Pancreatic beta-cells express a low affinity glucose transporter: functional consequences in normal and diabetic states.

The application of molecular biology to the study of membrane transport proteins has led to a rapid advance in our understanding of the mechanisms behind the regulation of blood glucose levels. Moreover the demonstration of lesions in the expression of GLUT2 in the islets from diabetic models has provided a focus for research efforts aimed at addressing the defects responsible for the development and onset of both type I and perhaps type II diabetes. The recent demonstration that an 'artificial beta-cell' can be engineered from anterior pituitary-derived cell lines by transfection with both the insulin cDNA and the cDNA encoding GLUT2 represents a significant advance in the development of potential therapies for type I diabetes [24].