Autor: |
Run Yu, Deepti Dhall, Nicholas N Nissen, Cuiqi Zhou, Song-Guang Ren |
Jazyk: |
angličtina |
Rok vydání: |
2011 |
Předmět: |
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Zdroj: |
PLoS ONE, Vol 6, Iss 8, p e23397 (2011) |
Druh dokumentu: |
article |
ISSN: |
1932-6203 |
DOI: |
10.1371/journal.pone.0023397 |
Popis: |
Inhibition of glucagon signaling causes hyperglucagonemia and pancreatic α cell hyperplasia in mice. We have recently demonstrated that a patient with an inactivating glucagon receptor mutation (P86S) also exhibits hyperglucagonemia and pancreatic α cell hyperplasia but further develops pancreatic neuroendocrine tumors (PNETs). To test the hypothesis that defective glucagon signaling causes PNETs, we studied the pancreata of mice deficient in glucagon receptor (Gcgr(-/-)) from 2 to 12 months, using WT and heterozygous mice as controls. At 2-3 months, Gcgr(-/-) mice exhibited normal islet morphology but the islets were mostly composed of α cells. At 5-7 months, dysplastic islets were evident in Gcgr(-/-) mice but absent in WT or heterozygous controls. At 10-12 months, gross PNETs (≥1 mm) were detected in most Gcgr(-/-) pancreata and micro-PNETs ( |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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