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)

Fatty liver can be determined by chronic abuse of alcohol, by means of direct action of the same on the level of membrane's proteins. The UDPG restores the levels of a membrane's component, the phosphoribosylpyrophosphate (PRPP), which normally results reduced in cellular cultures of rat's liver, after the addition of alcohol. It has been made a study on 40 patients (27 men and 13 women age medium 54 years) alcoholics for at least 1 year with a quantity of ethanol ingested less than 1 g gamma/die/kg of body weight with alternated values of serum GOT, GPT and gamma-GT and clinical aspects of a modest alcoholic hepatopathy, assigning through, at random in double blind, two groups of treatment: the first one with UDPG (400 mg/im/die for 30 days) the second one with placebo. It has been considered like variable of therapeutic effect the difference between basal value and the result at the end of treatment of these serum enzymes, it has been applied the Student's t test for the evaluation of the difference between treatments. It has been shown in the groups of patients analyzed with UDPG (not the group of placebo) reduction extremely significant for the gamma-GT (p = 0.00032) and GOT (p = 0.0138). In 5 treated cases, after an hepatic ultrasound imaging of comparison, at the end of the treatment, it has been demonstrated an apparent improvement of thickening of the echos; only 3/40 of the patients have certainly stopped to ingest alcoholic drinks.
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PMID:[Uridine diphosphate glucose (UDPG) in the treatment of hepatic disease from chronic alcohol abuse]. 208 Mar 8

Recent in vivo studies have demonstrated a strong negative correlation between liver triglyceride content and hepatic insulin sensitivity, but a causal relationship remains to be established. We therefore have examined parameters of direct hepatic insulin action on isolated steatotic livers from high-fat (HF)-fed rats compared with standard chow (SC)-fed controls. Direct hepatic action of insulin was assayed in Wistar rats after 6 wk of HF diet by measuring the insulin-induced suppression of epinephrine-induced hepatic glucose output in an isolated liver perfusion system. Insulin-induced activation of glycogen synthase was measured by quantifying the incorporation of radioactive UDP-glucose into glycogen in HF and SC liver lysates. HF diet induced visceral obesity, mild insulin resistance, and hepatic steatosis. Both suppression of epinephrine-induced glycogenolysis and activation of glycogen synthase by insulin were sustained in HF rats; no significant difference from SC controls could be detected. In conclusion, in our model, triglyceride accumulation into the liver was not sufficient to impair direct hepatic insulin action. The data argue for an important role of systemic factors in the regulation of hepatic glucose output and hepatic insulin sensitivity in vivo.
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PMID:Preserved direct hepatic insulin action in rats with diet-induced hepatic steatosis. 1472 26