Evidence map›Paper›PMID 28702330›Full record

ArticleMolecular metabolism2017

Neonatal GLP1R activation limits adult adiposity by durably altering hypothalamic architecture.

Andrea V Rozo, Daniella A Babu, PoMan A Suen, David N Groff, Randy J Seeley, Rebecca A Simmons, Patrick Seale, Rexford S Ahima, Doris A Stoffers

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 19 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

9 authors at 2 institutions in 1 country.

Andrea V RozoInstitute for Diabetes, Obesity and Metabolism and the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA, 19104, USA.
Daniella A BabuInstitute for Diabetes, Obesity and Metabolism and the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA, 19104, USA.
PoMan A SuenInstitute for Diabetes, Obesity and Metabolism and the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA, 19104, USA.
David N GroffInstitute for Diabetes, Obesity and Metabolism and the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA, 19104, USA.
Randy J SeeleyDepartment of Surgery, University of Michigan, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA.
Rebecca A SimmonsDepartment of Pediatrics, Division of Neonatology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA, 19104, USA.
Patrick SealeInstitute for Diabetes, Obesity and Metabolism and the Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA, 19104, USA.
Rexford S AhimaInstitute for Diabetes, Obesity and Metabolism and the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA, 19104, USA.
Doris A StoffersInstitute for Diabetes, Obesity and Metabolism and the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA, 19104, USA.
University of Pennsylvania · USUniversity of Michigan–Ann Arbor · US

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Patrick Seale · 1986 to 2026
$48.3M
TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Diabetes, Endocrine, and MetabolismT32DK007314 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI DORIS A STOFFERS, Patrick Seale · 1986 to 2026
$9.0M
Prevention of diabetes due to growth retardationR01DK062965 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI STOFFERS, DORIS A · 2004 to 2008
$1.8M
Metabolic Consequences of Neonatal Programming by a GLP1 Receptor AgonistF32DK085939 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI BABU, DANIELLA ANGELA · 2009 to 2011
$159k
NIDDK NIH HHS F32 DK085939NIDDK NIH HHS P30 DK019525NIDDK NIH HHS P30 DK020572NIDDK NIH HHS P30 DK050306NIDDK NIH HHS R01 DK062965NIDDK NIH HHS T32 DK007314
6 · The paper itself

Abstract

objectiveAdult obesity risk is influenced by alterations to fetal and neonatal environments. Modifying neonatal gut or neurohormone signaling pathways can have negative metabolic consequences in adulthood. Here we characterize the effect of neonatal activation of glucagon like peptide-1 (GLP-1) receptor (GLP1R) signaling on adult adiposity and metabolism.

methodsWild type C57BL/6 mice were injected with 1 nmol/kg Exendin-4 (Ex-4), a GLP1R agonist, for 6 consecutive days after birth. Growth, body composition, serum analysis, energy expenditure, food intake, and brain and fat pad histology and gene expression were assessed at multiple time points through 42 weeks. Similar analyses were conducted in a

resultsNeonatal administration of Ex-4 reduced adult body weight and fat mass, increased energy expenditure, and conferred protection from diet-induced obesity in female mice. This was associated with induction of brown adipose genes and increased noradrenergic fiber density in parametrial white adipose tissue (WAT). We further observed durable alterations in orexigenic and anorexigenic projections to the paraventricular hypothalamic nucleus (PVH). Genetic deletion of Glp1r in the PVH by Sim1-Cre abrogated the impact of neonatal Ex-4 on adult body weight, WAT browning, and hypothalamic architecture.

conclusionThese observations suggest that the acute activation of GLP1R in neonates durably alters hypothalamic architecture to limit adult weight gain and adiposity, identifying GLP1R as a therapeutic target for obesity prevention.

Indexed as

AdiposityGlucagon-Like Peptide-1 Receptor AgonistsAnimalsExenatideFemaleGlucagon-Like Peptide-1 ReceptorHypothalamusIncretinsMaleMiceMice, Inbred C57BLNeuronsOrexinsPeptidesVenomsExenatideGlp1r protein, mouseGlucagon-Like Peptide-1 ReceptorGlucagon-Like Peptide-1 Receptor AgonistsIncretinsOrexinsPeptidesVenomsBeige fatHypothalamic architectureIncretinMetabolismObesity

Identifiers

PMID28702330
PMCPMC5485307
OpenAlexW2616570371

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.