Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1983-8-26
pubmed:abstractText
To study the effect of chronic alcohol consumption on hepatic levels of thyroid hormones, female Sprague-Dawley rats (n = 24) were pair-fed nutritionally adequate liquid diets containing either ethanol (36% of total calories) or isocaloric carbohydrates for 21 days. Compared to controls, chronic alcohol consumption failed to result in a significant change of hepatic thyroid hormone levels (thyroxine: 14.7 +/- 1.81 ng per gm of liver wet weight vs. 15.0 +/- 1.59; triiodothyronine: 2.60 +/- 0.16 ng per gm of liver wet weight vs. 2.66 +/- 0.18). Similar results were obtained when the hepatic levels of thyroid hormones were expressed per total liver, per gram of liver protein or per 100 gm of body weight. Moreover, prolonged alcohol ingestion led to a significant reduction of serum total thyroxine by 31.6% (p less than 0.001), free thyroxine by 38.9% (p less than 0.02), total triiodothyronine by 40.2% (p less than 0.001) and free triiodothyronine by 56.1% (p less than 0.001) when compared to their pair-fed controls, whereas thyroid-stimulating hormone levels remained virtually unchanged. These data, therefore, clearly show that chronic alcohol consumption is incapable of creating a hyperthyroid hepatic state in rats, and limit the rationale for antithyroid treatment in patients with alcoholic liver disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
469-74
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Hepatic thyroid hormone levels following chronic alcohol consumption: direct experimental evidence in rats against the existence of a hyperthyroid hepatic state.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't