Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent reports described a high incidence of nonalcoholic steatohepatitis (NASH) in patients with obstructive sleep apnea. Accordingly, we hypothesized that recurrent and intermittent hypoxemia plays an important role in the pathogenesis of NASH. Our objective was construction of a practical and accurate experimental model to reproduce the key features of NASH in humans. Chemical hypoxemia through methemoglobinemia was induced by daily intraperitoneal injection of sodium nitrite (40 mg/kg) for 4 weeks in rats with fatty liver. The later was induced by 4-week feeding a choline-deficient high-fat diet (CDHF). Besides, the normal chow diets feeding groups were prepared with in the same manner except for CDHF feeding. The animal experiment was performed in four groups; Normal control, Hypoxemia, CDHF, and CDHF + hypoxemia. Nitrite was given for the later 4 weeks to each rat of Hypoxemia and CDHF + hypoxemia. CDHF + hypoxemia rats were confirmed to develop histological changes that resemble those of patients with NASH, together with biochemical liver dysfunction, while CDHF group was limited in mild steatosis, and Hypoxemia group liver was normal. Present study established a reproducible and useful NASH model resembling the main features of NASH in humans, and showed first that recurrent and intermittent hypoxemia aggravate fatty liver to steatohepatitis and liver fibrosis.
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PMID:A Novel Animal Model of Nonalcoholic Steatohepatitis (NASH): Hypoxemia Enhances the Development of NASH. 1990 25

Obesity is a major risk factor for many chronic metabolic diseases such as inflammation, insulin resistance (IR) and fatty liver injury. It was reported that obesity causes some variations on the serum levels of fetuin-A and is associated with arginine metabolism, especially arginase-1 levels. The aim of our study was to evaluate, the interaction and possible changes of these liver over produced proteins, fetuin-A and arginase-1 levels in obesity-related inflammatory status. Study groups were composed of individuals aged between 19 and 63 (n = 62). The control group included healthy subjects with BMI < 25, obese group included obese patients with BMI > 30 and with no other chronic disease. Biochemical markers were determined by an auto-analyzer. Adiponectin, fetuin-A, arginase-1, asymmetric dimethylarginine (ADMA), arginine, Hexanoyl-lysine (HEL) and leptin levels were measured with commercial ELISA immunoassay kits. Nitrite and nitrate were determined with colorimetric assay kit in serum samples. High sensitive C-reactive protein (hsCRP) levels and liver function enzymes activities were higher in the obese group in respect to the control group. Serum fetuin-A, arginase-1 and leptin levels were increased but adiponectin levels were decreased in obese subjects. Fetuin-A levels showed significant correlations with arginase-1 and HOMA-IR. Consequently, we carried out an investigation about higher serum fetuin-A and arginase-1 levels may have an important role in obesity and obesity-related liver damage.
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PMID:Serum fetuin-A and arginase-1 in human obesity model: Is there any interaction between inflammatory status and arginine metabolism? 2572 54