Evidence map›Paper›PMID 28747407›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2017

Chronic hindbrain administration of oxytocin is sufficient to elicit weight loss in diet-induced obese rats.

Zachary S Roberts, Tami Wolden-Hanson, Miles E Matsen, Vitaly Ryu, Cheryl H Vaughan, James L Graham, Peter J Havel, Daniel W Chukri, Michael W Schwartz, Gregory J Morton and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
9.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Zachary S RobertsVeterans Affairs Puget Sound Health Care System, Office of Research and Development, Medical Research Service, Department of Veterans Affairs Medical Center, Seattle, Washington.
Tami Wolden-HansonVeterans Affairs Puget Sound Health Care System, Office of Research and Development, Medical Research Service, Department of Veterans Affairs Medical Center, Seattle, Washington.
Miles E MatsenUniversity of Washington Diabetes Institute, University of Washington School of Medicine, Seattle, Washington.
Vitaly RyuDepartment of Biology, Georgia State University, Atlanta, Georgia; and.
Cheryl H VaughanDepartment of Biology, Georgia State University, Atlanta, Georgia; and.
James L GrahamDepartments of Nutrition and Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, California.
Peter J HavelDepartments of Nutrition and Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, California.
Daniel W ChukriVeterans Affairs Puget Sound Health Care System, Office of Research and Development, Medical Research Service, Department of Veterans Affairs Medical Center, Seattle, Washington.
Michael W SchwartzDivision of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, Washington.
Gregory J MortonDivision of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, Washington.
James E BlevinsVeterans Affairs Puget Sound Health Care System, Office of Research and Development, Medical Research Service, Department of Veterans Affairs Medical Center, Seattle, Washington; jeblevin@u.washington.edu.
University of Washington · USGeorgia State University · USUniversity of California, Davis · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
PILOT STUDY--CLINICAL NUTRITION RESEARCHP30DK035816 · NIDDK · UNIVERSITY OF WASHINGTON · PI Ellen A Schur · 1986 to 2026
$30.4M
Novel Brain Mechanisms Controlling Glucose HomeostasisR01DK083042 · NIDDK · UNIVERSITY OF WASHINGTON · PI SCHWARTZ, MICHAEL W · 2008 to 2025
$7.6M
Novel Anti-Diabetic Actions of Hypothalamic FGF19-FGFR1 SignalingR01DK101997 · NIDDK · UNIVERSITY OF WASHINGTON · PI SCHWARTZ, MICHAEL W · 2014 to 2018
$1.9M
NIDDK NIH HHS P30 DK017047NIDDK NIH HHS P30 DK035816NIDDK NIH HHS R01 DK083042NIDDK NIH HHS R01 DK101997
6 · The paper itself

Abstract

Oxytocin (OT) administration elicits weight loss in diet-induced obese (DIO) rodents, nonhuman primates, and humans by reducing energy intake and increasing energy expenditure. Although the neurocircuitry underlying these effects remains uncertain, OT neurons in the paraventricular nucleus are positioned to control both energy intake and sympathetic nervous system outflow to interscapular brown adipose tissue (BAT) through projections to the hindbrain nucleus of the solitary tract and spinal cord. The current work was undertaken to examine whether central OT increases BAT thermogenesis, whether this effect involves hindbrain OT receptors (OTRs), and whether such effects are associated with sustained weight loss following chronic administration. To assess OT-elicited changes in BAT thermogenesis, we measured the effects of intracerebroventricular administration of OT on interscapular BAT temperature in rats and mice. Because fourth ventricular (4V) infusion targets hindbrain OTRs, whereas third ventricular (3V) administration targets both forebrain and hindbrain OTRs, we compared responses to OT following chronic 3V infusion in DIO rats and mice and chronic 4V infusion in DIO rats. We report that chronic 4V infusion of OT into two distinct rat models recapitulates the effects of 3V OT to ameliorate DIO by reducing fat mass. While reduced food intake contributes to this effect, our finding that 4V OT also increases BAT thermogenesis suggests that increased energy expenditure may contribute as well. Collectively, these findings support the hypothesis that, in DIO rats, OT action in the hindbrain evokes sustained weight loss by reducing energy intake and increasing BAT thermogenesis.

Indexed as

Adipose Tissue, BrownAnimalsAppetite DepressantsDiet, High-FatDose-Response Relationship, DrugInfusions, IntraventricularMaleMiceMice, Inbred C57BLObesityOxytocinRatsRats, Long-EvansRats, Sprague-DawleyRhombencephalonSpecies SpecificityAppetite DepressantsOxytocinbrown adipose tissueobesityoxytocinthermogenesis

Identifiers

PMID28747407
PMCPMC5668612
OpenAlexW2737278723

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.