Exploring the Potential Effect of GLP1R Agonism on Common Aging-Related Diseases via Glucose Reduction: A Mendelian Randomization Study

Jan 11, 2025The journals of gerontology. Series A, Biological sciences and medical sciences

Possible Links Between GLP1R Activation, Lower Blood Sugar, and Common Aging Diseases

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Abstract

GLP1 receptor agonism is potentially positively associated with appendicular lean mass, whole-body fat-free mass, and lung function.

Appendicular lean mass may increase with GLP1 receptor agonism (Beta = 0.246).
Whole-body fat-free mass is potentially positively affected by GLP1 receptor agonism (Beta = 0.202).
Lung function, measured by forced vital capacity, shows a potential positive association with GLP1 receptor agonism (Beta = 0.179).
A potential negative association with myocardial infarction has been observed (odds ratio = 0.430).
The findings are exploratory and require further research to confirm and understand the biological mechanisms involved.

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BACKGROUND: Glucagon-like peptide-1 receptor agonists (GLP1RAs) are widely used in managing type 2 diabetes mellitus and weight control. Their potential in treating aging-related diseases has been gaining attention in recent years. However, the long-term effects of GLP1RAs on these diseases have yet to be fully revealed.

METHODS: Using a genetic variant in the GLP1R gene to model the long-term effects of GLP1RAs, this Mendelian randomization (MR) study systematically explored potential causal associations between GLP1R agonism and 12 aging-related diseases and indicators. Genetic summary data sets used in this study were obtained from previous genome-wide association studies.

RESULTS: The primary MR analysis results suggested that GLP1R agonism was potentially positively causally associated with appendicular lean mass (Beta = 0.246, 95% confidence interval [CI] = 0.096-0.396), whole-body fat-free mass (Beta = 0.202, 95% CI = 0.048-0.355), and lung function (forced vital capacity [FVC]; Beta = 0.179, 95% CI = 0.152-0.205; p < .05). Additionally, a potential negative causal association was observed with myocardial infarction (odds ratio = 0.430, 95% CI = 0.249-0.745; p < .05).

CONCLUSIONS: The present MR study provides exploratory evidence suggesting potential causal associations between GLP1R agonism and appendicular lean mass, whole-body fat-free mass, lung function (FVC), and myocardial infarction. Given the exploratory nature of these findings and the limitations of the MR methodology, further research is needed to validate these results and investigate the underlying biological mechanisms.

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Exploring the Potential Effect of GLP1R Agonism on Common Aging-Related Diseases via Glucose Reduction: A Mendelian Randomization Study

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