Xenin is a 25-amino acid peptide initially isolated from human gastric mucosa. Xenin is a gut hormone that can reduce food intake.
Xenin is abundantly expressed in gastric, duodenal, and jejunal mucosa, and is found at lower levels in the pancreas. Xenin is released into the circulation postprandially and has been reported to stimulatepancreatic endocrine and exocrine secretion, inhibit gastrin secretion, and influence gastrointestinal motility. Xenin is highly homologous to neurotensin. Xenin and neurotensin are reported to have similar biological effects[1].
Both intracerebroventricular and intraperitoneal administration of xenin inhibit fasting-induced hyperphagia in wild-type mice in a dose-dependent manner. The intraperitoneal injection of xenin also reduces nocturnal intake in ad libitum–fed wild-type mice. The intraperitoneal injection of xenin increases Fos immunoreactivity in hypothalamic nuclei, including the paraventricular nucleus and the arcuate nucleus. Xenin reduces food intake in agouti and ob/ob mice[2]. Gastric emptying rate is reduced by about 93% in xenin-treated mice compared to saline-treated control mice. The i.p. xenin injection significantly increases Fos-immunoreactive cells in the nucleus of the solitary tract of the brainstem, but not area postrema and dorsal motor nucleus of the vagus[3].
References:
[1]. Cooke JH, et al. Peripheral and central administration of xenin and neurotensin suppress food intake in rodents. Obesity (Silver Spring). 2009 Jun;17(6):1135-43.
[2]. Leckstrom A, et al. Xenin, a gastrointestinal peptide, regulates feeding independent of the melanocortinsignaling pathway. Diabetes. 2009 Jan;58(1):87-94.
[3]. Kim ER, et al. Xenin delays gastric emptying rate and activates the brainstem in mice. Neurosci Lett. 2010 Aug 30;481(1):59-63.