Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of a short-term ischemia of the pancreas for the pathogenesis of a hemorrhagic necrotising pancreatitis was investigated in 28 mongrel dogs. Ischemia of the pancreas in 20 minute intervals repeated three times did not leave any macroscopic, histologic or electron microscopic changes and no alterations of the level of the alpha-amylase, the lipase, and the glucose in the serum. An ischemia of 20 minutes' duration by starvation of the celiac artery and the superior mesenteric artery produces a hemorrhagic necrotising pancreatitis under the precondition of a following pancreatic edema by ligature of the pancreatic duct and secretomotoring with secretin and pancreozymin. The necrosis starts histologically in the perilobular adipose and affects the parenchyma later. Whether the lipase is the starting enzyme for the acute pancreatitis or only conditions the early adipose necrosis should be discussed after these findings. Already a fugitive pancreatic edema produces a hemorrhagic necrotising pancreatitis after previous ischemic damage.
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PMID:[Animal experiment studies on the role of ischemia in the pathogenesis of acute pancreatitis]. 633 88

The occurrence of a postoperative complication represents an additional stress factor for patients and leads in many cases rapidly to a malnutrition status. Thus a nutritional support is required as soon as the foreseeable duration of starvation has a longer duration than one week. Considering its lower risk of septic complications and lower cost, enteral feeding should be initiated as soon as possible. Appraisal of caloric needs with standard formulas often leads to inappropriate nutritional management. Therefore the requirements should be assessed by indirect calorimetry if available. Nutritional support is a part of the management of a postoperative septic patient. It must be initiated when initial phase of haemodynamic instability is amended. Branched chain amino acids, medium chain triglycerides and other specific nutrients have failed to demonstrate a real clinical beneficial effect. In case of acute respiratory failure, nutritional support must be cautious with regard to caloric load, as carbohydrates may increase CO2 production and lipids may worsen hypoxaemia. In case of postoperative acute renal failure, nutritional management is facilitated by continuous haemofiltration techniques allowing an unlimited nutrient intake. Solutions containing only essential amino acids are not recommended. During severe acute pancreatitis, enteral feeding is indicated when ileus does not permit the use of the intestinal tract. Jejunal access must be preferred to stomach or duodenum. Lipid emulsions can be used safely if serum triglyceride concentrations remain below 4 g.L-1 during infusion and below 2 g.L-1 between infusions.
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PMID:[Effect of postoperative complications on nutritional status: therapeutic consequences]. 748 37

Ketonaemia is well documented as a consequence of prolonged starvation, acute alcoholism, and uncontrolled diabetes mellitus. However, its occurrence in acute pancreatitis has not been described. In this report, three patients who manifested ketoacidosis at the time of presentation of acute pancreatitis are described. In none of these patients could ketoacidosis be attributed to any of the well known pathogenetic factors such as ethanol, diabetes mellitus or prolonged starvation. In one patient, both the serum ketone titres and increased anion gap persisted for several days during the recovery period, despite appropriate therapy (including restriction of oral intake or nasogastric suction, intravenous fluids, and analgesic administration), before declining in parallel with a decrease in serum lipase levels, and became undetectable following near normalisation of serum lipase. Therefore, we believe that pancreatic ketosis or ketoacidosis may be a distinct syndrome with ketogenesis being promoted and maintained by extremely high circulating pancreatic lipase concentrations.
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PMID:Pancreatic ketoacidosis: ketonemia associated with acute pancreatitis. 770 90

In experiment on 43 dogs while the loading with polysubstrate food mixtures it was established, that the food passage shunting and starvation enhances the incretory answer value, but cholestasis and starvation lowers the pancreatic secretory potency. The restorational operation conduction promotes elimination of the cholestasis influence, but aggravates the action of starvation. An acute pancreatitis was not noted.
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PMID:[Functional state of the pancreas and risks of occurrence of acute pancreatitis in early use of enteral tube feeding in surgery of bile ducts]. 1007 50

We have previously identified a new rat mRNA, provisionally named p8, which showed a strong, but transient, induction in the pancreas in response to acute pancreatitis. We report here the cloning and sequencing of the human p8 cDNA. The human p8 polypeptide is 82 amino acids long and shows an overall identity of 74% with the rat counterpart. The complete structure of the p8 gene was also established. The p8 gene comprises three exons separated by two introns and the gene was mapped to chromosome 16. Analysis of the p8 primary structure suggested the presence of a bipartite motif of nuclear targeting, indicating that p8 may function within the nucleus. This presumption has been confirmed by transfection of COS-7 cells with the p8 cDNA followed by immunostaining with specific antibodies. p8 mRNA expression is induced in some, but not all, cells by serum starvation and ceramide. To analyze the p8 function, we stably transfected HeLa cells with a p8 expression plasmid, and measured their growth and their sensitivity to apoptosis. Response to TNF alpha and staurosporine-induced apoptosis was not modified by p8 expression. However, cells expressing p8 grew significantly more rapidly.
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PMID:Cloning and expression of the human p8, a nuclear protein with mitogenic activity. 1009 51

In pancreatic acinar cells, chaperonin Cpn60 is present in all the cellular compartments involved in protein secretion as well as in mitochondria. To better understand the role Cpn60 plays in pancreatic secretion, we have evaluated its changes under experimental conditions known to alter pancreatic secretion. Quantitative protein A-gold immunocytochemistry was used to reveal Cpn60 in pancreatic acinar cells. Cpn60 immunolabelings in cellular compartments involved in secretion were found to decrease in acute pancreatitis as well as upon stimulation of secretion and in starvation conditions. A major increase in Cpn60 was recorded in diabetic condition. This was normalized by insulin treatment. Although in certain situations changes in secretory enzymes and in Cpn60 correlate well, in others, nonparallel secretion seemed to take place. In contrast, expression of mitochondrial Cpn60 in acinar cells appeared to remain stable in all conditions except starvation, where its levels decreased. Expression of Cpn60 in the secretory pathway and in mitochondria thus appears to behave differently, and Cpn60 in the secretory pathway must be important for quality control and integrity of secretion.
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PMID:Expression differences in mitochondrial and secretory chaperonin 60 (Cpn60) in pancreatic acinar cells. 1498 62

About 20% of acute pancreatitis cases develop necrosis and have a high risk of inflammatory and infectious complications and a high mortality rate. Acute pancreatitis has a variety of causes and despite years of research its pathogenesis remains complex and obscure. Both local and systemic inflammatory responses play key roles in the pathophysiology of this disorder. Treatment plans continue to rely on supportive care without proven specific therapies. Pancreatic rest and use of total parenteral nutrition (TPN) were the gold standard for nutritional support of these challenging patients. Because numerous studies in other critically ill patients demonstrated benefits of enteral nutrition, recent investigations compared TPN to enteral nutrition in acute pancreatitis. These studies indicated that enteral nutrition delivered into the jejunum was tolerated well, even in patients with severe acute pancreatitis. "Mild'' cases of pancreatitis should improve and tolerate oral nutrition within a few days. In contrast, "severe'' cases of pancreatitis or those with a protracted clinical course require nutritional support to aid in preventing adverse effects of starvation and nutrient deficiencies. Current recommendations are to attempt enteral nutrition in patients with acute pancreatitis prior to instituting TPN. Further studies to determine optimal nutrient composition are warranted and should investigate the possibility of modulating the inflammatory response induced by pancreatitis to improve outcomes.
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PMID:Nutritional support in acute pancreatitis: an update on management issues. 1608 59

Autophagy is a degradation process of cytoplasmic cellular constituents, which serves as a survival mechanism in starving cells, and it is characterized by sequestration of bulk cytoplasm and organelles in double-membrane vesicles called autophagosomes. Autophagy has been linked to a variety of pathological processes such as neurodegenerative diseases and tumorigenesis, which highlights its biological and medical importance. We have previously characterized the vacuole membrane protein 1 (VMP1) gene, which is highly activated in acute pancreatitis, a disease associated with morphological changes resembling autophagy. Here we show that VMP1 expression triggers autophagy in mammalian cells. VMP1 expression induces the formation of ultrastructural features of autophagy and recruitment of the microtubule-associated protein 1 light-chain 3 (LC3), which is inhibited after treatment with the autophagy inhibitor 3-methiladenine. VMP1 is induced by starvation and rapamycin treatments. Its expression is necessary for autophagy, because VMP1 small interfering RNA inhibits autophagosome formation under both autophagic stimuli. VMP1 is a transmembrane protein that co-localizes with LC3, a marker of the autophagosomes. It interacts with Beclin 1, a mammalian autophagy initiator, through the VMP1-Atg domain, which is essential for autophagosome formation. VMP1 endogenous expression co-localizes with LC3 in pancreas tissue undergoing pancreatitis-induced autophagy. Finally, VMP1 stable expression targeted to pancreas acinar cell in transgenic mice induces autophagosome formation. Our results identify VMP1 as a novel autophagy-related membrane protein involved in the initial steps of the mammalian cell autophagic process.
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PMID:The pancreatitis-induced vacuole membrane protein 1 triggers autophagy in mammalian cells. 1794 Feb 79

Autophagy is an evolutionarily preserved degradation process of cytoplasmic cellular constituents, which has been known for its role in protecting cells against stresses such as starvation and in eliminating defective subcellular structures. It is essentially a form of self-cannibalism - hence the name that means 'self-eating' - in which the cell breaks down its own components. By mostly morphological studies, autophagy has been linked to a variety of pathological processes such as neurodegenerative diseases and tumorigenesis, which highlights its biological and medical importance. However, whether autophagy protects from or causes disease is unclear. Autophagic morphology was described in human pancreatitis by Helin et al. in 1980. Actually, acute pancreatitis is one of the earlier pathological processes where autophagy has been described in a human tissue. Autophagy, autodigestion and cell death are early cellular events in acute pancreatitis. The aim of this review is to introduce a description of the autophagic process and to discuss the possible role of autophagy in acute pancreatitis.
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PMID:Autophagy and pancreas disease. 1871 76

Patients with acute pancreatitis usually present nutritional status impairment. In alcoholic pancreatitis this impairment is usually presented before hospital admission. In patients with long-term complicated pancreatitis, malnutrition develops during the course of the disease. Besides, these patients present an increased stress and protein hypercatabolism. Treatment of acute pancreatitis usually maintains patients in a short period of starvation. In mild pancreatitis, starvation is needed for a few days, beginning progressively oral feeding. These patients don't need special nutritional support, unless they were previously malnourished. Patients with severe acute pancreatitis should always receive artificial nutritional support in order to preserve the nutritional status as starvation will be maintained for more than one week. In this paper, we review the nutritional treatment in these situations, trying to answer some different questions: type of nutritional support, when it should be started and when it is indicated to withdraw.
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PMID:[Nutritional management of patients with acute pancreatitis: when the past is present]. 1871 11


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