Evidence map›Paper›PMID 27030669›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2016

GLP-1 and weight loss: unraveling the diverse neural circuitry.

Scott E Kanoski, Matthew R Hayes, Karolina P Skibicka

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed, 3 pooled it
8.3field-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

150 citing papers in PubMed, 3 syntheses or guidelines pooled it, 276 citations in OpenAlex.

  1. Pooled it
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  3. GLP-1a: Going beyond Traditional Use.International journal of molecular sciences · 2022
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  9. Impact of semaglutide on health outcomes and mood in obese heart failure patients: a retrospective analysis.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
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90 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Scott E KanoskiHuman and Evolutionary Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California; kanoski@usc.edu.
Matthew R HayesTranslational Neuroscience Program, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia Pennsylvania; and.
Karolina P SkibickaDepartment of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
University of Gothenburg · SEUniversity of Pennsylvania · USUniversity of Southern California · US

Funding

Higher-Order Neural Control of Food IntakeR01DK104897 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KANOSKI, SCOTT EDWARD · 2015 to 2024
$4.3M
Neuroendocrinology of Energy Balance ControlR01DK096139 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI HAYES, MATTHEW R · 2012 to 2016
$1.7M
Food intake control by leptin signaling in the hippocampusK01DK097147 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KANOSKI, SCOTT EDWARD · 2013 to 2015
$284k
Neuropeptidergic control of environmental stimulus-driven feeding behaviorR03DK102478 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KANOSKI, SCOTT EDWARD · 2014 to 2015
$165k
NIDDK NIH HHS K01 DK097147NIDDK NIH HHS R01 DK096139NIDDK NIH HHS R01 DK104897NIDDK NIH HHS R03 DK102478
6 · The paper itself

Abstract

Glucagon-like peptide-1 (GLP-1) is currently one of the most promising biological systems for the development of effective obesity pharmacotherapies. Long-acting GLP-1 analogs potently reduce food intake and body weight, and recent discoveries reveal that peripheral administration of these drugs reduces food intake largely through humoral pathways involving direct action on brain GLP-1 receptors (GLP-1R). Thus, it is of critical importance to understand the neural systems through which GLP-1 and long-acting GLP-1 analogs reduce food intake and body weight. In this review, we discuss several neural, physiological, cellular and molecular, as well as behavioral mechanisms through which peripheral and central GLP-1R signaling reduces feeding. Particular attention is devoted to discussion regarding the numerous neural substrates through which GLP-1 and GLP-1 analogs act to reduce food intake and body weight, including various hypothalamic nuclei (arcuate nucleus of the hypothalamus, periventricular hypothalamus, lateral hypothalamic area), hindbrain nuclei (parabrachial nucleus, medial nucleus tractus solitarius), hippocampus (ventral subregion; vHP), and nuclei embedded within the mesolimbic reward circuitry [ventral tegmental area (VTA) and nucleus accumbens (NAc)]. In some of these nuclei [VTA, NAc, and vHP], GLP-1R activation reduces food intake and body weight without concomitant nausea responses, suggesting that targeting these specific pathways may be of particular interest for future obesity pharmacotherapy. The widely distributed neural systems through which GLP-1 and GLP-1 analogs act to reduce body weight highlight the complexity of the neural systems regulating energy balance, as well as the challenges for developing effective obesity pharmacotherapies that reduce feeding without producing parallel negative side effects.

Indexed as

BrainGene Expression RegulationGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorHumansWeight LossGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorByettadipeptidyl peptidase-4exendin-4food rewardglucagon-like peptide-1liraglutideobesitySaxenda

Identifiers

PMID27030669
PMCPMC4888559
OpenAlexW2330887677

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.