Related Experiment Videos
Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26
D Marguet1, L Baggio, T Kobayashi
1Centre d'Immunologie de Marseille Luminy, Institut National de la Santé et de la Recherche Médicale-Centre National de la Recherche Scientifique Case 906, Parc Scientifique de Luminy, 13288 Marseille Cedex 9, France.
Summary
Dipeptidyl-peptidase IV (DPP IV or CD26) regulates blood glucose by controlling hormones like GLP-1. Its inhibition improves glucose tolerance, highlighting its role in diabetes therapy.
Area of Science:
- Biochemistry
- Endocrinology
- Immunology
Background:
- Dipeptidyl-peptidase IV (DPP IV or CD26) cleaves N-terminal dipeptides from proline/alanine-containing substrates.
- This enzyme regulates hormones like glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP).
Purpose of the Study:
- To investigate the role of CD26 in glucose homeostasis.
- To determine if CD26 is a viable therapeutic target for type II diabetes.
Main Methods:
- Targeted inactivation of the CD26 gene in mice.
- Administration of a pharmacological DPP IV inhibitor to wild-type and CD26(-/-) mice.
- Assessment of glucose tolerance and hormone levels (insulin, GLP-1).
Main Results:
- CD26(-/-) mice exhibited normal fasting glucose but reduced glycemic excursion post-glucose challenge.
- Increased levels of glucose-stimulated insulin and intact GLP-1 were observed in CD26(-/-) mice.
- DPP IV inhibitor improved glucose tolerance in wild-type mice but not CD26(-/-) mice, and also in GLP-1 receptor(-/-) mice.
Conclusions:
- CD26 plays a critical role in physiological glucose homeostasis.
- CD26 regulates blood glucose by influencing GLP-1 activity and other substrates.
- CD26 is a potential therapeutic target for type II diabetes.