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Connexin implication in the control of the murine beta-cell mass |
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Published in | Pediatric Research. 2011, vol. 70, no. 2, p. 142-7 | |
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 | |
Identifiers | PMID: 21527868 | |
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Research group | Couplage cellulaire et connexines (136) | |
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. 142-7. doi: 10.1203/PDR.0b013e318220f106 https://archive-ouverte.unige.ch/unige:25463 |