Underexpression of β Cell High K m Glucose Transporters in Noninsulin-Dependent Diabetes

• DOI: 10.1126/science.2237405
• Publication Date: 2006-10-05T22:10:14Z
• Authors: John H. Johnson; Atsushi Ogawa; Ling Chen; Lelio Orci; Christopher B. Ne...; Tausif Alam; Roger H. Unger
• Keywords: BETA (programming language); Carbohydrate Metabolism; Pathogenesis

The role of defective glucose transport in the pathogenesis noninsulin-dependent diabetes (NIDDM) was examined Zucker diabetic fatty rats, a model NIDDM. As human NIDDM, insulin secretion unresponsive to 20 mM glucose. Uptake 3- O -methylglucose by islet cells less than 19% controls. β cell transporter (GLUT-2) immunoreactivity and amount GLUT-2 messenger RNA were profoundly reduced. Whenever fewer 60% GLUT-2-positive, response absent hyperglycemia exceeded 11 plasma We conclude that NIDDM underexpression lowers high K m cells, thereby impairs glucose-stimulated prevents correction hyperglycemia.