GLP-1 Receptor Agonists: Effects on Cardiovascular Risk Reduction
Corresponding Author
Daniel Lorber
Division of Endocrinology, New York Hospital Queens, Flushing, NY, USA
Department of Medicine, Weill Medical College of Cornell University, New York, NY, USA
Correspondence
D. Lorber, M.D., F.A.C.P., C.D.E., Director, Endocrinology, New York Hospital Queens, 5945 161 Street, Flushing, NY 11365, USA.
Tel.: 718 762 3111;
Fax: 718 353 6315;
E-mail: [email protected]
Search for more papers by this authorCorresponding Author
Daniel Lorber
Division of Endocrinology, New York Hospital Queens, Flushing, NY, USA
Department of Medicine, Weill Medical College of Cornell University, New York, NY, USA
Correspondence
D. Lorber, M.D., F.A.C.P., C.D.E., Director, Endocrinology, New York Hospital Queens, 5945 161 Street, Flushing, NY 11365, USA.
Tel.: 718 762 3111;
Fax: 718 353 6315;
E-mail: [email protected]
Search for more papers by this authorRe-use of this article is permitted in accordance with the Terms and Conditions set out at http://wileyonlinelibrary.com/onlineopen#OnlineOpen_Terms
Summary
Comorbid obesity, dyslipidemia, and hypertension place patients with type 2 diabetes (T2DM) at greatly increased risk of cardiovascular (CV) disease-related morbidity and mortality. An urgent need exists for effective treatment for patients with T2DM that encompasses glycemic control, weight loss, and reduction in CV risk factors. The glucagon-like peptide-1 receptor agonists (GLP-1 RAs) liraglutide and exenatide are incretin-based antidiabetes agents. This review examines CV-associated effects of liraglutide and exenatide in animal models and clinical trials with patients with T2DM. Studies support the effectiveness of GLP-1 RAs in reducing hyperglycemia. Further, GLP-1 RAs represent a significant advance in T2DM treatment because they uniquely affect a broad array of CV risk factors through significant weight and systolic blood pressure reduction, improved lipid levels, and possibly, as shown in in vitro studies and animal models, through direct effects on cardiac myocytes and endothelium.
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