Ethanol feeding aggravates morphological and biochemical parameters in experimental chronic pancreatitis

Background and Aims: Instillation of trinitrobenzene sulfonic acid (TNBS) i nto the rat pancreatic ducts induces morphological changes resembling human chronic pancreatitis. In humans, alcoholism is commonly associated with ch ronic pancreatitis, but ethanol feeding fails to induce pancreatitis in exp erimental animals. We hypothesized that ethanol would manifest its pathogen etic effects on a duct-injured pancreas. Methods: Chronic pancreatitis was induced in rats by instillation of TNBS into pancreatic ducts. Thereafter, rats were fed a normal chow diet with or without ethanol supplementation. C ontrol rats received vehicle and a normal diet. A separate group of vehicle -treated rats were also fed with ethanol. At 2 and 4 weeks pancreata were e xcised and processed for morphological examination or for biochemical assay s. From crude homogenates, protein and hydroxyproline were quantified. Afte r sonication, homogenates were also assayed for amylase and DNA. An oral gl ucose tolerance test was performed on the fourth week. Results: TNBS induce d chronic fibrogenic pancreatitis that was associated with a reduction in p ancreatic weight, DNA, protein and amylase as compared to control rats. Eth anol feeding to TNBS-treated animals slowed weight gain, increased fasting glucose and impaired glucose tolerance test. Larger areas of gland atrophy were observed with a striking disruption of the normal architecture of the islets. Ethanol accelerated pancreatic involution and collagen deposition a s measured by total amylase, protein, DNA and hydroxyproline content. Concl usions: In TNBS chronic pancreatitis, active fibrogenesis is associated wit h progressive atrophy of glandular elements. Morphological and biochemical parameters are aggravated by sustained ethanol intake.