Secreted frizzled-related protein 4 reduces insulin secretion and is overexpressed in type 2 diabetes.

نویسندگان

  • Taman Mahdi
  • Sonja Hänzelmann
  • Albert Salehi
  • Sarheed J Muhammed
  • Thomas M Reinbothe
  • Yunzhao Tang
  • Annika S Axelsson
  • Yuedan Zhou
  • Xingjun Jing
  • Peter Almgren
  • Ulrika Krus
  • Jalal Taneera
  • Anna M Blom
  • Valeriya Lyssenko
  • Jonathan Lou S Esguerra
  • Ola Hansson
  • Lena Eliasson
  • Jonathan Derry
  • Enming Zhang
  • Claes B Wollheim
  • Leif Groop
  • Erik Renström
  • Anders H Rosengren
چکیده

A plethora of candidate genes have been identified for complex polygenic disorders, but the underlying disease mechanisms remain largely unknown. We explored the pathophysiology of type 2 diabetes (T2D) by analyzing global gene expression in human pancreatic islets. A group of coexpressed genes (module), enriched for interleukin-1-related genes, was associated with T2D and reduced insulin secretion. One of the module genes that was highly overexpressed in islets from T2D patients is SFRP4, which encodes secreted frizzled-related protein 4. SFRP4 expression correlated with inflammatory markers, and its release from islets was stimulated by interleukin-1β. Elevated systemic SFRP4 caused reduced glucose tolerance through decreased islet expression of Ca(2+) channels and suppressed insulin exocytosis. SFRP4 thus provides a link between islet inflammation and impaired insulin secretion. Moreover, the protein was increased in serum from T2D patients several years before the diagnosis, suggesting that SFRP4 could be a potential biomarker for islet dysfunction in T2D.

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عنوان ژورنال:
  • Cell metabolism

دوره 16 5  شماره 

صفحات  -

تاریخ انتشار 2012