Linked Life Data

17628538

Source:http://linkedlifedata.com/resource/pubmed/id/17628538

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-9-17
pubmed:abstractText
The aim of the present study was to investigate whether hyperlipidemia can cause acute pancreatitis or alter its severity. Male Wistar rats were fed a 3% cholesterol-enriched diet or a normal diet for 16 weeks. Edematous and necrotizing pancreatitis was induced with 3x75 mug/kg body weight of cholecystokinin s.c. and 2x2 g/kg body weight of L-arginine i.p., respectively, in separate groups of normal and hyperlipidemic rats. The severity of the pancreatitis was assessed. We studied the influence of hyperlipidemia on the formation of oxygen-derived free radicals, endogenous scavengers, nitric oxide synthases (NOS), peroxynitrite (ONOO(-)), heat shock protein 72 (HSP72) and nuclear factor-kappa B (NF-kappaB) activation in the pancreas during acute edematous and necrotizing pancreatitis. Hyperlipidemia did not worsen edematous, but aggravated necrotizing pancreatitis. The cholesterol-enriched diet significantly reduced the catalase and Mn-superoxide dismutase (SOD) and constitutive NOS (cNOS) activities and increased the inducible NOS (iNOS) in the pancreas relative to those in the rats on the normal diet. The pancreatic nitrotyrosine level, as a marker of ONOO(-), and the NF-kappaB DNA-binding activity in the pancreas, were significantly elevated in the cholesterol-fed rats. The pancreatic HSP72 expression during necrotizing pancreatitis was not influenced by the hyperlipidemia. The pancreatic Mn-SOD, Cu, Zn-SOD, glutathione peroxidase, total glutathione and cNOS activities were significantly reduced, while the catalase, iNOS and NF-kappaB DNA-binding activities were significantly increased in the animals with necrotizing pancreatitis on the cholesterol diet as compared with those with pancreatitis and receiving the normal diet. Hyperlipidemia induced with this cholesterol-enriched diet leads to decreases in endogenous scavenger and cNOS activities, results in iNOS and NF-kappaB activation and stimulates ONOO(-) generation in the pancreas, which may be responsible for the aggravation of acute necrotizing pancreatitis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
572
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
74-81
pubmed:meshHeading
pubmed-meshheading:17628538-Animals, pubmed-meshheading:17628538-Arginine, pubmed-meshheading:17628538-Catalase, pubmed-meshheading:17628538-Cholecystokinin, pubmed-meshheading:17628538-Cholesterol, Dietary, pubmed-meshheading:17628538-Free Radical Scavengers, pubmed-meshheading:17628538-HSP72 Heat-Shock Proteins, pubmed-meshheading:17628538-Hyperlipidemias, pubmed-meshheading:17628538-Male, pubmed-meshheading:17628538-NF-kappa B, pubmed-meshheading:17628538-Nitric Oxide Synthase, pubmed-meshheading:17628538-Oxidative Stress, pubmed-meshheading:17628538-Pancreas, pubmed-meshheading:17628538-Pancreatitis, Acute Necrotizing, pubmed-meshheading:17628538-Peroxynitrous Acid, pubmed-meshheading:17628538-Rats, pubmed-meshheading:17628538-Rats, Wistar, pubmed-meshheading:17628538-Superoxide Dismutase
pubmed:year
2007
pubmed:articleTitle
Hyperlipidemia induced by a cholesterol-rich diet aggravates necrotizing pancreatitis in rats.
pubmed:affiliation
First Department of Medicine, University of Szeged, Hungary. czal@in1st.szote.u-szeged.hu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't