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E Albright

Publications and source records attributed to E Albright.

21 records · Page 2Linked to original sources

Effect of dietary cholesterol on biliary cholesterol content and bile flow in the hypothyroid rat.

The hypothyroid rat model was used to investigate the effect of dietary-induced hypercholesterolemia on biliary cholesterol content and bile flow. Rats were divided into four dietary groups--diet A: Rat Chow; diet B: Rat Chow plus 0.1% propylthiouracil; diet C: Rat Chow plus 0.1% propylthiouracil, 0.3% taurocholate, 5% lard; diet D: Rat Chow plus 0.1% propylthiouracil, 0.3% taurocholate, 5% lard, and 1% cholesterol. After 6 wk, bile was collected and livers were excised for the preparation of membranes. In cholesterol-fed animals, biliary cholesterol content was increased. However, because of a significant decrease in the rate of bile flow that occurred in these animals, biliary cholesterol output was unchanged from the cholesterol output observed in control animals. Dietary cholesterol also caused a threefold increase in liver membrane cholesterol content and a 64% decrease in the activity of sodium-potassium-stimulated adenosine triphosphatase (Na+,K+-ATPase). In a separate group of animals, microsomes prepared from livers of control rats were incubated with phosphatidylserine liposomes, liposomes containing cholesterol, or buffer. The activity of Na+,K+-ATPase was increased in microsomes incubated with phosphatidylserine liposomes. However, when the cholesterol content of the microsomes was increased twofold by incubating the membranes with liposomes containing cholesterol, the stimulation of Na+,K+-ATPase activity was significantly decreased. The data suggest that in the cholesterol-fed hypothyroid rat, biliary cholesterol content is significantly increased; however, because of a decrease in the rate of bile flow, biliary cholesterol output is not changed. The decrease in bile flow is associated with an accumulation of cholesterol and a decrease in the activity of Na+,K+-ATPase in hepatic membranes.

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The effect of hypothyroidism and thyroxine replacement on hepatic and intestinal HMG-CoA reductase and ACAT activities and biliary lipids in the rat.

Hepatic and intestinal cholesterol metabolism were investigated in the hypothyroid and thyroxine-treated hypothyroid rat. Plasma cholesterol levels were significantly increased in hypothyroid animals. After thyroxine administration, plasma cholesterol levels were reduced to levels observed in euthyroid controls. Hypothyroidism caused a significant decrease in biliary cholesterol output, which was reversed with thyroxine treatment. In contrast, biliary bile acid output was unchanged by the thyroid status. Cholesterol synthesis, as estimated by HMG-CoA reductase activity, was decreased in the liver of hypothyroid animals. Thyroxine administration, however, significantly increased reductase activity returning it to control levels. Hypothyroidism did not affect HMG-CoA reductase activity in the intestine, but thyroxine administration markedly stimulated the activity of this enzyme in this organ. Cholesterol esterification, as estimated by ACAT activity, was decreased in the liver of hypothyroid rats, while intestinal ACAT activity was greatly increased. Thyroxine treatment reversed these effects of hypothyroidism on ACAT activity in both organs. An increase in microsomal cholesterol content in the intestine of hypothyroid rats was associated with the observed increase in intestinal ACAT activity. The percent of cholesterol that was absorbed in the intestine was not changed by the thyroid status of the animal. The data suggest that the changes observed in cholesterol metabolism in hypothyroid rats or hypothyroid rats treated with thyroxine for 1 week cannot account for the increase in plasma cholesterol levels observed in the hypothyroid rat. This implies that other factors that were not studied, such as changes in lipoprotein catabolism, are likely to contribute to the hypercholesterolemia of hypothyroidism.

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