PCSK9‐deficient mice exhibit impaired glucose tolerance and pancreatic islet abnormalities
2009; Wiley; Volume: 584; Issue: 4 Linguagem: Inglês
10.1016/j.febslet.2009.12.018
ISSN1873-3468
AutoresMajambu Mbikay, Francine Sirois, Janice Mayne, Gen‐Sheng Wang, Andrew Chen, Thilina Dewpura, Annik Prat, Nabil G. Seidah, Michel Chrètien, Fraser W. Scott,
Tópico(s)Lipoproteins and Cardiovascular Health
ResumoProprotein 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 β 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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