| Autor: |
Kerai, Mita D. J., Waterfield, Catherine J., Kenyon, Susan H., Asker, Daniel S., Timbrell, John A. |
| Předmět: |
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| Zdroj: |
Alcohol & Alcoholism; Jan2001, Vol. 36 Issue 1, p29-38, 10p, 10 Diagrams |
| Abstrakt: |
— Alcohol was administered chronically to female Sprague–Dawley rats in a nutritionally adequate totally liquid diet for 28 days. This resulted in significant hepatic steatosis and lipid peroxidation. β-Alanine, when co-administered with alcohol, seemed to increase hepatic steatosis, as assessed histologically, but decreased triglyceride levels as measured biochemically. In addition, β-alanine and especially alcohol co-administered with β-alanine, significantly increased homocysteine and cysteine excretion into urine throughout the 28-day period of ethanol administration. Serum homocysteine levels were significantly higher in alcohol- and alcohol plus β-alanine-treated animals compared to pair-fed control animals. Alcohol did not affect the urinary excretion of taurine, except after 21 days, when levels were reduced. Levels of liver taurine were markedly depleted in animals receiving alcohol and particularly alcohol plus β-alanine, compared to pair-fed controls. Liver and serum taurine levels were also markedly depleted in animals receiving β-alanine and alcohol plus β-alanine, compared to non-β-alanine-treated animals. There was evidence of slight cholestasis in animals treated with alcohol and more so with alcohol plus β-alanine, as indicated by raised serum alkaline phosphatase and bile acids. These in vivo findings demonstrate for the first time that animals treated with β-alanine may be more susceptible to ethanol-induced hepatic dysfunction, possibly as a result of taurine depletion. [ABSTRACT FROM PUBLISHER] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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