Weiner H, Novin D, Grijalva C V, Taché Y, Garrick T
West J Med. 1985 Aug;143(2):207-22.
The initiation and termination of feeding behavior are not fully understood. The stomach has been implicated as one source of signals regulating food intake. The sight and smell of food are potent stimuli to gastric acid secretion and contraction. The mouth, upper gastrointestinal tract and liver contain receptors regulating food intake; afferent information passes into the brain stem and into the brain areas. Lateral hypothalamic lesions abolish feeding, raise the body temperature and basal gastric acid secretion and produce gastric erosions. Vagotomy and administering propantheline bromide abolish the increased acid secretion after such lesions; they also alter the mucosal barrier permitting diffusion of protons into mucosal cells. Several of the neuropeptides via the central nervous system stimulate or inhibit gastric acid secretion through modulation of the autonomic nervous system. Most animal models of gastric erosions are associated with a reduced body temperature. Unknown is whether or not this association is the result of increased levels of thyrotropin-releasing hormone-a potent stimulus to gastric acid secretion and erosion formation when injected intracisternally.
进食行为的启动和终止尚未完全明确。胃被认为是调节食物摄入信号的一个来源。食物的视觉和嗅觉是胃酸分泌和胃收缩的有力刺激因素。口腔、上消化道和肝脏含有调节食物摄入的受体；传入信息传入脑干和脑区。下丘脑外侧损伤会导致进食停止、体温升高、基础胃酸分泌增加，并产生胃糜烂。迷走神经切断术和给予溴丙胺太林可消除此类损伤后胃酸分泌的增加；它们还会改变黏膜屏障，使质子扩散到黏膜细胞中。几种神经肽通过中枢神经系统，通过调节自主神经系统来刺激或抑制胃酸分泌。大多数胃糜烂的动物模型都与体温降低有关。尚不清楚这种关联是否是促甲状腺激素释放激素水平升高的结果，当脑池内注射促甲状腺激素释放激素时，它是胃酸分泌和糜烂形成的有力刺激因素。
