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

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.

DOI: 10.1016/j.febslet.2009.12.018
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@article{Mbikay2010PCSK9deficientME, title={PCSK9-deficient mice exhibit impaired glucose tolerance and pancreatic islet abnormalities.}, author={Majambu Mbikay and Francine Sirois and Janice Mayne and Gen-Sheng Wang and Andrew R. Chen and Thilina Dewpura and Annik Prat and Nabil G Seidah and Michel Chr{\'e}tien and Fraser W. Scott}, journal={FEBS letters}, year={2010}, volume={584 4}, pages={701-6} }