PMID- 19931305 OWN - NLM STAT- MEDLINE DCOM- 20100514 LR - 20220408 IS - 1879-016X (Electronic) IS - 0163-7258 (Linking) VI - 125 IP - 2 DP - 2010 Feb TI - Glycaemic control in type 2 diabetes: targets and new therapies. PG - 328-61 LID - 10.1016/j.pharmthera.2009.11.001 [doi] AB - Type 2 diabetes mellitus (T2DM) is a worldwide public health challenge. Despite the availability of many antidiabetes agents and pharmacotherapies targeting cardiovascular risk factors, the morbidity, mortality and economic consequences of T2DM are still a great burden to patients, society, health care systems and the economy. The need for new therapies for glycaemic control is compounded by the fact that existing treatments have limitations either because of their side effects (particularly weight gain and hypoglycaemia) or contraindications that limit their use. Furthermore, none of the current therapies have a significant impact on disease progression. Incretin-based therapies offer a new therapeutic approach to the management of T2DM, and there are also several even newer therapies in development. There are two groups of incretin-based therapies currently available; dipeptidyl peptidase-4 (DPP-4) inhibitors and GLP-1 analogues/mimetics. The former are given orally while the latter subcutaneously. These drugs result in glucose-dependent insulin secretion and glucose-dependent glucagon suppression, with consequent low risk of hypoglycaemia when used as mono- or combination therapy (except when used with sulphonylureas). In addition, they are either weight neutral in the case of DPP-4 inhibitors or cause weight loss in the case of incretin mimetics/analogues. Furthermore, animal studies have shown that these agents prolong beta cell survival which offers the theoretical possibility of slowing the progression to T2DM. In this article we will review the currently available antidiabetes agents with particular emphasis on incretin-based and future therapies. In addition, we will review and discuss the evidence relating to glycaemic control and cardiovascular disease. CI - 2009 Elsevier Inc. All rights reserved. FAU - Tahrani, Abd A AU - Tahrani AA AD - Department of Diabetes and Endocrinology, Heart of England NHS Foundation Trust, Birmingham, UK. a.a.tahrani@bham.ac.uk FAU - Piya, Milan K AU - Piya MK FAU - Kennedy, Amy AU - Kennedy A FAU - Barnett, Anthony H AU - Barnett AH LA - eng GR - RTF/01/094/DH_/Department of Health/United Kingdom GR - CAPMC/CIHR/Canada PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20091118 PL - England TA - Pharmacol Ther JT - Pharmacology & therapeutics JID - 7905840 RN - 0 (Dipeptidyl-Peptidase IV Inhibitors) RN - 0 (Hypoglycemic Agents) RN - 0 (Incretins) RN - 89750-14-1 (Glucagon-Like Peptide 1) SB - IM MH - Animals MH - Cardiovascular Diseases/etiology/prevention & control MH - Diabetes Mellitus, Type 2/complications/*drug therapy/physiopathology MH - Dipeptidyl-Peptidase IV Inhibitors/adverse effects/pharmacokinetics/*therapeutic use MH - Drug Administration Routes MH - Drug Interactions MH - Glucagon-Like Peptide 1/analogs & derivatives/therapeutic use MH - Humans MH - Hypoglycemic Agents/adverse effects/pharmacokinetics/*therapeutic use MH - Incretins/adverse effects/pharmacokinetics/*therapeutic use RF - 280 EDAT- 2009/11/26 06:00 MHDA- 2010/05/15 06:00 CRDT- 2009/11/26 06:00 PHST- 2009/11/02 00:00 [received] PHST- 2009/11/02 00:00 [accepted] PHST- 2009/11/26 06:00 [entrez] PHST- 2009/11/26 06:00 [pubmed] PHST- 2010/05/15 06:00 [medline] AID - S0163-7258(09)00211-3 [pii] AID - 10.1016/j.pharmthera.2009.11.001 [doi] PST - ppublish SO - Pharmacol Ther. 2010 Feb;125(2):328-61. doi: 10.1016/j.pharmthera.2009.11.001. Epub 2009 Nov 18.