The relationship of diabetes, loss of glucose-induced insulin secretion, and GLUT2.
Diabetes in humans and experimental animals invariably is associated with a loss of glucose-induced insulin secretion. It has been hypothesized that this reversible defect is an adaptation of beta cells to chronic hyperglycemia, a hypothesis that has been strengthened by studies in experimental models of diabetes. Recently, a marked underexpression of the beta-cell glucose transporter GLUT2 has been found in diabetic rodents. Although this finding provides an attractive potential explanation for the abnormal insulin secretion of diabetes, some problems with the hypothesis have emerged. Additional studies must be carried out to define the potentially pathogenic role of GLUT2.
Research Division, Joslin Diabetes Center, Boston, Massachusetts 02215.
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D000818:Animals; D003920:Diabetes Mellitus / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D015870:Gene Expression; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D009004:Monosaccharide Transport Proteins / Q000096:biosynthesis / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism
D007328:Insulin; D009004:Monosaccharide Transport Proteins; D012333:RNA, Messenger