Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (664 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A peptide of 36 or 37 amino acids that is derived from proglucagon and mainly produced by the intestinal L cells. glp-1(1-37 or 1-36) is further N-terminally truncated resulting in glp-1(7-37) or glp-1-(7-36) which can be amidated. These glp-1 peptides are known to enhance glucose-dependent insulin release, suppress glucagon release and gastric emptying, lower blood glucose, and reduce food intake.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Glucagon Like Peptide 1; GLP-1; GLP 1; Glucagon-Like Peptide-1.
Where it fits in the MeSH classification
- Broader topics
- Glucagon-Like Peptides
- Narrower topics
- Liraglutide
Related concepts
Research landscape
PubMed indexes 14,240 records tagged with the MeSH heading “Glucagon-Like Peptide 1” (counts retrieved 2026-10-31). 5,573 of them (39.1%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 6,221 records.
Reviews account for 3,059 records (21.5%) and meta-analyses for 397. Randomized controlled trials number 1,626 (11.4%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.
Show the data
| Period | Records |
|---|---|
| through 1999 | 579 |
| 2000-2009 | 1,867 |
| 2010-2019 | 6,221 |
| 2020 onward | 5,573 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,059 | 21.5% |
| Meta-analyses | 397 | 2.8% |
| Randomized controlled trials | 1,626 | 11.4% |
Method: PubMed query "Glucagon-Like Peptide 1"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Effects of GLP-1 Analogues and Agonists on the Gut Microbiota: A Systematic Review | 2025 | Systematic review Design not recorded in structured metadata | 72 | cc by PMID 40284168 · DOI · PMC12029897 |
| Liraglutide in mild to moderate Alzheimer's disease: a phase 2b clinical trial | 2026 | Randomized controlled trial Design not recorded in structured metadata | 62 | cc by PMID 41326666 · DOI · PMC12823385 |
| An endogenous GLP-1 circuit engages VTA GABA neurons to regulate mesolimbic dopamine neurons and attenuate cocaine seeking | 2025 | Research article Design not recorded in structured metadata | 55 | cc by PMID 40009667 · DOI · PMC11864183 |
Effects of GLP-1 Analogues and Agonists on the Gut Microbiota: A Systematic Review [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundGLP-1 analogues are a relatively new class of medications that form the cornerstone of diabetes treatment.
- Closing excerpt
- Further research is essential to confirm these findings and to better recognize their implications for the clinical outcomes of patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (282 words)
BackgroundGLP-1 analogues are a relatively new class of medications that form the cornerstone of diabetes treatment. They possess invaluable glucose-lowering properties without hypoglycemic effects as well as strong cardioprotective effects. The gut microbiome has become the focus of numerous studies, demonstrating its influence not only on the gut but also on the overall well-being of the entire body. However, the effects of GLP-1 analogs on gut microbiota remain uncertain.Scope of reviewOur systematic review (based on PRISMA guidelines) aimed to gather knowledge on the effects of GLP-1 analogue medications on the composition, richness, and abundance of gut microbiota in both animal and human models.ConclusionsThirty-eight studies were included in this systematic review. GLP-1 analogues have demonstrated a notable impact on the composition, richness, and diversity of gut microbiota. We can conclude, following the obtained research results of our study, that liraglutide promotes the growth of beneficial genera relevant for beneficial metabolic functions. Exenatide and exendin-4 administration showed various effects on the microbiome composition in animal and human studies. In animal models, it increased genera associated with improved metabolism; however, in human models, genera linked to better metabolic functions and escalated inflammation increased. Following dulaglutide administration, increases in Bacteroides, Akkermansia, and Ruminococcus, genera connected to an improved metabolic model, were significant. Finally, varied results were obtained after semaglutide treatment, in which A. muciniphila, known for its positive metabolic functions, increased; however, microbial diversity decreased. Semaglutide treatment provided various results indicating many confounding factors in semaglutide's impact on the gut microbiota. Results varied due to dissimilarities in the studied populations and the duration of the studies. Further research is essential to confirm these findings and to better recognize their implications for the clinical outcomes of patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40284168 · DOI · PMC12029897
Liraglutide in mild to moderate Alzheimer's disease: a phase 2b clinical trial [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Liraglutide, a glucagon-like peptide 1 (GLP-1) agonist and antidiabetic drug, has shown neuroprotective effects in animal models.
- Closing excerpt
- gov identifier: NCT01843075 .
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (224 words)
Liraglutide, a glucagon-like peptide 1 (GLP-1) agonist and antidiabetic drug, has shown neuroprotective effects in animal models. In this study, we aimed to evaluate the safety and efficacy of liraglutide in mild to moderate Alzheimer's disease syndrome. 'Evaluating liraglutide in Alzheimer's disease' (ELAD) is a multicenter, randomized, double-blind, placebo-controlled phase 2b trial in 204 participants with mild to moderate Alzheimer's disease syndrome with no diabetes. Participants received daily injections of liraglutide or placebo for 52 weeks. They underwent fluorodeoxyglucose positron emission tomography, magnetic resonance imaging and detailed neuropsychometric evaluations. The primary outcome was a change in cerebral glucose metabolic rate. Secondary outcomes were safety and tolerability and cognitive changes. The primary outcome showed no significant differences in cerebral glucose metabolism (difference = -0.17; 95% confidence interval: -0.39 to 0.06; P = 0.14) between the two groups. The secondary outcome-score on the Alzheimer's Disease Assessment Scale-Executive domain (ADAS-Exec)-performed better in liraglutide-treated patients compared to placebo (0.15; 95% confidence interval: 0.03-0.28; unadjusted P = 0.01). No significant differences were observed in Alzheimer's Disease Cooperative Study-Activities of Daily Living (ADCS-ADL) (-0.58; 95% confidence interval: -3.13 to 1.97; unadjusted P = 0.65) or Clinical Dementia Rating-Sum of Boxes (CDR-SoB) (-0.06; 95% confidence interval: -0.57 to 0.44; unadjusted P = 0.81) scores. Liraglutide was generally safe and well tolerated in non-diabetic patients with Alzheimer's disease. ClinicalTrials.gov identifier: NCT01843075 .
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41326666 · DOI · PMC12823385
An endogenous GLP-1 circuit engages VTA GABA neurons to regulate mesolimbic dopamine neurons and attenuate cocaine seeking [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Recent studies show that systemic administration of a glucagon-like peptide-1 receptor (GLP-1R) agonist is sufficient to attenuate cocaine seeking.
- Closing excerpt
- Together, these findings suggest that targeting central GLP-1 circuits may be an effective strategy toward reducing cocaine relapse and highlight a functional role of GABAergic GLP-1R-expressing midbrain neurons in drug seeking.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (158 words)
Recent studies show that systemic administration of a glucagon-like peptide-1 receptor (GLP-1R) agonist is sufficient to attenuate cocaine seeking. However, the neural mechanisms mediating these effects and the role of endogenous central GLP-1 signaling in cocaine seeking remain unknown. Here, we show that voluntary cocaine taking decreased plasma GLP-1 levels in rats and that chemogenetic activation of GLP-1-producing neurons in the nucleus tractus solitarius that project to the ventral tegmental area (VTA) decreased cocaine seeking. Single-nuclei transcriptomics and FISH studies revealed that GLP-1Rs are expressed primarily on GABA neurons in the VTA. Using in vivo fiber photometry, we found that the efficacy of a systemic GLP-1R agonist to attenuate cocaine seeking was associated with increased activity of VTA GABA neurons and decreased activity of VTA dopamine neurons. Together, these findings suggest that targeting central GLP-1 circuits may be an effective strategy toward reducing cocaine relapse and highlight a functional role of GABAergic GLP-1R-expressing midbrain neurons in drug seeking.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40009667 · DOI · PMC11864183
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Glucagon-like peptide 1 (GLP-1) [4]
- Research article Effects of glucagon-like peptide-1 receptor agonists on weight loss: systematic review and meta-analyses of randomised controlled trials [5]
- Research article GLP-1 physiology informs the pharmacotherapy of obesity [6]
- Research article Efficacy and Safety of GLP-1 Medicines for Type 2 Diabetes and Obesity [7]
- Research article Changes in lean body mass with glucagon-like peptide-1-based therapies and mitigation strategies [8]
- Research article Glucagon-like peptide-1: a multi-faceted anti-inflammatory agent [9]
References
- Gofron KK, Wasilewski A, Małgorzewicz S. Effects of GLP-1 Analogues and Agonists on the Gut Microbiota: A Systematic Review. . 2025. PMID 40284168 · DOI · PMC12029897
- Edison P, Femminella GD, Ritchie C, Nowell J, Holmes C, Walker Z, et al.. Liraglutide in mild to moderate Alzheimer's disease: a phase 2b clinical trial. . 2026. PMID 41326666 · DOI · PMC12823385
- Merkel R, Hernandez NS, Weir V, Zhang Y, Caffrey A, Rich MT, et al.. An endogenous GLP-1 circuit engages VTA GABA neurons to regulate mesolimbic dopamine neurons and attenuate cocaine seeking. . 2025. PMID 40009667 · DOI · PMC11864183
- Müller TD, Finan B, Bloom SR, D'Alessio D, Drucker DJ, Flatt PR, et al.. Glucagon-like peptide 1 (GLP-1). Mol Metab. 2019. PMID 31767182 · DOI · PMC6812410
- Vilsbøll T, Christensen M, Junker AE, Knop FK, Gluud LL. Effects of glucagon-like peptide-1 receptor agonists on weight loss: systematic review and meta-analyses of randomised controlled trials. BMJ. 2012. PMID 22236411 · DOI · PMC3256253
- Drucker DJ. GLP-1 physiology informs the pharmacotherapy of obesity. Mol Metab. 2022. PMID 34626851 · DOI · PMC8859548
- Drucker DJ. Efficacy and Safety of GLP-1 Medicines for Type 2 Diabetes and Obesity. Diabetes Care. 2024. PMID 38843460 · DOI
- Neeland IJ, Linge J, Birkenfeld AL. Changes in lean body mass with glucagon-like peptide-1-based therapies and mitigation strategies. Diabetes Obes Metab. 2024. PMID 38937282 · DOI
- Mehdi SF, Pusapati S, Anwar MS, Lohana D, Kumar P, Nandula SA, et al.. Glucagon-like peptide-1: a multi-faceted anti-inflammatory agent. Front Immunol. 2023. PMID 37266425 · DOI · PMC10230051
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.