Extrapancreatic contribution to glucose regulation by dipeptidyl peptidase 4 inhibition
(2016) In Cardiovascular Endocrinology 5(3). p.82-85- Abstract
Dipeptidyl peptidase 4 (DPP-4) inhibitors are now being clinically utilized as glucose-lowering medications for the treatment of type 2 diabetes. Their widespread use and effective glucose-lowering properties have led to great interest in the mechanism of action of this class of drug. Although it has been well accepted that DPP-4 inhibitors lower glucose in part by increasing postprandial insulin secretion and suppressing fasting and postprandial hyperglucagonemia, recent studies have suggested that DPP-4 inhibition has other metabolically beneficial properties that are extrapancreatic in nature. This review explores the changes in DPP-4 expression and activity in metabolic disease states and discusses the metabolic consequences of... (More)
Dipeptidyl peptidase 4 (DPP-4) inhibitors are now being clinically utilized as glucose-lowering medications for the treatment of type 2 diabetes. Their widespread use and effective glucose-lowering properties have led to great interest in the mechanism of action of this class of drug. Although it has been well accepted that DPP-4 inhibitors lower glucose in part by increasing postprandial insulin secretion and suppressing fasting and postprandial hyperglucagonemia, recent studies have suggested that DPP-4 inhibition has other metabolically beneficial properties that are extrapancreatic in nature. This review explores the changes in DPP-4 expression and activity in metabolic disease states and discusses the metabolic consequences of DPP-4 inhibition on a systemic and tissue-specific basis. It concludes that there is considerable scientific evidence and a growing body of clinical evidence to suggest that DPP-4 inhibition would be beneficial in a number of metabolic disorders in addition to type 2 diabetes.
(Less)
- author
- Omar, Bilal A. LU and Ahrén, Bo LU
- organization
- publishing date
- 2016
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- dipeptidyl peptidase-4, glucose, insulin, insulin sensitivity, liver
- in
- Cardiovascular Endocrinology
- volume
- 5
- issue
- 3
- pages
- 4 pages
- publisher
- Lippincott Williams & Wilkins
- external identifiers
-
- wos:000389477700005
- scopus:85000502014
- ISSN
- 2162-688X
- DOI
- 10.1097/XCE.0000000000000088
- language
- English
- LU publication?
- yes
- id
- 23ca0134-39dc-401d-b41b-aa7cf134c25f
- date added to LUP
- 2016-12-30 13:43:01
- date last changed
- 2024-01-04 20:08:51
@article{23ca0134-39dc-401d-b41b-aa7cf134c25f,
abstract = {{<p>Dipeptidyl peptidase 4 (DPP-4) inhibitors are now being clinically utilized as glucose-lowering medications for the treatment of type 2 diabetes. Their widespread use and effective glucose-lowering properties have led to great interest in the mechanism of action of this class of drug. Although it has been well accepted that DPP-4 inhibitors lower glucose in part by increasing postprandial insulin secretion and suppressing fasting and postprandial hyperglucagonemia, recent studies have suggested that DPP-4 inhibition has other metabolically beneficial properties that are extrapancreatic in nature. This review explores the changes in DPP-4 expression and activity in metabolic disease states and discusses the metabolic consequences of DPP-4 inhibition on a systemic and tissue-specific basis. It concludes that there is considerable scientific evidence and a growing body of clinical evidence to suggest that DPP-4 inhibition would be beneficial in a number of metabolic disorders in addition to type 2 diabetes.</p>}},
author = {{Omar, Bilal A. and Ahrén, Bo}},
issn = {{2162-688X}},
keywords = {{dipeptidyl peptidase-4; glucose; insulin; insulin sensitivity; liver}},
language = {{eng}},
number = {{3}},
pages = {{82--85}},
publisher = {{Lippincott Williams & Wilkins}},
series = {{Cardiovascular Endocrinology}},
title = {{Extrapancreatic contribution to glucose regulation by dipeptidyl peptidase 4 inhibition}},
url = {{http://dx.doi.org/10.1097/XCE.0000000000000088}},
doi = {{10.1097/XCE.0000000000000088}},
volume = {{5}},
year = {{2016}},
}