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

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_name

Diabetes

journal_title

Diabetes

authors

Portha B,Giroix MH,Serradas P,Gangnerau MN,Movassat J,Rajas F,Bailbe D,Plachot C,Mithieux G,Marie JC

doi

10.2337/diabetes.50.2007.s89

subject

Has Abstract

pub_date

2001-02-01 00:00:00

pages

S89-93

eissn

0012-1797

issn

1939-327X

journal_volume

50 Suppl 1

pub_type

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