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Endocrinology. 2017 Sep 1;158(9):2826-2836. doi: 10.1210/en.2017-00200.

Effects of Endogenous Oxytocin Receptor Signaling in Nucleus Tractus Solitarius on Satiation-Mediated Feeding and Thermogenic Control in Male Rats.

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Department of Psychology, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104.


Central oxytocin receptor (OT-R) signaling reduces food intake and increases energy expenditure, but the central sites and mechanisms mediating these effects are unresolved. We showed previously that pharmacological activation of OT-R in hindbrain/nucleus tractus solitarius (NTS) amplifies the intake-inhibitory effects of gastrointestinal (GI) satiation signals. Unexplored were the energetic effects of hindbrain OT-R agonism and the physiological relevance of NTS OT-R signaling on food intake and energy expenditure control. Using a virally mediated OT-R knockdown (KD) strategy and a range of behavioral paradigms, this study examined the role of endogenous NTS OT-R signaling on satiation-mediated food intake inhibition and thermogenic control. Results showed that, compared with controls, NTS OT-R KD rats consumed larger meals, were less responsive to the intake-inhibitory effects of a self-ingested preload, and consumed more chow following a 24-hour fast. These data indicate that NTS OT-R signaling is necessary for normal satiation control. Whereas both control and NTS OT-R KD rats increased core temperature following high-fat diet maintenance (relative to chow maintenance), the percent increase in core temperature was greater in control compared with NTS OT-R KD rats during the light cycle. Hindbrain oxytocin agonist delivery increased core temperature in both control and NTS OT-R KD rats and the percent increase relative to vehicle treatment was not significantly different between groups. Together, data reveal a critical role for endogenous NTS OT-R signaling in mediating the intake-inhibitory effects of endogenous GI satiation signals and in diet-induced thermogenesis.

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