Reach further, in an Open Access Journal Endocrinology, Diabetes & Metabolism Case Reports

ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2010) 22 S15.2 

Wnt-signaling and the metabolic syndrome

Sven Schinner

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Wnt-signaling has been discovered as a regulator of adipocyte biology, pancreatic β-cell proliferation and insulin secretion. In addition, this pathway has been implicated in the regulation of aldosterone and cortisol secretion by the adrenal cortex. There is evidence that Wnt-signaling molecules can mediate a crosstalk between adipocytes and endocrine cells like pancreatic β-cells and adrenocortical cells.

In addition, the recent genome-wide association studies in humans affected by diabetes mellitus type 2 have pointed out that variations in the TCF7L2 gene have the strongest association with the diabetic phenotype. TCF7L2 is a transcription factor in the canonical Wnt-signaling pathway and can be coactivated by β-catenin. It is not yet completely understood how variants in the TCF7L2 gene can contribute to the diabetic phenotype but the available data suggest impaired insulin secretion as the underlying cause.

Finally, a link between the Wnt-signaling pathway and the incretin system has been found on the cellular level. Incretin-based therapies are novel therapeutic approaches to type 2 diabetes mellitus. Current data imply that GLP-1 agonists exert their effects on pancreatic β-cells in part through the canonical Wnt-signaling pathway. In summary, the recent data on Wnt-signaling as a novel regulator of metabolic control will be discussed in this talk.

*Correspondence to Dr Sven Schinner, Department of Endocrinology, Diabetes and Rheumatology, University Hospital Düsseldorf, Moorenstraße 5, 40225 Düsseldorf, Germany, Tel.: +49-211-8117810, Fax: +49-211-8117860, e-mail:

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