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DPP-4 inhibition and islet function

Ahrén, Bo LU (2012) In Journal of Diabetes Investigation 3(1). p.3-10
Abstract
During recent years, dipeptidyl peptidase-4 (DPP-4) inhibition has been included in the clinical management of type 2 diabetes, both as monotherapy and as add-on to several other therapies. DPP-4 inhibition prevents the inactivation of the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). This results in stimulation of insulin secretion and inhibition of glucagon secretion, and there is also a potential beta-cell preservation effect, as judged from rodent studies; that is, it might target the key islet dysfunction in the disease. In type 2 diabetes. This reduces 24-h glucose levels and reduces HbA1c by approximate to 0.81.1% from baseline levels of 7.78.5%. DPP-4 inhibition is safe,... (More)
During recent years, dipeptidyl peptidase-4 (DPP-4) inhibition has been included in the clinical management of type 2 diabetes, both as monotherapy and as add-on to several other therapies. DPP-4 inhibition prevents the inactivation of the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). This results in stimulation of insulin secretion and inhibition of glucagon secretion, and there is also a potential beta-cell preservation effect, as judged from rodent studies; that is, it might target the key islet dysfunction in the disease. In type 2 diabetes. This reduces 24-h glucose levels and reduces HbA1c by approximate to 0.81.1% from baseline levels of 7.78.5%. DPP-4 inhibition is safe, with a very low risk for adverse events including hypoglycemia, and it prevents weight gain. The present review summarizes the studies on the influence of DPP-4 inhibition on islet function. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00184.x, 2012) (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Dipeptidyl peptidase-4 inhibition, Glucagon secretion, Insulin secretion
in
Journal of Diabetes Investigation
volume
3
issue
1
pages
3 - 10
publisher
Wiley-Blackwell
external identifiers
  • wos:000300678900002
  • scopus:84857226676
ISSN
2040-1116
DOI
10.1111/j.2040-1124.2011.00184.x
language
English
LU publication?
yes
id
2a2910d5-19d6-4bd4-a427-d88f7a1c053e (old id 2403206)
date added to LUP
2012-04-02 09:27:29
date last changed
2017-01-01 03:51:33
@article{2a2910d5-19d6-4bd4-a427-d88f7a1c053e,
  abstract     = {During recent years, dipeptidyl peptidase-4 (DPP-4) inhibition has been included in the clinical management of type 2 diabetes, both as monotherapy and as add-on to several other therapies. DPP-4 inhibition prevents the inactivation of the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). This results in stimulation of insulin secretion and inhibition of glucagon secretion, and there is also a potential beta-cell preservation effect, as judged from rodent studies; that is, it might target the key islet dysfunction in the disease. In type 2 diabetes. This reduces 24-h glucose levels and reduces HbA1c by approximate to 0.81.1% from baseline levels of 7.78.5%. DPP-4 inhibition is safe, with a very low risk for adverse events including hypoglycemia, and it prevents weight gain. The present review summarizes the studies on the influence of DPP-4 inhibition on islet function. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00184.x, 2012)},
  author       = {Ahrén, Bo},
  issn         = {2040-1116},
  keyword      = {Dipeptidyl peptidase-4 inhibition,Glucagon secretion,Insulin secretion},
  language     = {eng},
  number       = {1},
  pages        = {3--10},
  publisher    = {Wiley-Blackwell},
  series       = {Journal of Diabetes Investigation},
  title        = {DPP-4 inhibition and islet function},
  url          = {http://dx.doi.org/10.1111/j.2040-1124.2011.00184.x},
  volume       = {3},
  year         = {2012},
}