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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Female, albino mice were fed a choline-deficient diet containing 0.5% DL-ethionine. All animals died within 5 days due to the development of an acute hemorrhagic pancreatis with fat necrosis throughout the peritoneal cavity. The apancreatitis was characterized by a massive necrosis of the exocrine parenchyma with intense hemorrhage and inflammatory reaction of the stroma. The sequence of histologic and ultrastructural alterations occurring in the acinar cells of the pancreas were studied in mice fed the diet for 1, 2, and 3 days. Major findings consited of accumulation of zymogen granules, vacuolation due to foci of cytoplasmic degradation, and alterations in the morphology of the zymogen granules. The pancreatitis appears to be due to intraparenchymal activation of zymogens, resulting from a synergistic action of choline deficiency with the basic toxicity of ethionine toward the acinar cells of the pancreas. The experimental model simulates closely the acute hemorrhagic pancreatitis with fat necrosis occurring in humans and may prove useful for exploring the pathogenesis of this condition.
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PMID:Acute hemorrhagic pancreatitis (massive necrosis) with fat necrosis induced in mice by DL-ethionine fed with a choline-deficient diet. 109 37

The influence of several factors on the development of acute hemorrhagic pancreatitis (pancreatic necrosis) with fat necrosis in mice fed DL-ethionine with a choline-deficient diet has been investigated. The results showed that: a) the incidence of the induced disease is dependent upon the age and sex of the animals and the dietary level of ethionine; b) 100% of young female mice fed 0.5% ethionine develop acute hemorrhagic pancreatitis and die within 5 days; c) the incidence is only 10 to 20% when 0.5% ethionine is fed with either a choline-supplemented diet or with laboratory chow; and d) development of pancreatic pathology is completely prevented by the inclusion in the diet of 0.5% methionine but not by the inclusion of 0.5% adenine. Possible mechanisms whereby choline deficiency potentiates the pancreatotoxicity of ethionine in mice are discussed.
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PMID:Acute hemorrhagic pancreatic necrosis in mice. Influence of the age and sex of the animals and of dietary ethionine, choline, methionine, and adenine sulfate. 118 Mar 34

The earliest changes noted during the evolution of pancreatitis induced by feeding mice a choline-deficient ethionine-supplemented (CDE) diet are an increase in the number of zymogen granules in pancreatic acinar cells and an increase in digestive enzyme content of the pancreas. We have studied the processes of protein and digestive enzyme synthesis and discharge at varying times after institution of the CDE diet, a choline-deficient diet (CD), and a diet containing ethionine but not choline-deficient (E). Both the CDE and E diets increased digestive enzyme content within 12 h of their institution. Both the CDE and E diets reduced the rate of protein and amylase synthesis and caused a marked reduction in the rate of protein and amylase discharge from the pancreas. These changes were greatest and were noted earliest in the CDE diet group. A marked reduction in secretagogue-induced in vivo and in vitro amylase discharge followed ingestion of either the CDE or E diet. These studies indicate that the increased pancreatic content of digestive enzymes noted after ingestion of the CDE and E diets results from an ethionine-induced decrease in the rat of digestive enzyme discharge. This phenomenon is enhanced by simultaneous choline deficiency. Subsequent intrapancreatic activation of zymogens may couple these changes in enzyme content to the development of hemorrhagic pancreatitis.
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PMID:Effects of ethionine on digestive enzyme synthesis and discharge by mouse pancreas. 615 94

Serum activities of amylase, lipase, phospholipase A2 and transaminases were measured in mice with diet-induced acute pancreatitis. To study the role of choline deficiency, one control group received only a choline-deficient diet (CD diet), another group received the choline-deficient diet with 0.5% DL-ethionine (CDE), and a third group received the choline-deficient diet and was given ethionine intraperitoneally. Serum amylase activities increased after 1 day of treatment in all experimental groups. In contrast, lipase activity rose later in the groups receiving ethionine either in the diet or intraperitoneally. In the CDE group there were significant changes in phospholipase A2 on the fourth day after test feeding was started, but no rise was seen in the other groups. Correspondingly, in the group receiving the CD diet alone and the group receiving intraperitoneal ethionine the mortality was significantly lower than in the group receiving ethionine in the diet. In all experimental groups there was a significant rise in serum transaminases (ASAT, ALAT). The rise in ALAT on day 4 was significantly higher in the CDE group than in the other two groups. The mortality rate in the CDE diet group on day 4 was 91%. In the animals to which ethionine was given intraperitoneally the corresponding mortality was 21%. In the CD diet group all animals survived for more than 4 days. The present results suggest that serum lipase and phospholipase A2 activities correlate better with the severity of diet-induced pancreatitis than do serum amylase levels. The most severe cases of the disease seemed to be associated with a rise in serum phospholipase A2 activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum phospholipase A2 in diet-induced pancreatitis. 620 20