Abstract
Islet adaptations to pregnancy were explored in C57BL6/J mice lacking functional receptors for glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP). Pregnant wild type mice and GIPRKO mice exhibited marked increases in islet and beta cell area, numbers of medium/large sized islets, with positive effects on Ki67/Tunel ratio favouring beta cell growth and enhanced pancreatic insulin content. Alpha cell area and glucagon content were unchanged but prohormone convertases PC2 and PC1/3 together with significant amounts of GLP-1 and GIP were detected in alpha cells. Knockout of GLP-1R abolished these islet adaptations and paradoxically decreased pancreatic insulin, GLP-1 and GIP. This was associated with abolition of normal pregnancy-induced increases in plasma GIP, L-cell numbers, and intestinal GIP and GLP-1 stores. These data indicate that GLP-1 but not GIP is a key mediator of beta cell mass expansion and related adaptations in pregnancy, triggered in part by generation of intra-islet GLP-1.
Original language | English |
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Article number | e96863 |
Number of pages | 10 |
Journal | PLoS ONE |
Volume | 9 |
Issue number | 6 |
DOIs | |
Publication status | Published (in print/issue) - 13 Jun 2014 |
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Charlotte Moffett
- School of Biomedical Sciences - Lecturer in Pharmacology and Molecular Pathology
- Faculty Of Life & Health Sciences - Lecturer
Person: Academic