Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase.
Arch Pharm (Weinheim)
; 349(6): 410-3, 2016 Jun.
Article
en En
| MEDLINE
| ID: mdl-27100796
Diabetes mellitus is one of the most rapidly increasing diseases worldwide, whereby approximately 90-95% of patients suffer from type 2 diabetes. Considering its micro- and macrovascular complications like blindness and myocardial infarction, a reliable anti-diabetic treatment is needed. Maintaining the function and the mass of the insulin producing beta-cells despite elevated levels of beta-cell-toxic prediabetic signals represents a desirable mechanism of action of anti-diabetic drugs. The dual leucine zipper kinase (DLK) inhibits the action of two transcription factors within the beta-cell, thereby interfering with insulin secretion and production and the conservation of beta-cell mass. Furthermore, DLK action is regulated by prediabetic signals. Hence, the inhibition of this kinase might protect beta-cells against beta-cell-toxic prediabetic signals and prevent the development of diabetes. DLK might thus present a novel drug target for the treatment of diabetes mellitus type 2.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Quinasas Quinasa Quinasa PAM
/
Células Secretoras de Insulina
Límite:
Humans
Idioma:
En
Revista:
Arch Pharm (Weinheim)
Año:
2016
Tipo del documento:
Article
País de afiliación:
Alemania
Pais de publicación:
Alemania