Scientific article
Meta-analysis
OA Policy
English

Connexin implication in the control of the murine beta-cell mass

Published in

Pediatric research, vol. 70, no. 2, p. 142-147

Publication date

2011

Abstract

Diabetes develops when the insulin needs of peripheral cells exceed the availability or action of the hormone. This situation results from the death of most beta-cells in type 1 diabetes, and from an inability of the beta-cell mass to adapt to increasing insulin needs in type 2 and gestational diabetes. We analyzed several lines of transgenic mice and showed that connexins (Cxs), the transmembrane proteins that form gap junctions, are implicated in the modulation of the beta-cell mass. Specifically, we found that the native Cx36 does not alter islet size or insulin content, whereas the Cx43 isoform increases both parameters, and Cx32 has a similar effect only when combined with GH. These findings open interesting perspectives for the in vitro and in vivo regulation of the beta-cell mass.

Keywords

  • Animals
  • Cell Size
  • Connexin 43/genetics/metabolism
  • Connexins/genetics/metabolism
  • Crosses, Genetic
  • Diabetes Mellitus/metabolism
  • Fluorescent Antibody Technique
  • Growth Hormone/metabolism
  • Insulin/metabolism
  • Insulin-Secreting Cells/cytology/metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Radioimmunoassay
  • Statistics, Nonparametric

Citation (ISO format)

KLEE, Philippe et al. Connexin implication in the control of the murine beta-cell mass. In: Pediatric research, 2011, vol. 70, n° 2, p. 142–147. doi: 10.1203/PDR.0b013e318220f106

Main files (1)

Article (Published version)

Identifiers

Journal ISSN

0031-3998
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Technical informations

Creation

24/10/2012 18:31:00

First validation

24/10/2012 18:31:00

Update

14/03/2023 19:56:42

Status update

14/03/2023 19:56:41

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