Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 1699546

Experimental alcoholic skeletal muscle myopathy is characterised by a rapid and sustained decrease in muscle RNA content.

J S Marway·V R Preedy·T J Peters
View original source ↗Export metadata ↓

Abstract

An investigation was made into the effects of ethanol feeding (36% of total calories) on skeletal muscle. From 7 to 42 days, muscle weights and protein and DNA contents of alcohol-treated rats were significantly lower (10-23%) than pair-fed controls (with glucose as 36% of total calories). Ethanol feeding markedly reduced muscle RNA content by 22-34%, when compared to controls. Muscle RNA content of ethanol-fed rats at 7, 14, 28 and 42 days of treatment was significantly lower than initial values (i.e. at 3 days) by 22-38%. Thus, ethanol feeding caused an initial net loss and thereafter a reduction in the rate of accretion of RNA. The marked and sustained loss in the muscle protein synthetic apparatus may be a precipitating event in the development of experimental skeletal muscle myopathy.

Explore related subjects

AlcoholismAnimalsDNA ReplicationDose-Response Relationship, DrugEthanolMaleMuscle ProteinsMusclesMuscular AtrophyRNARatsRats, Inbred StrainsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J S Marway, V R Preedy, T J Peters. 1990. Experimental alcoholic skeletal muscle myopathy is characterised by a rapid and sustained decrease in muscle RNA content.. https://pubmed.ncbi.nlm.nih.gov/1699546/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1992

Long-term mortality after transfusion-associated non-A, non-B hepatitis. The National Heart, Lung, and Blood Institute Study Group.

BACKGROUND: Acute non-A, non-B hepatitis after blood transfusion often progresses to chronic hepatitis and sometimes culminates in cirrhosis or even hepatocellular carcinoma. However, the frequency of these sequelae and their effects on mortality are not known. METHODS: We traced patients with transfusion-related non-A, non-B hepatitis who had been identified in five major prospective studies conducted in the United States between 1967 and 1980. We matched each patient with two control subjects (identified as the first and second controls) who received transfusions but who did not have hepatitis. The mortality rates in the three groups were determined with use of data from the National Death Index and Social Security Death Tapes. Cause-specific mortality was determined by reviewing death certificates. RESULTS: Vital status was established for over 94 percent of the 568 patients who had had non-A, non-B hepatitis and the two control groups (526 first controls and 458 second controls). After an average follow-up of 18 years, the estimate by life-table analysis of mortality from all causes was 51 percent for those with transfusion-associated non-A, non-B hepatitis, as compared with 52 percent for the first controls and 50 percent for the second controls. The survival curves for the three groups were virtually the same. Mortality related to liver disease was 3.3, 1.1, and 2.0 percent, respectively, among the three groups (P = 0.033 for the comparison of the group with non-A, non-B hepatitis with the combined control group). Seventy-one percent of the deaths related to liver disease occurred among patients with chronic alcoholism. CONCLUSIONS: In this long-term follow-up study, there was no increase in mortality from all causes after transfusion-associated non-A, non-B hepatitis, although there was a small but statistically significant increase in the number of deaths related to liver disease.

Alcoholism↗