Injection of triton WR-1339 into rats leads to a rapid increase in the cholesterol, cholate, and various lipid fractions of their blood. The increase in cholesterol is confined to the blood itself. The cholesteremic effect of triton was not dependent upon a prior accumulation of cholate in plasma. The liver was found to be the source of the excess cholesterol but the rate of cholesterol synthesis, the excretion of cholate, and the cholesterol content of the liver were not changed by injection of triton. The cholesteremic effect of triton is not due to alteration in the intestinal excretion of cholesterol. Transfer of blood between "tritonized" and normal rats leads to a disappearance of the hypercholesteremia in the former and its appearance in the latter animals. The plasma proteins of rats injected with triton are markedly changed qualitatively. Heparin was found to inhibit the hypercholesteremic effect of triton. The hypercholesteremia following triton injection appears to be due to a fundamental physicochemical change in the plasma proteins produced by injection of this detergent.

Animals↗

PubMed1953

Observations concerning the production and excretion of cholesterol in mammals. IX. The mechanism of the hypercholesteremic effect of cholic acid.

Accumulation of cholate in plasma is the immediate cause of hypercholesteremia in the rat with bile duct ligation and in the normal rat given intravenous sodium cholate. The hypercholesteremia induced by cholate administration does not appear to be dependent upon any preceding change in the rates of absorption, excretion, synthesis, or redistribution of cholesterol in the tissues of the animal. Cholate administration seems to induce hypercholesteremia by impeding the normal rate of passage of cholesterol from the plasma into the liver; this impedance is probably due to an alteration of the cholesterol-binding power of plasma proteins induced by cholate. The chemical and physiological implications of this finding are discussed.

Animals↗

PubMed1953

Observations concerning the production and excretion of cholesterol in mammals. X. Factors affecting the absorption and fate of ingested cholesterol.

The absorption of oral cholesterol by rats was followed directly by analyses of the thoracic lymph and indirectly by calculating the deficit of fecal cholesterol under the amount fed. The two methods checked within about 20 per cent, with fecal analyses indicating the greater absorption. The absorbed cholesterol was found to be deposited in the liver, only very minor quantities being found in other organs or plasma. Bile is necessary for normal absorption of cholesterol, although very small amounts are absorbed even in its absence. Excess oral cholic acid increases the absorption of cholesterol by otherwise normal animals. The rat absorbs about 47 per cent of a single 50 mg. dose of cholesterol and about 34 per cent of a 100 mg. dose.

Animals↗

PubMed1953