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Acta cir. bras ; 31(10): 655-660, Oct. 2016. tab, graf
Article in English | LILACS | ID: biblio-827647

ABSTRACT

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.


Subject(s)
Animals , Female , Pancreatitis/etiology , Hypertriglyceridemia/complications , Hyperlipoproteinemia Type I/complications , Pancreatitis/pathology , Time Factors , Triglycerides/blood , Severity of Illness Index , Acute Disease , Disease Models, Animal , Heterozygote , Amylases/blood , Hyperlipoproteinemia Type I/genetics , Mice, Inbred C57BL
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