous / Q000008:administration & dosage / Q000494:pharmacology; D006727:Hormone Antagonists / Q000494:pharmacology; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D007441:Intubation, Gastrointestinal; D008055:Lipids / Q000008:administration & dosage / Q000494:pharmacology*; D008196:Lymph / Q000502:physiology; D008297:Male; D009474:Neurons / Q000378:metabolism*; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000378:metabolism; D020442:Poloxamer / Q000494:pharmacology; D011377:Proglumide / Q000031:analogs & derivatives / Q000494:pharmacology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011949:Receptors, Cholecystokinin / Q000037:antagonists & inhibitors / Q000378:metabolism; D017552:Solitary Nucleus / Q000187:drug effects / Q000378:metabolism; D013501:Surface-Active Agents / Q000494:pharmacology; D014697:Ventromedial Hypothalamic Nucleus / Q000187:drug effects / Q000378:metabolism
chemical_list: D002914:Chylomicrons; D005217:Fat Emulsions, Intravenous; D006727:Hormone Antagonists; D008055:Lipids; D016760:Proto-Oncogene Proteins c-fos; D011949:Receptors, Cholecystokinin; D013501:Surface-Active Agents; D020442:Poloxamer; D011377:Proglumide; C048181:lorglumide