Abstract

A major satiety hormone, cholecystokinin (CCK) is well known to be released by electroacupuncture (EA) stimulation at certain body sites which elicits profound psychophysiological responses. Previous clinical and animal studies have shown that EA stimulation reduces food intake and body weight in both normal and obese subjects. The aim of the present study was to elucidate the satiety effect of EA stimulation and its mechanism related to CCK in rats. Here we show that EA stimulation at "Zusanli" (ST36) acupoint significantly reduced 30-min and 60-min food intake in 48-h fasted Sprague-Dawley rats, and such effect was reversed by a lorglumide (CCK-1 receptor antagonist, 10 mg/kg, i.p.) pretreatment. The ST36 EA stimulation-induced satiety was not observed in CCK-1 receptor knockout, Otsuka Long-Evans Tokushima Fatty rats, but in their controls, Long-Evans Tokushima Otsuka rats. Subdiaphragmatic vagotomy also blocked the satiety effect of ST36 EA stimulation in Sprague-Dawley rats. These results suggest that ST36 EA stimulation elicits satiety in rats and this is mediated by the endogenous CCK signaling pathway. © 2008 Elsevier Inc. All rights reserved.

Author keywords

Cholecystokinin; Electroacupuncture; Lorglumide; Otsuka Long-Evans Tokushima Fatty rat; Satiety; Vagotomy

Indexed keywords

EMTREE drug terms: cholecystokinin; lorglumide

EMTREE medical terms: animal experiment; article; controlled study; drug effect; electroacupuncture; food intake; male; nonhuman; priority journal; rat; satiety; stimulation

MeSH: Animals; Cholecystokinin; Electroacupuncture; Fasting; Male; Proglumide; Rats; Rats, Inbred OLETF; Rats, Sprague-Dawley; Satiation
Medline is the source for the MeSH terms of this document.

Species Index: Animalia; Rattus

Chemicals and CAS Registry Numbers: cholecystokinin, 9011-97-6, 93443-27-7; lorglumide, 97964-56-2;Cholecystokinin, 9011-97-6; lorglumide, 97964-56-2; Proglumide, 6620-60-6