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

Pediatr Res. 2011 Aug;70(2):142-7. doi: 10.1203/PDR.0b013e318220f106.

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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

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

Substances

  • Connexin 43
  • Connexins
  • Insulin
  • connexin 32
  • connexin 36
  • Growth Hormone