trypsinogen has been researched along with Obesity* in 5 studies
2 review(s) available for trypsinogen and Obesity
Article | Year |
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Acute pancreatitis.
Acute pancreatitis (AP) is an important cause of morbidity and mortality worldwide and the annual incidence appears to be increasing. It presents as a mild self-limiting illness in 80% of patients. However, one-fifth of these develop a severe complicated life-threatening disease requiring intensive and prolonged therapeutic intervention. Alcohol and gallstone disease remain the commonest causes of AP but metabolic abnormalities, obesity and genetic susceptibility are thought be increasingly important aetiological factors. The prompt diagnosis of AP and stratification of disease severity is essential in directing rapid delivery of appropriate therapeutic measures. In this review, the range of diagnostic and prognostic assays, severity scoring systems and radiological investigations used in current clinical practice are described, highlighting their strengths and weaknesses. Increased understanding of the complex pathophysiology of AP has generated an array of new potential diagnostic assays and these are discussed. The multidisciplinary approach to management of severe pancreatitis is outlined, including areas of controversy and novel treatments. Topics: Acute Disease; Alcohol Drinking; Amylases; Autolysis; Gallstones; Genetic Predisposition to Disease; Humans; Hypercalcemia; Hyperlipidemias; Lipase; Obesity; Pancreatitis; Prognosis; Trypsin; Trypsinogen | 2011 |
[Mechanism of onset and aggravation of acute pancreatitis].
Topics: Acute Disease; Alleles; Carrier Proteins; Cytokines; Humans; Immune System Diseases; Inflammation Mediators; Lipopolysaccharide Receptors; Macrophage Migration-Inhibitory Factors; Mutation; Obesity; Pancreatitis; Severity of Illness Index; Toll-Like Receptors; Trypsin; Trypsin Inhibitor, Kazal Pancreatic; Trypsinogen | 2008 |
3 other study(ies) available for trypsinogen and Obesity
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Influence of B-cell impairment on pancreatic acini in NOD mice and streptozotocin-induced diabetic rats.
Exocrine pancreatic function insufficiency, even of short duration, has been reported in juvenile-onset insulin dependent diabetic patients. To evaluate the status of pancreatic acini under decreased B-cell function, tissue insulin, amylase, chymotrypsinogen and trypsinogen in the pancreas were measured in streptozotocin-induced diabetic rats and non-obese diabetic mice in various conditions. In streptozotocin diabetic rats, a dissociation of three enzyme contents was demonstrated in the condition with discontinuation of insulin injection, i.e., a marked decrease in amylase, a significant increase in chymotrypsinogen, but no significant change in trypsinogen. This dissociation was markedly improved in the insulin-treated condition. In non-obese diabetic mice, these enzyme contents were not significantly changed although severe insulitis together with the marked decrease in insulin content was observed. These data show that the cessation of B-cell function alone does not cause insufficiency of exocrine pancreas. Topics: Amylases; Animals; Chymotrypsinogen; Diabetes Mellitus; Diabetes Mellitus, Experimental; Female; Insulin; Islets of Langerhans; Mice; Mice, Inbred Strains; Obesity; Pancreas; Rats; Rats, Inbred Lew; Trypsinogen | 1988 |
Pancreatic growth and enzyme profiles in weanling rats with normophagic hypothalamic obesity.
Weanling male rats with ventromedial hypothalamic lesions (VMNL rats) and sham-operated controls were killed 1, 2, 4, and 5 weeks postoperatively. The VMNL rats developed normophagic hypothalamic obesity in the presence of normal body weight and reduced linear growth. In both VMNL and control rats, pancreatic weight and protein content increased with time but were lower in the lesioned animals. Pancreatic DNA content was arrested in VMNL rats and remained so during the remainder of the experiment. The only significant enzyme changes (trypsinogen, amylase, and lipase) were evident in higher trypsinogen concentration in VMNL rats during 2 and 4 weeks after lesion production. In view of previous data on both hypophysectomized and VMNL rats and the known role of the ventromedial hypothalamic nucleus in neuroendocrine and neuroautonomic function, it is speculated that the changes observed here are in part due to disruption of neuroendocrine and in part due to disturbance of neuroautonomic control systems. Topics: Amylases; Animals; DNA; Hypophysectomy; Hypothalamus; Male; Obesity; Pancreas; Rats; Rats, Inbred Strains; Trypsinogen | 1984 |
[Levels of pancreatic hydrolases in pancreas and small bowel of two types of obese mice with hyperinsulinism: the obese-hyperglycemic Bar-Harbor mouse (OH) and the New-Zealand mouse (NZO)].
Topics: Amylases; Animals; Chymotrypsin; Female; Hydrolases; Hyperglycemia; Hyperinsulinism; Intestine, Small; Lipase; Male; Mice; Obesity; Pancreas; Ribonucleases; Species Specificity; Trypsin; Trypsinogen | 1968 |