Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase

Elke Oetjen

doi:10.1002/ardp.201600053

Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase

Standard

Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase. / Oetjen, Elke.

In: ARCH PHARM, Vol. 349, No. 6, 06.2016, p. 410-3.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Oetjen, E 2016, 'Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase', ARCH PHARM, vol. 349, no. 6, pp. 410-3. https://doi.org/10.1002/ardp.201600053

APA

Oetjen, E. (2016). Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase. ARCH PHARM, 349(6), 410-3. https://doi.org/10.1002/ardp.201600053

Vancouver

Oetjen E. Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase. ARCH PHARM. 2016 Jun;349(6):410-3. https://doi.org/10.1002/ardp.201600053

Bibtex

@article{5cc0ba878dab4efc8110fa26b94bc25a,

title = "Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase",

abstract = "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.",

keywords = "Journal Article, Review",

author = "Elke Oetjen",

note = "{\textcopyright} 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.",

year = "2016",

month = jun,

doi = "10.1002/ardp.201600053",

language = "English",

volume = "349",

pages = "410--3",

journal = "ARCH PHARM",

issn = "0365-6233",

publisher = "Wiley-VCH Verlag GmbH",

number = "6",

}

RIS

TY - JOUR

T1 - Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase

AU - Oetjen, Elke

PY - 2016/6

Y1 - 2016/6

N2 - 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.

AB - 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.

KW - Journal Article

KW - Review

U2 - 10.1002/ardp.201600053

DO - 10.1002/ardp.201600053

M3 - SCORING: Journal article

C2 - 27100796

VL - 349

SP - 410

EP - 413

JO - ARCH PHARM

JF - ARCH PHARM

SN - 0365-6233

IS - 6

ER -