Conversely, genes normally suppressed in β-cells, such as lactate dehydrogenase-A, hexokinase I, glucose-6-phosphatase, stress genes (heme oxygenase-1, A20, and Fas), and the transcription factor c-Myc, were markedly increased. At the same time points, high hyperglycemia rats showed a global alteration in gene expression with decreased mRNA for insulin, IAPP, islet-associated transcription factors (pancreatic and duodenal homeobox-1, BETA2/NeuroD, Nk圆.1, and hepatocyte nuclear factor 1α), β-cell metabolic enzymes (glucose transporter 2, glucokinase, mitochondrial glycerol phosphate dehydrogenase, and pyruvate carboxylase), and ion channels/pumps (Kir6.2, VDCCβ, and sarcoplasmic reticulum Ca 2+-ATPase 3). β-Cell hypertrophy was present at both 4 and 14 weeks. Px rats developed different degrees of hyperglycemia low hyperglycemia was assigned to Px rats with fed blood glucose levels less than 150 mg/dl, and high hyperglycemia was assigned above 150 mg/dl. Islets were isolated, and mRNA was extracted from rats 4 and 14 weeks after Px or sham Px surgery. Here we examined the effects of the duration of hyperglycemia on gene expression in islets of partially pancreatectomized (Px) rats. ![]() ![]() We have proposed that hyperglycemia-induced dedifferentiation of β-cells is a critical factor for the loss of insulin secretory function in diabetes.
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