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)

Three groups of freshly calved dairy cows suffering from fatty liver syndrome of different stages were examined for serum cholic acid (SCA) levels to assess the value of SCA-determination as a diagnostic approach to fatty liver syndrome. A. Comparison of the SCS levels between cows with and without ketonuria: Cows with ketonuria (n = 13) and with elevated plasma ASAT activity, indicating a moderate liver damage, showed a rise of their mean SCA level to 35.3 (+/- 14.9) mumol/l. Freshly calved cows without ketonuria (n = 10) had at the same time a mean SCA level of 17.9 (+/- 6.4) mumol/l, falling practically into the physiological range. The SCA level increased above the physiological range in 10 of the 13 cases with ketonuria, in seven of them even more than twice. B. Interrelationship between SCA level and hepatic lipid content: Increase in hepatic total lipid (TL) was always associated with SCA-elevation. The mean SCA level was 55 (+/- 22.0) mumol/l in cases of severe fatty liver (TL = 200-280 g/kg), and 39.5 (+/- 6.0) mumol/l in the moderate form (TL = 180-200 g/kg) of the syndrome. C. Peripartal SCA levels of cows with fatty liver: Clinically healthy cows (n = 6) with ketonuria and an elevation of serum ASAT and FFA concentrations had a mean SCA level of 35-45 mumol/l. One cow of this group, which developed acute fatty liver syndrome and died within the period of study, showed an extreme SCA level of 100 mumol/l in it's terminal stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cholic acid levels in the serum of dairy cows with metabolically-caused liver diseases]. 204 69

Improving the protection of marginal liver grafts during static cold storage is a major hurdle to increase the donor pool of organs. The endothelium glycocalyx quality of preservation influences future inflammatory and oxidative responses. One cellular pathway responsible for the formation of nitric oxide by endothelial cells is dependent on the stimulation of proteoglycans present in the glycocalyx. We investigated the impact of the glycocalyx preservation in static cold storage of fatty liver preserved in different preservation solutions on the endothelium-mediated production of NO. Zucker fatty rat livers were preserved 24 h in static cold storage in either Institut Georges Lopez-1 (IGL-1) (n = 10), IGL-0 (i.e., without PEG35) (n = 5) or Histidine-Tryptophan-Ketoglutarate (HTK) (n = 10) preservation solutions before being processed for analysis. For Sham group (n = 5), the fatty livers were immediately analyzed after procurement. The level of transaminases and nitrites/nitrates were measured in the washing perfusate. Glycocalyx proteins expressions, Syndecan-1, glypican-1 and heparan sulfate (HS), were determined in the tissue (ELISA). Steatotic livers preserved 24 h in IGL-1 preservation solution have a significant lower level of transaminases (aspartate aminotransferase (AST), alanine aminotransferase (ALT)) and less histological damages than steatotic livers preserved 24 h with HTK (p = 0.0152). The syndecan-1 is significantly better preserved in IGL-1 group compared to HTK (p < 0.0001) and we observed the same tendency compared to IGL-0. No significant differences were observed with glypican-1. HS expression in HTK group was significantly higher compared to the three other groups. HS level in IGL-1 was even lower than IGL-0 (p = 0.0005) which was similar to Sham group. The better protection of the glycocalyx proteins in IGL-1 group was correlated with a higher production of NO than HTK (p = 0.0055) or IGL-0 (p = 0.0433). IGL-1 protective mechanisms through the formation of NO could be due to its better protective effects on the glycocalyx during SCS compared to other preservation solutions. This beneficial effect could involve the preservation state of syndecan-1 and the internalization of HS.
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PMID:Glycocalyx Preservation and NO Production in Fatty Livers-The Protective Role of High Molecular Polyethylene Glycol in Cold Ischemia Injury. 3010 65