Pathophysiology of SPINK mutations in pancreatic development and disease.

Journal Article (Review)

The endogenous pancreatic trypsin inhibitor, SPINK, is believed to limit enzyme activity in the pancreas and reduce the risk of pancreatitis. Recently, mutations in the SPINK1 gene have been associated with development of both acute and chronic pancreatitis. In most patients with SPINK1 mutations, the genetic variants do not cause the disease independently, but may act in concert with other genetic or environmental factors. Recent studies, using mice in which the trypsin inhibitor gene has been deleted or overexpressed, provide novel insights into the role of SPINK in pancreatic development and pancreatitis.

Full Text

Duke Authors

Cited Authors

  • Liddle, RA

Published Date

  • June 2006

Published In

Volume / Issue

  • 35 / 2

Start / End Page

  • 345 - x

PubMed ID

  • 16632097

International Standard Serial Number (ISSN)

  • 0889-8529

Digital Object Identifier (DOI)

  • 10.1016/j.ecl.2006.02.012

Language

  • eng

Conference Location

  • United States