Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Dec 28;13(1):65.
doi: 10.3390/cells13010065.

GLP1 Receptor Agonists-Effects beyond Obesity and Diabetes

Affiliations
Review

GLP1 Receptor Agonists-Effects beyond Obesity and Diabetes

Sydney S Wilbon et al. Cells. .

Abstract

Glucagon-like peptide-1 receptor agonists (GLP1RA) have been transformative for patients and clinicians in treating type-2 diabetes and obesity. Drugs of this class, the bioavailability of which is continuously improving, enable weight loss and control blood glucose with minimal unwanted side effects. Since adopting GLP1RA for treating metabolic diseases, animal and clinical studies have revealed their beneficial effects on several other pathologies, including cardiovascular diseases, neurodegeneration, kidney disease, and cancer. A notable commonality between these diseases is their association with older age. Clinical trials and preclinical data suggest that GLP1RA may improve outcomes in these aging-related diseases. Some of the benefits of GLP1RA may be indirect due to their effects on obesity and glucose metabolism. However, there is building evidence that GLP1RA may also act directly on multiple organs implicated in aging-related pathology. This review aims to compile the studies reporting the effects of GLP1RA on aging-related diseases and discuss potential underlying mechanisms.

Keywords: GLP-1 receptor agonist; aging; cancer; cardiovascular disease; diabetes; incretin; neurodegenerative disease; obesity.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The dichotomous effects of GLP1 receptor agonists (GLP1RA). Effects are labeled with blue font, with resulting physiological changes marked in bold. GLP1R is expressed in some but not all cell populations of organs shown. Direct signaling reported to have positive effects is indicated by blue connections. Effects unclear from literature or remaining to be tested/confirmed are marked with “?”. Indirect effects downstream of GLP1RA signaling are shown as black connections. GLP1RA have also been shown to decrease inflammation in multiple organs, which also likely contributes to their indirect beneficial effects.

References

    1. Chia C.W., Egan J.M., Ferrucci L. Age-Related Changes in Glucose Metabolism, Hyperglycemia, and Cardiovascular Risk. Circ. Res. 2018;123:886–904. doi: 10.1161/CIRCRESAHA.118.312806. - DOI - PMC - PubMed
    1. Palta P., Huang E.S., Kalyani R.R., Golden S.H., Yeh H.C. Hemoglobin A(1c) and Mortality in Older Adults With and Without Diabetes: Results From the National Health and Nutrition Examination Surveys (1988–2011) Diabetes Care. 2017;40:453–460. doi: 10.2337/dci16-0042. - DOI - PMC - PubMed
    1. Edwards C.M., Todd J.F., Mahmoudi M., Wang Z., Wang R.M., Ghatei M.A., Bloom S.R. Glucagon-like peptide 1 has a physiological role in the control of postprandial glucose in humans: Studies with the antagonist exendin 9-39. Diabetes. 1999;48:86–93. doi: 10.2337/diabetes.48.1.86. - DOI - PubMed
    1. Muller T.D., Finan B., Bloom S.R., D’Alessio D., Drucker D.J., Flatt P.R., Fritsche A., Gribble F., Grill H.J., Habener J.F., et al. Glucagon-like peptide 1 (GLP-1) Mol. Metab. 2019;30:72–130. doi: 10.1016/j.molmet.2019.09.010. - DOI - PMC - PubMed
    1. Knudsen L.B., Nielsen P.F., Huusfeldt P.O., Johansen N.L., Madsen K., Pedersen F.Z., Thogersen H., Wilken M., Agerso H. Potent derivatives of glucagon-like peptide-1 with pharmacokinetic properties suitable for once daily administration. J. Med. Chem. 2000;43:1664–1669. doi: 10.1021/jm9909645. - DOI - PubMed

Publication types