Measurement of Gastric Acid Secretion in the Anaesthetized Rat

Adami, Maristella; Coruzzi, Gabriella

doi:10.1002/0471140856.tx2105s45

Cited by 1 publication

(1 citation statement)

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“…In addition to vagal, endocrine, and paracrine influences, gastric acid secretion is influenced by a variety of factors, including blood pressure and local blood flow (1,31,43). Additionally, all common general anesthetics have some impact on gastrointestinal secretory function (31).…”

Section: Discussionmentioning

confidence: 99%

Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats

Xia

Fritze

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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MW. Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats. Am J Physiol Gastrointest Liver Physiol 303: G570 -G577, 2012. First published June 21, 2012; doi:10.1152/ajpgi.00178.2012.-Nesfatin-1, a novel hypothalamic peptide, inhibits nocturnal feeding behavior and gastrointestinal motility in rodents. The effects of nesfatin-1 on gastrointestinal secretory function, including gastric acid production, have not been evaluated. Nesfatin-1 was injected into the fourth intracerebral ventricle (4V) of chronically cannulated rats to identify a nesfatin dose sufficient to inhibit food intake. Nesfatin-1 (2 g) inhibited dark-phase food intake, in a dose-dependent fashion, for Ͼ3 h. Gastric acid production was evaluated in urethane-anesthetized rats. Nesfatin-1 (2 g) was introduced via the 4V following endocrine stimulation of gastric acid secretion by pentagastrin (2 g·kg Ϫ1 ·h Ϫ1 iv), vagal stimulation with 2-deoxy-D-glucose (200 mg/kg sc), or no stimulus. Gastric secretions were collected via gastric cannula and neutralized by titration to determine acid content. Nesfatin-1 did not affect basal and pentagastrin-stimulated gastric acid secretion, whereas 2-deoxy-D-glucosestimulated gastric acid production was inhibited by nesfatin-1 in a dose-dependent manner. c-Fos immunofluorescence in brain sections was used to evaluate in vivo neuronal activation by nesfatin-1 administered via the 4V. Nesfatin-1 caused activation of efferent vagal neurons, as evidenced by a 16-fold increase in the mean number of c-Fos-positive neurons in the dorsal motor nucleus of the vagus (DMNV) in nesfatin-1-treated animals vs. controls (P Ͻ 0.01). Finally, nesfatin-induced Ca 2ϩ signaling was evaluated in primary cultured DMNV neurons from neonatal rats. Nesfatin-1 caused dosedependent Ca 2ϩ increments in 95% of cultured DMNV neurons. These studies demonstrate that central administration of nesfatin-1, at doses sufficient to inhibit food intake, results in inhibition of vagally stimulated secretion of gastric acid. Nesfatin-1 activates DMNV efferent vagal neurons in vivo and triggers Ca 2ϩ signaling in cultured DMNV neurons. gastric hormones; intracellular calcium; dorsal motor nucleus of the vagus NESFATIN-1, an 82-amino acid peptide derived from the parent peptide nucleobindin-2, was first identified as a satiety molecule in the hypothalamus by Oh et al. (33). Inhibition of rodent nocturnal feeding behavior by nesfatin-1 administered into the intracranial ventricles has been consistently observed (18,25,34,40,42). Most centrally acting peptides that influence food intake also regulate the processes of digestion, including gastrointestinal motility and secretory function (45). In rodents, nesfatin-1 inhibits gastroduodenal motility and gastric empty-

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