Exendin‐4 decreases liver inflammation and atherosclerosis development simultaneously by reducing macrophage infiltration
Open accessAbstract
Background and Purpose: The aetiology of inflammation in the liver and vessel wall, leading to non‐alcoholic steatohepatitis (NASH) and atherosclerosis, respectively, shares common mechanisms including macrophage infiltration. To treat both disorders simultaneously, it is highly important to tackle the inflammatory status. Exendin‐4, a glucagon‐like peptide‐1 (GLP‐1) receptor agonist, reduces hepatic steatosis and has been suggested to reduce atherosclerosis; however, its effects on liver inflammation are underexplored. Here, we tested the hypothesis that exendin‐4 reduces inflammation in both the liver and vessel wall, and investigated the common underlying mechanism. Experimental Approach: Female APOE*3‐L eiden.CETP mice, a model with human‐like lipoprotein metabolism, were fed a cholesterol‐containing W estern‐type diet for 5 weeks to induce atherosclerosis and subsequently treated for 4 weeks with exendin‐4. Key Results: Exendin‐4 modestly improved dyslipidaemia, but markedly decreased atherosclerotic lesion severity and area (−33%), accompanied by a reduction in monocyte adhesion to the vessel wall (−42%) and macrophage content in the plaque (−44%). Furthermore, exendin‐4 reduced hepatic lipid content and inflammation as well as hepatic CD68+ (−18%) and F 4/80+ (−25%) macrophage content. This was accompanied by less monocyte recruitment from the circulation as the Mac‐1+ macrophage content was decreased (−36%). Finally, exendin‐4 reduced hepatic chemokine expression in vivo and suppressed oxidized low‐density lipoprotein accumulation in peritoneal macrophages in vitro, effects dependent on the GLP‐1 receptor. Conclusions and Implications: Exendin‐4 reduces inflammation in both the liver and vessel wall by reducing macrophage recruitment and activation. These data suggest that exendin‐4 could be a valuable strategy to treat NASH and atherosclerosis simultaneously.
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In APOE*3-Leiden.CETP mice fed a cholesterol-containing high-fat diet, 4 weeks of daily 50 μg/kg exenatide protected against hepatic inflammation, as indicated by decreased CD68+, F4/80+, and CD18+/CD11b+ staining and reduced Tnf, Il1b, and Il6 mRNA levels in the liver.
“In APOE*3-Leiden.CETP mice fed a cholesterol-containing high-fat diet that promotes atherosclerosis, 4 weeks of daily 50 μg/kg exenatide treatment protected against hepatic inflammation, as indicated by a decrease in CD68+, F4/80+, and CD18+/CD11b+ staining, as well as reduced Tnf, Il1b, and Il6 mRNA levels in the liver (67).”
From Antiinflammatory actions of glucagon-like peptide-1–based therapies beyond metabolic benefits (2025) · cites this paper as [67]
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Experimental — accuracy not yet measuredExendin-4 (50 μg/kg/day) treatment resulted in a reduction of atherosclerosis development and the number of monocytes adhering to the endothelium wall in the aortic root in western-type diet-fed APOE*3-Leiden.CETP mice.
“Exendin-4 (50 μg/kg/day) treatment resulted in a reduction of atherosclerosis development and the number of monocytes adhering to the endothelium wall in the aortic root in western-type diet-fed APOE∗3-Leiden.CETP(E3L.CETP) mice [63].”
From Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control (2016) · cites this paper as [63]
Exendin-4 treatment reduced hepatic expression of the inflammatory markers TNF-α, IL-1β, and IL-6 and macrophage markers, CD68, and F4/80 in the liver of mice fed a western-type diet.
“Exendin-4 treatment reduced hepatic expression of the inflammatory markers TNF-α, IL-1β, and IL-6 and macrophage markers, cluster of differentiation 68 (CD68), and F4/80 in the liver of mice fed a western-type diet [63].”
From Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control (2016) · cites this paper as [63]
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- Authors
- Wang, Y., Parlevliet, E. T., Geerling, J. J., van der Tuin, S. J. L., Zhang, H., Bieghs, V, Jawad, A. H. M., Shiri‐Sverdlov, R., Bot, I., de Jager, S. C. A., Havekes, L. M., Romijn, J. A., Willems van Dijk, K., & Rensen, P. C. N.
- Affiliations
- Leiden University Medical Center (NL)
- Department of Endocrinology and Metabolic Diseases Leiden University Medical Center Leiden The Netherlands
- Maastricht University (NL)
- Division of Biopharmaceutics Leiden/Amsterdam Center for Drug Research Leiden The Netherlands
- Netherlands Organisation for Applied Scientific Research (NL)
- Corresponding author
- Rensen, P C N
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2014-01-13
- Volume
- 171
- Issue
- 3
- Pages
- 723-734
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC3969084
- OpenAlex
- W2161872363
- Cited by
- 126
- References
- 39
- Citations by year
- 2026: 9 · 2025: 10 · 2024: 14 · 2023: 12 · 2022: 9 · 2021: 10 · 2020: 3 · 2019: 10 · 2018: 13 · 2017: 16 · 2016: 11 · 2015: 6 · 2014: 3
- FWCI
- 3.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- TNO Repository (submittedVersion)
- Research Publications (Maastricht University) (submittedVersion)
- Funders
- Netherlands Heart Foundation (2007B81, 2009T038)
- Dutch Diabetes Foundation (2007.00.010)
- Center for Translational Molecular Medicine
- Project PREDICCt (01C-104)
- Center of Medical Systems Biology
- Netherlands Consortium for Systems Biology
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- exendin-4, GLP-1 receptor agonists, nonalcoholic steatohepatitis, atherosclerosis, liver inflammation, macrophage infiltration, monocyte recruitment, hepatic steatosis, oxidized LDL, chemokines, dyslipidemia, APOE*3-Leiden.CETP mice, Western diet, peritoneal macrophages
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Exenatide, Animals, Anti-Inflammatory Agents, Non-Steroidal, Hypolipidemic Agents, Diet, Atherogenic, Disease Models, Animal, Drug Implants, Endothelium, Vascular, Fatty Liver, Female, Humans, Liver, Macrophage Activation, Macrophages, Mice, Transgenic, Peptides, Random Allocation, Venoms, Receptors, Glucagon, Dyslipidemias, Atherosclerosis, Mice, Apolipoprotein E3, Cholesterol Ester Transfer Proteins, Non-alcoholic Fatty Liver Disease
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