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      Peripheral oxytocin activates vagal afferent neurons to suppress feeding in normal and leptin-resistant mice: a route for ameliorating hyperphagia and obesity.

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          Abstract

          Oxytocin (Oxt), a neuropeptide produced in the hypothalamus, is implicated in regulation of feeding. Recent studies have shown that peripheral administration of Oxt suppresses feeding and, when infused subchronically, ameliorates hyperphagic obesity. However, the route through which peripheral Oxt informs the brain is obscure. This study aimed to explore whether vagal afferents mediate the sensing and anorexigenic effect of peripherally injected Oxt in mice. Intraperitoneal Oxt injection suppressed food intake and increased c-Fos expression in nucleus tractus solitarius to which vagal afferents project. The Oxt-induced feeding suppression and c-Fos expression in nucleus tractus solitarius were blunted in mice whose vagal afferent nerves were blocked by subdiaphragmatic vagotomy or capsaicin treatment. Oxt induced membrane depolarization and increases in cytosolic Ca(2+) concentration ([Ca(2+)]i) in single vagal afferent neurons. The Oxt-induced [Ca(2+)]i increases were markedly suppressed by Oxt receptor antagonist. These Oxt-responsive neurons also responded to cholecystokinin-8 and contained cocaine- and amphetamine-regulated transcript. In obese diabetic db/db mice, leptin failed to increase, but Oxt increased [Ca(2+)]i in vagal afferent neurons, and single or subchronic infusion of Oxt decreased food intake and body weight gain. These results demonstrate that peripheral Oxt injection suppresses food intake by activating vagal afferent neurons and thereby ameliorates obesity in leptin-resistant db/db mice. The peripheral Oxt-regulated vagal afferent neuron provides a novel target for treating hyperphagia and obesity.

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          Author and article information

          Journal
          Am. J. Physiol. Regul. Integr. Comp. Physiol.
          American journal of physiology. Regulatory, integrative and comparative physiology
          1522-1490
          0363-6119
          Mar 1 2015
          : 308
          : 5
          Affiliations
          [1 ] Division of Integrative Physiology, Department of Physiology, Jichi Medical University School of Medicine, Tochigi, Japan;
          [2 ] First Department of Medicine, Saitama Medical Center, Jichi Medical University School of Medicine, Saitama, Japan;
          [3 ] Health Science Service Center, Kanazawa University, Ishikawa, Japan; and.
          [4 ] Division of Integrative Physiology, Department of Physiology, Jichi Medical University School of Medicine, Tochigi, Japan; Division of Adaptation Development, Department of Developmental Physiology, National Institute for Physiological Sciences, Aichi, Japan tyada@jichi.ac.jp.
          Article
          ajpregu.00344.2014
          10.1152/ajpregu.00344.2014
          25540101
          Copyright © 2015 the American Physiological Society.

          food intake, leptin, nodose ganglion, obesity, oxytocin

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