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

Acta Cir Bras. 2016 Oct;31(10):655-660. doi: 10.1590/S0102-865020160100000003.

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.

MeSH terms

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

Substances

  • Triglycerides
  • Amylases