The vagal afferent pathway does not play a major role in the induction of satiety by intestinal fatty acid in rats.
Intestinal infusion of long-chain fatty acids (LCFAs) strongly suppresses food intake and gut motility. Vagal afferents and cholecystokinin (CCK) signaling pathway are considered to play important roles in intestinal LCFA-induced satiety. Here, we first investigated the influence of vagus nerve on satiety following intestinal LCFA infusion in rats. Jejunal infusion of linoleic acid (LA) at 200 microL/h for 7 h suppressed food intake and the effect lasted for 24 h. The satiety induced by jejunal LA infusion occurred in a dose dependent manner. In contrast, the anorectic effect induced by octanoic acid, a medium-chain fatty acid, was weaker than that induced by LA. The reduction in food intake induced by jejunal LA infusion was not attenuated in rats treated with vagotomy, the ablation of bilateral subdiaphragmatic vagal trunks. Jejunal LA-induced satiety could also be observed in rats with bilateral midbrain transections, which ablates fibers between the hindbrain and hypothalamus. These findings suggest that the vagus nerve and fibers ascending from the hindbrain to the hypothalamus do not play a major role in intestinal LCFA-induced satiety. Jejunal LA infusion also reduced food intake in CCK-A receptor-deficient OLETF rats, suggesting that CCK signaling pathway is not critical for intestinal LCFA-induced anorexia. In conclusion, this study indicates that the vagus nerve and the CCK signaling pathway do not play major roles in conveying satiety signals induced by intestinal LCFA to the brain in rats.
Ogawa
Nobuya
N
Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, Kiyotake, Miyazaki 889-1692, Japan.
Yamaguchi
Hideki
H
Shimbara
Takuya
T
Toshinai
Koji
K
Kakutani
Makoto
M
Yonemori
Fumihiko
F
Nakazato
Masamitsu
M
D000818:Animals; D001069:Appetite Regulation / Q000187:drug effects / Q000502:physiology; D002766:Cholecystokinin / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005227:Fatty Acids / Q000378:metabolism* / Q000494:pharmacology; D007031:Hypothalamus / Q000502:physiology; D007421:Intestine, Small / Q000294:innervation* / Q000502:physiology*; D008297:Male; D009434:Neural Pathways / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D043886:Receptor, Cholecystokinin A / Q000187:drug effects / Q000378:metabolism; D012528:Satiety Response / Q000187:drug effects / Q000502:physiology*; D011984:Sensory Receptor Cells / Q000187:drug effects / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D017552:Solitary Nucleus / Q000502:physiology; D013997:Time Factors; D014628:Vagotomy; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology*; D017833:Visceral Afferents / Q000187:drug effects / Q000502:physiology*; D017962:alpha-Linolenic Acid / Q000378:metabolism / Q000494:pharmacology
D005227:Fatty Acids; D043886:Receptor, Cholecystokinin A; D017962:alpha-Linolenic Acid; D002766:Cholecystokinin