beta-cell function and viability in the spontaneously diabetic GK rat: information from the GK/Par colony.

• B Portha

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

• M H Giroix

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

• P Serradas

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

• M N Gangnerau

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

• J Movassat

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

• F Rajas

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

• D Bailbe

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

• C Plachot

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

• G Mithieux

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

• J C Marie

  Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université D. Diderot, Paris, France. [e-mail]

Abstract

The GK rat model of type 2 diabetes is especially convenient to dissect the pathogenic mechanism necessary for the emergence of overt diabetes because all adult rats obtained in our department (GK/Par colony) to date have stable basal mild hyperglycemia and because overt diabetes is preceded by a period of normoglycemia, ranging from birth to weaning. The purpose of this article is to sum up the information so far available related to the biology of the beta-cell in the GK/Par rat. In terms of beta-cell function, there is no major intrinsic secretory defect in the prediabetic GK/Par beta-cell, and the lack of beta-cell reactivity to glucose (which reflects multiple intracellular abnormalities), as seen during the adult period when the GK/Par rats are overtly diabetic, represents an acquired defect (perhaps glucotoxicity). In terms of beta-cell population, the earliest alteration so far detected in the GK/Par rat targets the size of the beta-cell population. Several convergent data suggest that the permanently reduced beta-cell mass in the GK/Par rat reflects a limitation of beta-cell neogenesis during early fetal life, and it is conceivable that some genes among the set involved in GK diabetes belong to the subset of genes controlling early beta-cell development.

Journal

• Diabetes

  Diabetes 50 (suppl_1), S89-, 2001-02-01

  American Diabetes Association

Keywords

• Endocrinology, Diabetes and Metabolism
• Internal Medicine

Details

• CRID: 1360574094913612416
• NII Article ID: 30026264415
• DOI: 10.2337/diabetes.50.2007.s89
• ISSN: 1939327X
• ISSN: 00121797
• Web Site: https://journals.org/diabetes/diabetes/article-pdf/50/suppl_1/S89/533177/s89.pdf
• Web Site: https://diabetesjournals.org/diabetes/article-pdf/50/suppl_1/S89/533177/s89.pdf
• Data Source:
  • Crossref
  • CiNii Articles