The effect of glucagon-like peptide 1 on cardiovascular risk

Research output: Contribution to journalJournal articleResearchpeer-review

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The effect of glucagon-like peptide 1 on cardiovascular risk. / Sivertsen, Jacob; Rosenmeier, Jaya; Holst, Jens Juul; Vilsbøll, Tina.

In: Nature Reviews Cardiology, Vol. 9, No. 4, 04.2012, p. 209-22.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Sivertsen, J, Rosenmeier, J, Holst, JJ & Vilsbøll, T 2012, 'The effect of glucagon-like peptide 1 on cardiovascular risk', Nature Reviews Cardiology, vol. 9, no. 4, pp. 209-22. https://doi.org/10.1038/nrcardio.2011.211

APA

Sivertsen, J., Rosenmeier, J., Holst, J. J., & Vilsbøll, T. (2012). The effect of glucagon-like peptide 1 on cardiovascular risk. Nature Reviews Cardiology, 9(4), 209-22. https://doi.org/10.1038/nrcardio.2011.211

Vancouver

Sivertsen J, Rosenmeier J, Holst JJ, Vilsbøll T. The effect of glucagon-like peptide 1 on cardiovascular risk. Nature Reviews Cardiology. 2012 Apr;9(4):209-22. https://doi.org/10.1038/nrcardio.2011.211

Author

Sivertsen, Jacob ; Rosenmeier, Jaya ; Holst, Jens Juul ; Vilsbøll, Tina. / The effect of glucagon-like peptide 1 on cardiovascular risk. In: Nature Reviews Cardiology. 2012 ; Vol. 9, No. 4. pp. 209-22.

Bibtex

@article{f9c0248f2e174b09b8adb96e09c7ebbf,
title = "The effect of glucagon-like peptide 1 on cardiovascular risk",
abstract = "Glucagon-like peptide 1 (GLP-1) is an incretin hormone responsible for amplification of insulin secretion when nutrients are given orally, as opposed to intravenously, and it retains its insulinotropic activity in patients with type 2 diabetes mellitus. GLP-1-based therapies, such as GLP-1 receptor agonists and inhibitors of dipeptidyl peptidase 4, an enzyme that degrades endogenous GLP-1, have established effectiveness in lowering glucose levels and are routinely used to treat patients with type 2 diabetes. These agents regulate glucose metabolism through multiple mechanisms and have several effects on cardiovascular parameters. These effects, possibly independent of the glucose-lowering activity, include changes in blood pressure, endothelial function, body weight, cardiac metabolism, lipid metabolism, left ventricular function, atherosclerosis, and the response to ischemia-reperfusion injury. Thus, GLP-1-based therapies could potentially target both diabetes and cardiovascular disease. This Review highlights the mechanisms targeted by GLP-1-based therapies, and emphasizes current developments in incretin research that are relevant to cardiovascular risk and disease, as well as treatment with GLP-1 receptor agonists.",
keywords = "Animals, Blood Glucose, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Evidence-Based Medicine, Glucagon-Like Peptide 1, Humans, Hypoglycemic Agents, Receptors, Glucagon, Risk Assessment, Risk Factors, Treatment Outcome",
author = "Jacob Sivertsen and Jaya Rosenmeier and Holst, {Jens Juul} and Tina Vilsb{\o}ll",
year = "2012",
month = "4",
doi = "10.1038/nrcardio.2011.211",
language = "English",
volume = "9",
pages = "209--22",
journal = "Nature Reviews Cardiology",
issn = "1759-5002",
publisher = "nature publishing group",
number = "4",

}

RIS

TY - JOUR

T1 - The effect of glucagon-like peptide 1 on cardiovascular risk

AU - Sivertsen, Jacob

AU - Rosenmeier, Jaya

AU - Holst, Jens Juul

AU - Vilsbøll, Tina

PY - 2012/4

Y1 - 2012/4

N2 - Glucagon-like peptide 1 (GLP-1) is an incretin hormone responsible for amplification of insulin secretion when nutrients are given orally, as opposed to intravenously, and it retains its insulinotropic activity in patients with type 2 diabetes mellitus. GLP-1-based therapies, such as GLP-1 receptor agonists and inhibitors of dipeptidyl peptidase 4, an enzyme that degrades endogenous GLP-1, have established effectiveness in lowering glucose levels and are routinely used to treat patients with type 2 diabetes. These agents regulate glucose metabolism through multiple mechanisms and have several effects on cardiovascular parameters. These effects, possibly independent of the glucose-lowering activity, include changes in blood pressure, endothelial function, body weight, cardiac metabolism, lipid metabolism, left ventricular function, atherosclerosis, and the response to ischemia-reperfusion injury. Thus, GLP-1-based therapies could potentially target both diabetes and cardiovascular disease. This Review highlights the mechanisms targeted by GLP-1-based therapies, and emphasizes current developments in incretin research that are relevant to cardiovascular risk and disease, as well as treatment with GLP-1 receptor agonists.

AB - Glucagon-like peptide 1 (GLP-1) is an incretin hormone responsible for amplification of insulin secretion when nutrients are given orally, as opposed to intravenously, and it retains its insulinotropic activity in patients with type 2 diabetes mellitus. GLP-1-based therapies, such as GLP-1 receptor agonists and inhibitors of dipeptidyl peptidase 4, an enzyme that degrades endogenous GLP-1, have established effectiveness in lowering glucose levels and are routinely used to treat patients with type 2 diabetes. These agents regulate glucose metabolism through multiple mechanisms and have several effects on cardiovascular parameters. These effects, possibly independent of the glucose-lowering activity, include changes in blood pressure, endothelial function, body weight, cardiac metabolism, lipid metabolism, left ventricular function, atherosclerosis, and the response to ischemia-reperfusion injury. Thus, GLP-1-based therapies could potentially target both diabetes and cardiovascular disease. This Review highlights the mechanisms targeted by GLP-1-based therapies, and emphasizes current developments in incretin research that are relevant to cardiovascular risk and disease, as well as treatment with GLP-1 receptor agonists.

KW - Animals

KW - Blood Glucose

KW - Cardiovascular Diseases

KW - Diabetes Mellitus, Type 2

KW - Evidence-Based Medicine

KW - Glucagon-Like Peptide 1

KW - Humans

KW - Hypoglycemic Agents

KW - Receptors, Glucagon

KW - Risk Assessment

KW - Risk Factors

KW - Treatment Outcome

U2 - 10.1038/nrcardio.2011.211

DO - 10.1038/nrcardio.2011.211

M3 - Journal article

VL - 9

SP - 209

EP - 222

JO - Nature Reviews Cardiology

JF - Nature Reviews Cardiology

SN - 1759-5002

IS - 4

ER -

ID: 117854840