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GLP-1 receptor agonists and reduction of cardiometabolic risk: Potential underlying mechanisms.

Biochim Biophys Acta Mol Basis Dis · 2018

Last updated 2026-05-28

GLP-1 receptor agonists, a type of incretin-based therapy for type 2 diabetes, help lower blood sugar without increasing the risk of low blood sugar. Studies show they also reduce body weight, blood pressure, harmful blood fats, inflammation, and other factors linked to heart disease, potentially lowering the risk of cardiovascular events.

AI summary of the abstract below.

JournalBiochim Biophys Acta Mol Basis Dis, 2018
Citations115
Relative citation ratio5.05
NIH percentile92
Molecules
Conditions studied Type 2 Diabetes, Obesity, Cardiovascular Risk Reduction, Chronic Kidney Disease, Mash

Abstract

Type 2 diabetes mellitus (T2DM) is a metabolic condition with an elevated impact on cardiovascular (CV) risk. The innovative therapeutic approaches for T2DM - incretin-based therapies (IBTs), including glucagon-like peptide 1 (GLP-1) receptor agonists, have become popular and more widely used in recent years. The available scientific data from clinical studies and clinical practice highlights their beyond glucose-lowering effects, which is achieved without any increase in hypoglycaemia. The former effects include reduction in body weight, lipids, blood pressure, inflammatory markers, oxidative stress, endothelial dysfunction, and subclinical atherosclerosis, thus reducing and potentially preventing CV events. In fact, the introduction of IBTs is one of the key moments in the history of diabetes research and treatment. Such therapeutic strategies allow customization of antidiabetic treatment to each patient's need and therefore obtain better metabolic control with reduced CV risk. The aim of the present paper is to provide a comprehensive overview of the effects of GLP-1RA on various cardiometabolic markers and overall CV risk, with particular attention on recent CV outcome studies and potential mechanisms. In particular, the effects of liraglutide on formation and progression of atherosclerotic plaque and mechanisms explaining its cardioprotective effects are highlighted.

Verbatim abstract via PubMed 29778663 ↗