Key result
LPL deficiency increases caerulein-induced serum amylase ~47%, worsening pancreatic inflammation.
Why the study?
The relationship between hypertriglyceridemia and acute pancreatitis pathogenesis remains to be elucidated.
Does LPL deficiency increase susceptibility to caerulein-induced acute pancreatitis and alter the serum metabolome in mice?
Population
Lipoprotein lipase-deficient heterozygous mice and wild-type mice
Comparison
LPL-deficient mice injected with caerulein vs wild-type mice injected with caerulein and healthy controls
Design
Preclinical animal model study using GC/MS metabolomic analysis
Authors
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Novel LPL-deficient mouse model shows increased pancreatitis susceptibility; leaves open human relevance.
Does LPL deficiency increase susceptibility to caerulein-induced acute pancreatitis and alter the serum metabolome in mice?
Absolute Event Rate: 3685.06% vs 2500.89%
p-value: p=<0.05
LPL-deficient heterozygous mice exhibit enhanced susceptibility to caerulein-induced acute pancreatitis, with distinct serum metabolomic changes reflecting altered energy, fat, and amino acid metabolism.
Tang et al. (2013) studied Hyperlipidemic acute pancreatitis (n=28). Caerulein injection in LPL-deficient mice vs. Caerulein injection in wild-type mice was evaluated on Plasma amylase levels (µ/l) 12 hours after injection (p=<0.05). Caerulein induced significantly higher levels of serum amylase (3685.06 vs 2500.89 µ/l, P<0.05) and more severe pancreatic inflammation in LPL-deficient mice compared to wild-type mice.
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