PMID- 28575174
OWN - NLM
STAT- MEDLINE
DCOM- 20171002
LR  - 20181211
IS  - 1945-7170 (Electronic)
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 158
IP  - 9
DP  - 2017 Sep 1
TI  - Effects of Endogenous Oxytocin Receptor Signaling in Nucleus Tractus Solitarius 
      on Satiation-Mediated Feeding and Thermogenic Control in Male Rats.
PG  - 2826-2836
LID - 10.1210/en.2017-00200 [doi]
AB  - 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.
CI  - Copyright (c) 2017 Endocrine Society.
FAU - Ong, Zhi Yi
AU  - Ong ZY
AD  - Department of Psychology, University of Pennsylvania, Philadelphia, Pennsylvania 
      19104.
FAU - Bongiorno, Diana M
AU  - Bongiorno DM
AD  - Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 
      19104.
FAU - Hernando, Mary Ann
AU  - Hernando MA
AD  - Perelman School of Medicine, University of Pennsylvania, Philadelphia, 
      Pennsylvania 19104.
FAU - Grill, Harvey J
AU  - Grill HJ
AD  - Department of Psychology, University of Pennsylvania, Philadelphia, Pennsylvania 
      19104.
LA  - eng
GR  - R01 DK021397/DK/NIDDK NIH HHS/United States
GR  - R56 DK021397/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Receptors, Oxytocin)
SB  - IM
CIN - Endocrinology. 2017 Sep 1;158(9):2713-2715. PMID: 28911180
MH  - Animals
MH  - Appetite Regulation/genetics
MH  - Diet, High-Fat
MH  - Eating/*genetics
MH  - Energy Metabolism/physiology
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Rats, Transgenic
MH  - Receptors, Oxytocin/genetics/*physiology
MH  - Satiation/*physiology
MH  - Signal Transduction/genetics
MH  - Solitary Nucleus/*metabolism
MH  - Thermogenesis/*genetics
PMC - PMC5659667
EDAT- 2017/06/03 06:00
MHDA- 2017/10/03 06:00
PMCR- 2018/09/01
CRDT- 2017/06/03 06:00
PHST- 2017/02/23 00:00 [received]
PHST- 2017/05/24 00:00 [accepted]
PHST- 2017/06/03 06:00 [pubmed]
PHST- 2017/10/03 06:00 [medline]
PHST- 2017/06/03 06:00 [entrez]
PHST- 2018/09/01 00:00 [pmc-release]
AID - 3857690 [pii]
AID - endo_201700200 [pii]
AID - 10.1210/en.2017-00200 [doi]
PST - ppublish
SO  - Endocrinology. 2017 Sep 1;158(9):2826-2836. doi: 10.1210/en.2017-00200.