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Scientific article
English

Defective insulin secretion in pancreatic beta cells lacking type 1 IGF receptor

Published inThe Journal of clinical investigation, vol. 110, no. 7, p. 1011-1019
Publication date2002
Abstract

Defective insulin secretion is a feature of type 2 diabetes that results from inadequate compensatory increase of beta cell mass and impaired glucose-dependent insulin release. beta cell proliferation and secretion are thought to be regulated by signaling through receptor tyrosine kinases. In this regard, we sought to examine the potential proliferative and/or antiapoptotic role of IGFs in beta cells by tissue-specific conditional mutagenesis ablating type 1 IGF receptor (IGF1R) signaling. Unexpectedly, lack of functional IGF1R did not affect beta cell mass, but resulted in age-dependent impairment of glucose tolerance, associated with a decrease of glucose- and arginine-dependent insulin release. These observations reveal a requirement of IGF1R-mediated signaling for insulin secretion.

Keywords
  • Animals
  • Exocytosis
  • Glucose Transporter Type 2
  • Insulin/ secretion
  • Islets of Langerhans/ secretion
  • Mice
  • Monosaccharide Transport Proteins/analysis
  • Phenotype
  • RNA, Messenger/analysis
  • Receptor, IGF Type 1/deficiency/genetics/ physiology
Citation (ISO format)
XUAN, Shouhong et al. Defective insulin secretion in pancreatic beta cells lacking type 1 IGF receptor. In: The Journal of clinical investigation, 2002, vol. 110, n° 7, p. 1011–1019. doi: 10.1172/JCI15276
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ISSN of the journal0021-9738
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