KATP channel-deficient pancreatic {beta}-cells are streptozotocin resistant because of lower GLUT2 activity.

KATP channel-deficient pancreatic {beta}-cells are streptozotocin resistant because of lower GLUT2 activity. Research Abstract Details 

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KATP channel-deficient pancreatic {beta}-cells are streptozotocin resistant because of lower GLUT2 activity. Abstract Text:

Jin Xu,Li Zhang,Andrew Chou,Tim Allaby,Guy Bélanger,Jerry Radziuk,Bernard J Jasmin,Takashi Miki,Susumo Seino,Jean-Marc Renaud,

In wild-type mice, a single injection of streptozotocin (STZ, 200 mg/kg body wt) caused within 4 days severe hyperglycemia, hypoinsulinemia, significant glucose intolerance, loss of body weight, and the disappearance of pancreatic beta-cells. However, in ATP-sensitive K(+) channel (K(ATP) channel)-deficient mice (Kir6.2(-/-) mice), STZ had none of these effects. Exposing isolated pancreatic islets to STZ caused severe damage in wild-type but not in Kir6.2(-/-) islets. Following a single injection, plasma STZ levels were slightly less in Kir6.2(-/-) mice than in wild-type mice. Despite the difference in plasma STZ, wild-type and Kir6.2(-/-) liver accumulated the same amount of STZ, whereas Kir6.2(-/-) pancreas accumulated 4.1-fold less STZ than wild-type pancreas. Kir6.2(-/-) isolated pancreatic islets also transported less glucose than wild-type ones. Quantification of glucose transporter 2 (GLUT2) protein content by Western blot using an antibody with an epitope in the extracellular loop showed no significant difference in GLUT2 content between wild-type and Kir6.2(-/-) pancreatic islets. However, visualization by immunofluorescence with the same antibody gave rise to 32% less fluorescence in Kir6.2(-/-) pancreatic islets. The fluorescence intensity using another antibody, with an epitope in the COOH terminus, was 5.6 times less in Kir6.2(-/-) than in wild-type pancreatic islets. We conclude that 1) Kir6.2(-/-) mice are STZ resistant because of a decrease in STZ transport by GLUT2 in pancreatic beta-cells and 2) the decreased transport is due to a downregulation of GLUT2 activity involving an effect at the COOH terminus.

KATP channel-deficient pancreatic {beta}-cells are streptozotocin resistant because of lower GLUT2 activity. Publishing Authors By Initials

J Xu,L Zhang,A Chou,T Allaby,G Bélanger,J Radziuk,BJ Jasmin,T Miki,S Seino,JM Renaud,

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KATP channel-deficient pancreatic {beta}-cells are streptozotocin resistant because of lower GLUT2 activity. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: American journal of physiology. Endocrinology and

VOLUME: 294

Page Numbers: E326-35

Journal Abbreviation: Am. J. Physiol. Endocrinol. Me

ISSN: 0193-1849

DAY: 27

MONTH: 11

YEAR: 2007

KATP channel-deficient pancreatic {beta}-cells are streptozotocin resistant because of lower GLUT2 activity. Information

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LANGUAGE: eng

NlmUniqueID: 100901226

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AFFILIATION: Dept. of Cellular and Molecular Medicine, Univ. of Ottawa, 451 Smyth Rd., Ottawa, ON, Canada K1H 8M5. jmrenaud@uottawa.ca).

Country: United States

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MEDLINETA: Am J Physiol Endocrinol Metab

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