BACKGROUND: Studies in patients with acute pancreatitis have shown a correlation between obesity and serious complications or a fatal outcome. However, the mechanisms by which obesity aggravates acute pancreatitis are not known. In the present study we used the sodium taurocholate model of pancreatitis to examine the effect of obesity on severity and outcome in acute experimental pancreatitis (AEP). METHODS: AEP was induced at two degrees of severity 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 diet, genetically obese (GO) rats or lean control rats. Surviving animals were 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 rats had a significantly lower 72-h survival rate than the high-fat obese (HFO) or lean control (LC) groups (GO 25% versus HFO 73%, P < 0.05; GO 25% versus LC 100%, P < 0.001). Survival rates in the high-dose experiment correlated strongly with basal liver fat content (R2 = 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 pancreatitis that was related to the magnitude of the pancreatic insult. The sodium taurocholate model in obese rats would be useful for future mechanistic studies of the effect of obesity on pancreatitis.
BACKGROUND: Studies in patients with acute pancreatitis have shown a correlation between obesity and serious complications or a fatal outcome. However, the mechanisms by which obesity aggravates acute pancreatitis are not known. In the present study we used the sodium taurocholate model of pancreatitis to examine the effect of obesity on severity and outcome in acute experimental pancreatitis (AEP). METHODS: AEP was induced at two degrees of severity 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 diet, genetically obese (GO) rats or lean control rats. Surviving animals were 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 rats had a significantly lower 72-h survival rate than the high-fat obese (HFO) or lean control (LC) groups (GO 25% versus HFO 73%, P < 0.05; GO 25% versus LC 100%, P < 0.001). Survival rates in the high-dose experiment correlated strongly with basal liver fat content (R2 = 0.86). Pancreatic histology showed significantly more fat necrosis and a higher total pathological mean score in the HFOrats than in the LC animals (both P < 0.05). CONCLUSIONS:Obesity had a negative influence on the outcome of necrotizing pancreatitis that was related to the magnitude of the pancreatic insult. The sodium taurocholate model in obeserats would be useful for future mechanistic studies of the effect of obesity on pancreatitis.
Authors: Maria Pini; Davina H Rhodes; Karla J Castellanos; Andrew R Hall; Robert J Cabay; Rohini Chennuri; Eileen F Grady; Giamila Fantuzzi Journal: J Leukoc Biol Date: 2012-03-16 Impact factor: 4.962
Authors: Hayder H Al-Azzawi; Terence E Wade; Deborah A Swartz-Basile; Sue Wang; Henry A Pitt; Nicholas J Zyromski Journal: Dig Dis Sci Date: 2011-02-24 Impact factor: 3.199
Authors: Hayder H Al-Azzawi; Kathryn M Ziegler; Deborah A Swartz-Basile; Sue Wang; Henry A Pitt; Nicholas J Zyromski Journal: J Gastrointest Surg Date: 2011-06-10 Impact factor: 3.452
Authors: Nicholas J Zyromski; Abhishek Mathur; Henry A Pitt; Terence E Wade; Sue Wang; Deborah A Swartz-Basile; Andrew D Prather; Keith D Lillemoe Journal: J Gastrointest Surg Date: 2009-02-19 Impact factor: 3.452