PMID- 23216746
OWN - NLM
STAT- MEDLINE
DCOM- 20140110
LR  - 20220330
IS  - 1463-1326 (Electronic)
IS  - 1462-8902 (Linking)
VI  - 15
IP  - 7
DP  - 2013 Jul
TI  - Extra-pancreatic effects of incretin-based therapies: potential benefit for 
      cardiovascular-risk management in type 2 diabetes.
PG  - 593-606
LID - 10.1111/dom.12050 [doi]
AB  - Development of cardiovascular disease is one of the major complications of type 2 
      diabetes mellitus (T2DM). The chronic hyperglycaemic state is often accompanied 
      by dyslipidaemia, hypertension, low-grade systemic inflammation and oxidative 
      stress which collectively result in a high risk of micro- and macrovascular 
      complications. Current glucose-lowering agents do not sufficiently address 
      fore-mentioned macrovascular-risk factors. Recently, new therapeutic agents were 
      introduced, based on the incretin hormone glucagon-like peptide-1 (GLP-1), that 
      is, the GLP-1 receptor agonists (GLP-1RA) and dipeptidyl-peptidase 4 (DPP-4) 
      inhibitors. Beside its effect on pancreatic insulin secretion, GLP-1 exerts 
      several extra-pancreatic effects such as slowing down gastric emptying, promoting 
      satiety and reducing food intake and weight loss. Also, GLP-1 and GLP-1RA were 
      shown to improve cardiovascular-risk profiles, by reducing body fat content, 
      blood pressure, circulating lipids and inflammatory markers in patients with 
      T2DM. This review summarizes the presently known evidence with regard to 
      extra-pancreatic effects of the incretin-based agents, focusing on the actions 
      that improve the cardiovascular-risk profile. We present available data from 
      clinical trials of at least 24 week duration, but also findings from small-sized 
      clinical 'proof of principle' studies. We conclude that GLP-1 RA and to a lesser 
      extent DPP-4 inhibitors are promising agents with regard to their effects on body 
      weight, blood pressure and lipids, which collectively ameliorate the 
      cardiovascular-risk profile and as such may have added value in the treatment of 
      T2DM. However, large-sized long-term outcome studies are warranted to show the 
      true added value of these agents in the treatment of patients with T2DM.
CI  - (c) 2012 Blackwell Publishing Ltd.
FAU - van Genugten, R E
AU  - van Genugten RE
AD  - Department of Internal Medicine, Diabetes Center, VU University Medical Center, 
      Amsterdam, the Netherlands. r.vangenugten@vumc.nl
FAU - Moller-Goede, D L
AU  - Moller-Goede DL
FAU - van Raalte, D H
AU  - van Raalte DH
FAU - Diamant, M
AU  - Diamant M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20130121
PL  - England
TA  - Diabetes Obes Metab
JT  - Diabetes, obesity & metabolism
JID - 100883645
RN  - 0 (Dipeptidyl-Peptidase IV Inhibitors)
RN  - 0 (GLP1R protein, human)
RN  - 0 (Glucagon-Like Peptide-1 Receptor)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Incretins)
RN  - 0 (Receptors, Glucagon)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/complications/epidemiology/*prevention & control
MH  - Diabetes Mellitus, Type 2/complications/*drug therapy/physiopathology
MH  - Diabetic Angiopathies/epidemiology/prevention & control
MH  - Diabetic Cardiomyopathies/epidemiology/prevention & control
MH  - Dipeptidyl-Peptidase IV Inhibitors/therapeutic use
MH  - Endothelium, Vascular/*drug effects/physiopathology
MH  - Glucagon-Like Peptide-1 Receptor
MH  - Heart/*drug effects/physiopathology
MH  - Humans
MH  - Hypoglycemic Agents/agonists/*therapeutic use
MH  - Incretins/agonists/*therapeutic use
MH  - Receptors, Glucagon/agonists
MH  - Risk Factors
EDAT- 2012/12/12 06:00
MHDA- 2014/01/11 06:00
CRDT- 2012/12/11 06:00
PHST- 2012/08/09 00:00 [received]
PHST- 2012/09/17 00:00 [revised]
PHST- 2012/11/30 00:00 [accepted]
PHST- 2012/12/11 06:00 [entrez]
PHST- 2012/12/12 06:00 [pubmed]
PHST- 2014/01/11 06:00 [medline]
AID - 10.1111/dom.12050 [doi]
PST - ppublish
SO  - Diabetes Obes Metab. 2013 Jul;15(7):593-606. doi: 10.1111/dom.12050. Epub 2013 
      Jan 21.