SLC2A2 mutations can cause neonatal diabetes, suggesting GLUT2 may have a role in human insulin secretion-Reference-Cited by-同舟云学术

SLC2A2 mutations can cause neonatal diabetes, suggesting GLUT2 may have a role in human insulin secretion

Published:2012-06-02 Issue:9 Volume:55 Page:2381-2385
ISSN:0012-186X
Container-title:Diabetologia
language:en
Short-container-title:Diabetologia

Author:

Sansbury F. H.,Flanagan S. E.,Houghton J. A. L.,Shuixian Shen F. L.,Al-Senani A. M. S.,Habeb A. M.,Abdullah M.,Kariminejad A.,Ellard S.,Hattersley A. T.

Publisher

Springer Science and Business Media LLC

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

Link

http://link.springer.com/content/pdf/10.1007/s00125-012-2595-0.pdf

Reference25 articles.

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2. Guillam M-T, Hümmler E, Schaerer E et al (1997) Early diabetes and abnormal postnatal pancreatic islet development in mice lacking Glut-2. Nat Genet 17:327–330

3. Guillam M-T, Dupraz P, Thorens B (2000) Glucose uptake, utilization, and signaling in GLUT2-null islets. Diabetes 49:1485–1491

4. De Vos A, Heimberg H, Quartier E et al (1995) Human and rat beta cells differ in glucose transporter but not in glucokinase gene expression. J Clin Invest 96:2489–2495

5. Richardson CC, Hussain K, Jones PM et al (2007) Low levels of glucose transporters and K+ ATP channels in human pancreatic beta cells early in development. Diabetologia 50:1000–1005

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