Levin Fredrik, Edholm Therese, Ehrström Marcus, Wallin Berndt, Schmidt Peter T, Kirchgessner Annette M, Hilsted Linda M, Hellström Per M, Näslund Erik
Department of Surgery, Karolinska Institutet Danderyd Hospital, SE-182 88 Stockholm, Sweden.
Regul Pept. 2005 Nov;131(1-3):59-65. doi: 10.1016/j.regpep.2005.06.001.
Ghrelin is a gut peptide that is secreted from the stomach and stimulates food intake. There are ghrelin receptors throughout the gut and intracerebroventricular ghrelin has been shown to increase gastric acid secretion. The aim of the present study was to examine the effects of peripherally administered ghrelin on gastric emptying of a non-nutrient and nutrient liquid, as well as, basal and pentagastrin-stimulated gastric acid secretion in awake rats. In addition, gastric contractility was studied in vitro. Rats equipped with a gastric fistula were subjected to an intravenous infusion of ghrelin (10-500 pmol kg(-1) min(-1)) during saline or pentagastrin (90 pmol kg(-1) min(-1)) infusion. After administration of polyethylene glycol (PEG) 4000 with 51Cr as radioactive marker, or a liquid nutrient with (51)Cr, gastric retention was measured after a 20-min infusion of ghrelin (500 pmol kg(-1) min(-1)). In vitro isometric contractions of segments of rat gastric fundus were studied (10(-9) to 10(-6) M). Ghrelin had no effect on basal acid secretion, but at 500 pmol kg(-1) min(-1) ghrelin significantly decreased pentagastrin-stimulated acid secretion. Ghrelin had no effect on gastric emptying of the nutrient liquid, but significantly increased gastric emptying of the non-nutrient liquid. Ghrelin contracted fundus muscle strips dose-dependently (pD2 of 6.93+/-0.7). Ghrelin IV decreased plasma orexin A concentrations and increased plasma somatostatin concentrations. Plasma gastrin concentrations were unchanged during ghrelin infusion. Thus, ghrelin seems to not only effect food intake but also gastric motor and secretory function indicating a multifunctional role for ghrelin in energy homeostasis.
胃饥饿素是一种由胃分泌的肠道肽，可刺激食物摄入。肠道各处都有胃饥饿素受体，且已证实脑室内注射胃饥饿素可增加胃酸分泌。本研究的目的是检测外周给予胃饥饿素对清醒大鼠非营养性和营养性液体胃排空以及基础胃酸分泌和五肽胃泌素刺激的胃酸分泌的影响。此外，还进行了体外胃收缩性研究。给装有胃瘘的大鼠在输注生理盐水或五肽胃泌素（90 pmol·kg⁻¹·min⁻¹）期间静脉输注胃饥饿素（10 - 500 pmol·kg⁻¹·min⁻¹）。在给予以⁵¹Cr作为放射性标记的聚乙二醇（PEG）4000或含⁵¹Cr的液体营养物后，在输注胃饥饿素（500 pmol·kg⁻¹·min⁻¹）20分钟后测量胃潴留情况。研究了大鼠胃底段的体外等长收缩（10⁻⁹至10⁻⁶ M）。胃饥饿素对基础胃酸分泌无影响，但在500 pmol·kg⁻¹·min⁻¹时，胃饥饿素显著降低五肽胃泌素刺激的胃酸分泌。胃饥饿素对营养液的胃排空无影响，但显著增加非营养液的胃排空。胃饥饿素使胃底肌条剂量依赖性收缩（pD2为6.93±0.7）。静脉注射胃饥饿素可降低血浆食欲素A浓度并增加血浆生长抑素浓度。在输注胃饥饿素期间血浆胃泌素浓度未改变。因此，胃饥饿素似乎不仅影响食物摄入，还影响胃运动和分泌功能，表明胃饥饿素在能量稳态中具有多功能作用。
