ETHANOL-INDUCED ACTIVATION OF ADENINE-NUCLEOTIDE TURNOVER - EVIDENCE FOR A ROLE OF ACETATE
ETHANOL-INDUCED ACTIVATION OF ADENINE-NUCLEOTIDE TURNOVER - EVIDENCE FOR A ROLE OF ACETATE
复制标题
DOI:
10.1172/jci111512
复制
发表时间:
1984-01-01
影响因子:
15.9
通讯作者:
FOX, IH
中科院分区:
文献类型:
--
作者:
PUIG, JG;FOX, IH
Consumption of alcohol causes hyperuricemia by decreasing urate excretion and increasing its production. Previous studies indicate that ethanol administration increases uric acid production by increasing ATP degradation to uric acid precursors. To test the hypothesis that ethanol-induced increased urate production results from acetate metabolism and enhanced adenosine triphosphate turnover, i.v. sodium acetate, sodium chloride and ethanol (0.1 mmol/kg per min for 1 h) were given to 5 normal [human] subjects. Acetate plasma levels increased from 0.04 .+-. 0.1 mM (mean .+-. SE) to peak values of 0.35 .+-. 0.07 mM and to 0.08 .+-. 0.01 mM during acetate and ethanol infusions, respectively. Urinary oxypurines increased to 223 .+-. 13% and 316 .+-. 44% of the baseline values during acetate and ethanol infusions, respectively. Urinary radioactivity from the adenine nucleotide pool labeled with [8-14C]adenine increased to 171 .+-. 27% and to 128 .+-. 8% of the baseline values after acetate and ethanol infusions. Both ethanol and acetate evidently increases purine nucleotide degradation by enhancing the turnover of the adenine nucleotide pool. Acetate metabolism may contribute to the increased production of urate associated with ethanol intake. [Alcohol consumption as a cause of gouty arthritis is discussed.].