Reidelberger R D
Department of Veterans Affairs Medical Center, Omaha, Nebraska 68105.
Am J Physiol. 1992 Dec;263(6 Pt 2):R1354-8. doi: 10.1152/ajpregu.1992.263.6.R1354.
The hypothesis that peripherally administered cholecystokinin C-terminal octapeptide (CCK-8) and endogenous CCK act by the same abdominal vagal mechanism to produce satiety was tested by injecting rats with CCK-8 or the type A CCK receptor antagonist MK-329 after they had received bilateral subdiaphragmatic vagotomies. CCK-8 (8 nmol/kg ip) inhibited 1-h food intake by 60%; vagotomy and MK-329 (0.5 mg/kg sc) each completely blocked this effect. In contrast, vagotomy did not alter the stimulatory effect of MK-329 (0.5 mg/kg sc) on feeding; 3-h cumulative intake in control and vagotomized animals was increased by 25 and 34%, respectively. These results suggest that satiety is mediated in part by an endogenous CCK action that is independent of abdominal vagal innervation.
通过在大鼠接受双侧膈下迷走神经切断术后给它们注射胆囊收缩素C末端八肽(CCK - 8)或A型胆囊收缩素受体拮抗剂MK - 329,来检验外周给予的CCK - 8和内源性CCK通过相同的腹部迷走神经机制产生饱腹感这一假设。CCK - 8(8 nmol/kg腹腔注射)使1小时食物摄入量减少60%;迷走神经切断术和MK - 329(0.5 mg/kg皮下注射)均完全阻断了这一效应。相比之下,迷走神经切断术并未改变MK - 329(0.5 mg/kg皮下注射)对进食的刺激作用;对照动物和迷走神经切断术后动物的3小时累积摄入量分别增加了25%和34%。这些结果表明,饱腹感部分是由一种独立于腹部迷走神经支配的内源性CCK作用介导的。