Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 2814-2821 |
| Number of pages | 8 |
| Journal | BIOCHIMICA ET BIOPHYSICA ACTA. MOLECULAR BASIS OF DISEASE |
| Volume | 1864 |
| Publication status | Published - 2018 |
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All Science Journal Classification (ASJC) codes
- Molecular Medicine
- Molecular Biology
Cite this
GLP-1 receptor agonists and reduction of cardiometabolic risk: Potential underlying mechanisms. / Nikolic, Dragana; Rizzo, Manfredi; Patti, Angelo Maria; Montalto, Giuseppe; Rizzo, Manfredi; Mcadams, Brooke S.; Cosentino, Francesco; Rizvi, Ali A.; Rizzo, Manfredi; Mannina, Carlo.
In: BIOCHIMICA ET BIOPHYSICA ACTA. MOLECULAR BASIS OF DISEASE, Vol. 1864, 2018, p. 2814-2821.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - GLP-1 receptor agonists and reduction of cardiometabolic risk: Potential underlying mechanisms
AU - Nikolic, Dragana
AU - Rizzo, Manfredi
AU - Patti, Angelo Maria
AU - Montalto, Giuseppe
AU - Rizzo, Manfredi
AU - Mcadams, Brooke S.
AU - Cosentino, Francesco
AU - Rizvi, Ali A.
AU - Rizzo, Manfredi
AU - Mannina, Carlo
PY - 2018
Y1 - 2018
N2 - 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.
AB - 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.
UR - http://hdl.handle.net/10447/299148
UR - http://www.elsevier.com/locate/bbadis
M3 - Article
VL - 1864
SP - 2814
EP - 2821
JO - Biochimica et Biophysica Acta - Molecular Basis of Disease
JF - Biochimica et Biophysica Acta - Molecular Basis of Disease
SN - 0925-4439
ER -