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Publication : PCSK9-deficient mice exhibit impaired glucose tolerance and pancreatic islet abnormalities.

First Author  Mbikay M Year  2010
Journal  FEBS Lett Volume  584
Issue  4 Pages  701-6
PubMed ID  20026049 Mgi Jnum  J:157666
Mgi Id  MGI:4431328 Doi  10.1016/j.febslet.2009.12.018
Citation  Mbikay M, et al. (2010) PCSK9-deficient mice exhibit impaired glucose tolerance and pancreatic islet abnormalities. FEBS Lett 584(4):701-6
abstractText  Proprotein convertase subtilisin/kexin type 9 (PCSK9), a liver-secreted plasma enzyme, restricts hepatic uptake of low-density lipoprotein (LDL) cholesterol by promoting the degradation of LDL receptors (LDLR). PCSK9 and LDLR are also expressed in insulin-producing pancreatic islet beta cells, possibly affecting the function of these cells. Here we show that, compared to control mice, PCSK9-null male mice over 4 months of age carried more LDLR and less insulin in their pancreas; they were hypoinsulinemic, hyperglycemic and glucose-intolerant; their islets exhibited signs of malformation, apoptosis and inflammation. Collectively, these observations suggest that PCSK9 may be necessary for the normal function of pancreatic islets.
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