Key result
LPL deficiency worsens acute pancreatitis via chylomicron- and free fatty acid-mediated acinar injury.
Why the study?
The exact pathogenetic mechanism of recurrent pancreatitis in severe hypertriglyceridaemia due to lipoprotein lipase deficiency has not been defined.
Population
Lipoprotein lipase-deficient and wild-type mice and isolated pancreatic acinar cells
Comparison
LPL-deficient mice vs wild-type mice; addition of free fatty acids or chylomicrons vs control; orlistat treatment vs no treatment
Design
Preclinical experimental study
Authors
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LPL deficiency heightens caerulein-induced pancreatitis severity in mice; leaves open whether chylomicron lipase pathways translate to human recurrent pancreatitis risk.
LPL-deficient mice with severe hypertriglyceridaemia have enhanced susceptibility to acute pancreatitis, driven by chylomicrons and free fatty acids causing pancreatic cell injury.
Wang et al. (2008) studied Severe hypertriglyceridaemia and recurrent pancreatitis. Lipoprotein lipase (LPL) deficiency vs. Wild-type mice was evaluated on Susceptibility to pancreatitis (amylase release and pancreatic pathological scores). LPL-deficient mice with severe hypertriglyceridaemia display enhanced susceptibility to acute pancreatitis, with high levels of chylomicrons and free fatty acids resulting in pancreatic cell injury.
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