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Horm Metab Res 2000; 32(2): 53-56
DOI: 10.1055/s-2007-978588
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© Georg Thieme Verlag Stuttgart · New York

Glucose-Induced Insulin mRNA Accumulation is Impaired in Islets from Neonatal Streptozotocin-Treated Rats

I. Briaud1 , 2 , C. Rouault2 , D. Bailbé3 , B. Portha3 , G. Reach2 , V. Poitout1 , 2
  • 1Pacific Northwest Research Institute, Seattle WA, USA
  • 2INSERM U341, Hôtel-Dieu, Paris, France
  • 3CNRS ESA 7059, Université Paris 7 D. Diderot, Paris, France
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1999

1999

Publication Date:
19 April 2007 (online)

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According to the “glucose toxicity” hypothesis, hyperglycemia contributes to defective β-cell function in type 2, non-insulin-dependent diabetes mellitus. This concept is supported by substantial data in rodent models of diabetes. However, the ability of glucose to stimulate the accumulation of insulin mRNA, a critical feature of normal β-cell physiology, has not been investigated in in vivo models with chronic hyperglycemia. The aim of this study was to determine whether glucose-induced insulin mRNA accumulation is impaired in the neonatal streptozotocin-treated rat (n0-STZ rat), a model of non-obese, non-insulin-dependent diabetes mellitus. Islets of Langerhans isolated from n0-STZ and control rats were cultured for 24 h in the presence of 2.8 or 16.7 mmol/l glucose, and insulin mRNA levels were measured by Northern analysis. Insulin mRNA levels were increased more than twofold by glucose in control islets. In contrast, no significant effect of glucose was found on insulin mRNA levels in n0-STZ islets. We conclude that insulin gene regulation by glucose is impaired in n0-STZ rat islets.

Key words

NIDDM - Insulin Gene - Glucose Toxicity - Islets of Langerhans

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