Background: Studies in patients with acute pancreatitis have shown a correl
ation between obesity and serious complications or a fatal outcome. However
, the mechanisms by which obesity aggravates acute pancreatitis are not kno
wn. In the present study we used the sodium taurocholate model of pancreati
tis to examine the effect of obesity on severity and outcome in acute exper
imental pancreatitis (AEP). Methods: AEP was induced at two degrees of seve
rity by retrograde infusion of sodium taurocholate (0.2 ml x 3% or 0.4 ml x
3.5%) into the pancreatic duct of rats with obesity induced by high-fat di
et, genetically obese (GO) rats or lean control rats. Surviving animals wer
e sacrificed 72 h after induction of pancreatitis. Results: In the low-dose
experiment, there were no significant differences in pancreatic histology
or survival rate between the groups. In the high-dose experiment, the GO ra
ts had a significantly lower 72-h survival rate than the high-fat obese (HF
O) or lean control (LC) groups (GO 25% versus HFO 73%. P < 0.05: GO 25% ver
sus LC 100%, P < 0.001). Survival rates in the high-dose experiment correla
ted strongly with basal liver fat content (R-2=0.86). Pancreatic histology
showed significantly more fat necrosis and a higher total pathological mean
score in the HFO rats than in the LC animals (both P < 0.05). Conclusions:
Obesity had a negative influence on the outcome of necrotizing pancreatiti
s that was related to the magnitude of the pancreatic insult. The sodium ta
urocholate model in obese rats would be useful for future mechanistic studi
es of the effect of obesity on pancreatitis.