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Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes
Open accessAbstract
Aims/hypothesis Obesity and insulin resistance are associated with low-grade chronic inflammation. Glucagon-like peptide-1 (GLP-1) is known to reduce insulin resistance. We investigated whether GLP-1 has anti-inflammatory effects on adipose tissue, including adipocytes and adipose tissue macrophages (ATM).Methods We administered a recombinant adenovirus (rAd) producing GLP-1 (rAd-GLP-1) to an ob/ob mouse model of diabetes. We examined insulin sensitivity, body fat mass, the infiltration of ATM and metabolic profiles. We analysed the mRNA expression of inflammatory cytokines, lipogenic genes, and M1 and M2 macrophage-specific genes in adipose tissue by real-time quantitative PCR. We also examined the activation of nuclear factor κB (NF-κB), extracellular signal-regulated kinase 1/2 and Jun N-terminal kinase (JNK) in vivo and in vitro.Results Fat mass, adipocyte size and mRNA expression of lipogenic genes were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Macrophage populations (F4/80(+) and F4/80(+)CD11b(+)CD11c(+) cells), as well as the expression and production of IL-6, TNF-α and monocyte chemoattractant protein-1, were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Expression of M1-specific mRNAs was significantly reduced, but that of M2-specific mRNAs was unchanged in rAd-GLP-1-treated ob/ob mice. NF-κB and JNK activation was significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Lipopolysaccharide-induced inflammation was reduced by the GLP-1 receptor agonist, exendin-4, in 3T3-L1 adipocytes and ATM.Conclusions/interpretation We suggest that GLP-1 reduces macrophage infiltration and directly inhibits inflammatory pathways in adipocytes and ATM, possibly contributing to the improvement of insulin sensitivity.
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“In the adipose tissue of GLP-1-treated ob/ob mice expressing recombinant adenovirus, for instance, GLP-1RA has been shown to decrease the production of TNF-α, IL-6, and IL-1β, all of which are significant mediators of inflammation.”
From Anti-inflammatory role of glucagon-like peptide 1 receptor agonists and its clinical implications (2024) · cites this paper as [38]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“antiinflammatory benefits have been observed in various preclinical models, such as obesity, atherosclerosis, steatohepatitis, and nephritis, even in the absence of direct immune cell targeting (27–32).”
From Antiinflammatory actions of glucagon-like peptide-1–based therapies beyond metabolic benefits (2025) · cites this paper as [27]
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“It was reported that GLP-1 shows anti-inflammatory effects on pancreatic islets and adipose tissue, contributing to lowering glucose levels in diabetes [18–20].”
From Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control (2016) · cites this paper as [18]
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“Administration of a recombinant adenovirus producing GLP-1 (4 × 109 PFU/mouse) to ob/ob mice reduced the macrophage population and production of TNF-α, MCP-1, and IL-6 in adipose tissue via inhibition of nuclear factor-kappa B (NF-κB) activation and phosphorylation of ERK1/2 and c-Jun N-terminal kinases [18].”
From Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control (2016) · cites this paper as [18]
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In the citing paper
“GLP-1 receptor agonists may potentially reduce inflammation and oxidative stress in adipose tissue by affecting the expression of cytokines, chemokines, and macrophage infiltration, with prolonged GLP-1 action potentially alleviating obesity-related adipose tissue inflammation while enhancing the expression of anti-inflammatory genes [17,18]”
From New Developments in Pharmacological Treatment of Obesity and Type 2 Diabetes—Beyond and within GLP-1 Receptor Agonists (2024) · cites this paper as [17]
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“Similar antiinflammatory effects of GLP-1 have been reported in human macrophage cell lines (66), and systemic effects of GLP-1 agonists on macrophage infiltration have been previously reported (67).”
From GLP-1 agonists in the treatment of chronic kidney disease in type 2 diabetes and obesity (2025) · cites this paper as [67]
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“Treatment of Huh7 and HepG2 hepatoma cells with exenatide decreased intracellular lipid accumulation [181,182] by enhancing fatty acid oxidation and reducing lipogenesis [160,161,179,183].”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [182]
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“Treatment with GLP-1 RAs is also able to reduce macrophage infiltration of adipose tissue and inhibit inflammatory pathways in adipocytes, concurring to ameliorate insulin sensitivity [138].”
From GLP-1 Receptor Agonists in Non-Alcoholic Fatty Liver Disease: Current Evidence and Future Perspectives (2023) · cites this paper as [138]
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“In fact, new research suggests that GLP-1 RAs may reduce the production of pro-inflammatory cytokines and immune cell infiltration to reduce inflammation in many tissues, including AT [73].”
From Adipose Tissue: A Novel Target of the Incretin Axis? A Paradigm Shift in Obesity-Linked Insulin Resistance (2024) · cites this paper as [73]
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“Furthermore, GLP-1 RAs prevent resident macrophages in AT from being activated by nuclear factor-kappa B (NF-κB) [73].”
From Adipose Tissue: A Novel Target of the Incretin Axis? A Paradigm Shift in Obesity-Linked Insulin Resistance (2024) · cites this paper as [73]
In the citing paper
“Studies have shown that GLP-1 and its analogs have anti-inflammatory properties.”
From The Role of Glp-1 Receptor Agonists in Insulin Resistance with Concomitant Obesity Treatment in Polycystic Ovary Syndrome (2022) · cites this paper as [101]
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Metadata
- Authors
- Lee, Y.-S., Park, M.-S., Choung, J.-S., Kim, S.-S., Oh, H.-H., Choi, C.-S., Ha, S.-Y., Kang, Y., Kim, Y., & Jun, H.-S.
- Affiliations
- Gachon University (KR)
- Gachon University Gil Medical Center (KR)
- Ajou University (KR)
- Seoul National University (KR)
- Corresponding author
- Jun, H.-S.
- Venue
- Diabetologia
- Published
- 2012-06-22
- Volume
- 55
- Issue
- 9
- Pages
- 2456-2468
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W1993624198
- Cited by
- 319
- References
- 47
- Citations by year
- 2026: 31 · 2025: 34 · 2024: 35 · 2023: 29 · 2022: 25 · 2021: 24 · 2020: 17 · 2019: 26 · 2018: 17 · 2017: 15 · 2016: 17 · 2015: 17 · 2014: 18 · 2013: 12 · 2012: 2
- FWCI
- 11.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- AJOU Open Repository (Ajou University) (submittedVersion)
- Funders
- National Research Foundation
- National Research Foundation of Korea (A062260)
- Korea Science and Engineering Foundation
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- glucagon-like peptide-1, adipose tissue macrophages, adipose tissue inflammation, obesity, type 2 diabetes, insulin resistance, ob/ob mice, adipocyte size, lipogenic gene expression, macrophage polarization, NF-κB, JNK, exendin-4, lipopolysaccharide-induced inflammation, adipocyte inflammation, adipose tissue mass
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Adipose Tissue, Animals, Anti-Inflammatory Agents, Gene Expression Regulation, Inflammation, Insulin Resistance, Macrophages, Mice, Obese, Obesity, NF-kappa B, Receptors, Glucagon, Body Fat Distribution, Mice, Glucagon-Like Peptide 1, Real-Time Polymerase Chain Reaction
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