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FEBS Lett. 2010 Feb 19;584(4):701-6. doi: 10.1016/j.febslet.2009.12.018. Epub 2009 Dec 16.

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

Author information

1
Ottawa Hospital Research Institute, Ottawa, Ontario, Canada. mmbikay@ohri.ca

Abstract

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.

PMID:
20026049
DOI:
10.1016/j.febslet.2009.12.018
[Indexed for MEDLINE]
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