Lipoprotein lipase gene-deficient mice with hypertriglyceridaemia associated with acute pancreatitis

• Autor(a) principal: Tang,Maochun
• Data de Publicação: 2016
• Outros Autores: Zong,Pengfei, Zhang,Ting, Wang,Dongyan, Wang,Yuhui, Zhao,Yan
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Acta Cirúrgica Brasileira (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502016001000655
• topic: Hypertriglyceridemia; Pancreatitis; Lipoprotein Lipase; Mice

ABSTRACT PURPOSE: To investigate the severity of pancreatitis in lipoprotein lipase (LPL)-deficient hypertriglyceridaemic (HTG) heterozygous mice and to establish an experimental animal model for HTG pancreatitis study. METHODS: LPL-deficient HTG heterozygous mice were rescued by somatic gene transfer and mated with wild-type mice. The plasma amylase, triglyceride, and pathologic changes in the pancreas of the LPL-deficient HTG heterozygous mice were compared with those of wild-type mice to assess the severity of pancreatitis. In addition, acute pancreatitis (AP) was induced by caerulein (50 µg/kg) for further assessment. RESULTS: The levels of plasma amylase and triglyceride were significantly higher in the LPL-deficient HTG heterozygous mice. According to the pancreatic histopathologic scores, the LPL-deficient HTG heterozygous mice showed more severe pathologic damage than the wild-type mice. CONCLUSIONS: Lipoprotein lipase deficient heterozygous mice developed severe caerulein-induced pancreatitis. In addition, their high triglyceride levels were stable. Therefore, LPL-deficient HTG heterozygous mice are a useful experimental model for studying HTG pancreatitis.