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].
