Ascorbic Acid Alleviates Pancreatic Damage Induced by Dibutyltin Dichloride (DBTC) in Rats

PURPOSE: Because previous studies have reported depleted antioxidant capacity in patients with chronic pancreatitis (CP), prevention of free radical production has gained importance in antifibrotic treatment strategies for CP. The aim of this study was to investigate the effects of ascorbic acid on oxidative capacity and pancreatic damage in experimental CP. MATERIALS AND METHODS: CP was induced in male Sprague-Dawley rats by infusion of dibutyltin dichloride (DBTC) into the tail vein. Ascorbic acid was given intraperitoneally at a daily dose of 10mg/kg body weight. The treatment groups were as follows: group 1, DBTC plus intraperitoneal physiologic saline; group 2, DBTC plus intraperitoneal ascorbic acid; group 3, solvent plus intraperitoneal physiologic saline; group 4, no operation plus intraperitoneal physiologic saline. Each group contained 15 animals. Treatment was started after CP was established. After 4 weeks of treatment, serum hyaluronic acid and laminin levels were determined by radioimmunoassay, pancreatic tissue oxidative stress was analyzed, and the degree of pancreatic damage was determined. RESULTS: Ascorbic acid treatment markedly increased superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) concentrations in pancreatic tissue (p < 0.01 for both). Significant serum hyaluronic acid and laminin reductions were observed in group 2 as compared with group 1 (p < 0.05). However, the serum hyaluronic acid and laminin levels remained elevated when compared with those of groups 3 and 4 (p < 0.05). Histopathologic scores were also lower in animals with CP that underwent ascorbic acid-treatment (p < 0.05). CONCLUSION: Ascorbic acid treatment alleviated the degree of oxidative stress and pancreatic damage in rat CP. Antioxidant treatment might be considered a potential option to improve the pathologic process in CP.

A pancreaticographic study of malnutrition-related diabetes mellitus.

Pancreatic involvement is considered to be the hallmark of malnutrition-related diabetes mellitus (MRDM). Of the 2 subgroups of the disease, fibrocalculous pancreatic diabetes (FCPD) is characterized by pancreatic calcification. The nature of pancreatic abnormalities in MRDM have not been studied extensively in Indian patients. The present study was designed to compare pancreatic abnormalities (exocrine and endocrine) including endoscopic retrograde pancreaticography in patients with FCPD and protein deficient pancreatic diabetes (PDPD), in relation to controls. Ten patients each of FCPD and PDPD were studied with regard to clinical features, biochemical exocrine and endocrine pancreatic responses, C-peptide response, islet cell antibody, and pancreatographic changes. Five normal pancreatograms were taken as control. Clinical and biochemical features in patient with FCPD and PDPD were as follows: pain in 8 and 2 patients, respectively; the mean duration of diabetes was similar in both groups (62.28 +/- 71.92 months V. 72 +/- 50.9 months); and faecal fat excretion and insulin requirements were comparable in both groups. The main pancreatic duct was dilated in 6 of 10 patient with FCPD and only 1 of 10 with PDPD on ultrasonography. On pancreatography the duct was dilated in 9 of 10 patients with FCPD and only 1 of 10 patients with PDPD. The number of side branches was reduced in all cases with MRDM; in those with FCPD, these were stunted and dilated while in PDPD side branches are thin and spastic. We conclude that pancreatic ductal changes involving the main duct and side branches are more frequent in patients with FCPD as compared to those with PDPD.