DPP-4 inhibitor therapy: new directions in the treatment of type 2 diabetes

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DPP-4 inhibitor therapy: new directions in the treatment of type 2 diabetes. / Deacon, Carolyn F; Carr, Richard D; Holst, Jens Juul.

In: Frontiers in Bioscience, Vol. 13, 2008, p. 1780-94.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Deacon, CF, Carr, RD & Holst, JJ 2008, 'DPP-4 inhibitor therapy: new directions in the treatment of type 2 diabetes', Frontiers in Bioscience, vol. 13, pp. 1780-94.

APA

Deacon, C. F., Carr, R. D., & Holst, J. J. (2008). DPP-4 inhibitor therapy: new directions in the treatment of type 2 diabetes. Frontiers in Bioscience, 13, 1780-94.

Vancouver

Deacon CF, Carr RD, Holst JJ. DPP-4 inhibitor therapy: new directions in the treatment of type 2 diabetes. Frontiers in Bioscience. 2008;13:1780-94.

Author

Deacon, Carolyn F ; Carr, Richard D ; Holst, Jens Juul. / DPP-4 inhibitor therapy: new directions in the treatment of type 2 diabetes. In: Frontiers in Bioscience. 2008 ; Vol. 13. pp. 1780-94.

Bibtex

@article{711d9100c50e11dd8ca2000ea68e967b,
title = "DPP-4 inhibitor therapy: new directions in the treatment of type 2 diabetes",
abstract = "Many patients with type 2 diabetes fail to achieve adequate glycaemic control with available treatments, even when used in combination, and eventually develop microvascular and macrovascular diabetic complications. Even intensive interventions to control glycaemia reduce macrovascular complications only minimally. There is, therefore, a need for new agents that more effectively treat the disease, as well as target its prevention, its progression, and its associated complications. One emerging area of interest is centred upon the actions of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which enhance meal-induced insulin secretion and have trophic effects on the beta-cell. GLP-1 also inhibits glucagon secretion, and suppresses food intake and appetite. Two new classes of agents have recently gained regulatory approval for therapy of type 2 diabetes; long-acting stable analogues of GLP-1, the so-called incretin mimetics, and inhibitors of dipeptidyl peptidase 4 (DPP-4, the enzyme responsible for the rapid degradation of the incretin hormones), the so-called incretin enhancers. This article focuses on DPP-4 inhibitors.",
author = "Deacon, {Carolyn F} and Carr, {Richard D} and Holst, {Jens Juul}",
note = "Keywords: Animals; Antigens, CD26; Diabetes Mellitus, Type 2; Disease Models, Animal; Enzyme Inhibitors; Gastric Inhibitory Polypeptide; Glucose; Humans; Hypoglycemic Agents; Incretins; Insulin; Insulin Resistance; Islets of Langerhans; Mice; Rats",
year = "2008",
language = "English",
volume = "13",
pages = "1780--94",
journal = "Frontiers in Bioscience",
issn = "1093-9946",
publisher = "Frontiers in Bioscience",

}

RIS

TY - JOUR

T1 - DPP-4 inhibitor therapy: new directions in the treatment of type 2 diabetes

AU - Deacon, Carolyn F

AU - Carr, Richard D

AU - Holst, Jens Juul

N1 - Keywords: Animals; Antigens, CD26; Diabetes Mellitus, Type 2; Disease Models, Animal; Enzyme Inhibitors; Gastric Inhibitory Polypeptide; Glucose; Humans; Hypoglycemic Agents; Incretins; Insulin; Insulin Resistance; Islets of Langerhans; Mice; Rats

PY - 2008

Y1 - 2008

N2 - Many patients with type 2 diabetes fail to achieve adequate glycaemic control with available treatments, even when used in combination, and eventually develop microvascular and macrovascular diabetic complications. Even intensive interventions to control glycaemia reduce macrovascular complications only minimally. There is, therefore, a need for new agents that more effectively treat the disease, as well as target its prevention, its progression, and its associated complications. One emerging area of interest is centred upon the actions of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which enhance meal-induced insulin secretion and have trophic effects on the beta-cell. GLP-1 also inhibits glucagon secretion, and suppresses food intake and appetite. Two new classes of agents have recently gained regulatory approval for therapy of type 2 diabetes; long-acting stable analogues of GLP-1, the so-called incretin mimetics, and inhibitors of dipeptidyl peptidase 4 (DPP-4, the enzyme responsible for the rapid degradation of the incretin hormones), the so-called incretin enhancers. This article focuses on DPP-4 inhibitors.

AB - Many patients with type 2 diabetes fail to achieve adequate glycaemic control with available treatments, even when used in combination, and eventually develop microvascular and macrovascular diabetic complications. Even intensive interventions to control glycaemia reduce macrovascular complications only minimally. There is, therefore, a need for new agents that more effectively treat the disease, as well as target its prevention, its progression, and its associated complications. One emerging area of interest is centred upon the actions of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which enhance meal-induced insulin secretion and have trophic effects on the beta-cell. GLP-1 also inhibits glucagon secretion, and suppresses food intake and appetite. Two new classes of agents have recently gained regulatory approval for therapy of type 2 diabetes; long-acting stable analogues of GLP-1, the so-called incretin mimetics, and inhibitors of dipeptidyl peptidase 4 (DPP-4, the enzyme responsible for the rapid degradation of the incretin hormones), the so-called incretin enhancers. This article focuses on DPP-4 inhibitors.

M3 - Journal article

C2 - 17981667

VL - 13

SP - 1780

EP - 1794

JO - Frontiers in Bioscience

JF - Frontiers in Bioscience

SN - 1093-9946

ER -

ID: 8933143