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

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


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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Appetite Regulation / genetics
  • Diet, High-Fat
  • Eating / genetics*
  • Energy Metabolism / physiology
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Rats, Transgenic
  • Receptors, Oxytocin / genetics
  • Receptors, Oxytocin / physiology*
  • Satiation / physiology*
  • Signal Transduction / genetics
  • Solitary Nucleus / metabolism*
  • Thermogenesis / genetics*


  • Receptors, Oxytocin