Biomedical subjects
Publications and source records attributed to C Lutton.
New studies have permit to reevaluate the importance of the digestive tract in each of the mechanisms regulating cholesterol turnover. Particularly, the role of the digestive trace in the rat cholesterol synthesis was underestimated. Is there a similar situation in man?
By an isotopic equilibrium method turnover rates of rats cholesterol have been determined in 30 various experimental conditions. A deductive analysis of these overall old data discovers that absorption coefficient of dietary cholesterol is a determinative parameter of cholesterol dynamic equilibrium. Synthesis which takes places chiefly in the intestine, fecal external secretion and fecal excretion of cholesterol are linearly increasing when the absorption coefficient is decreasing. Two types of exception have been noted. The most interesting concerns the case where there is a supplementary synthesis. For pregnant of lactating female rats placenta or mammary glands are directly interested. For rats with ligated bile duct or feed with cholestryramine, liver must be incriminated. These two last cases are the alone on 30 where hepatic synthesis play very probably a notable role in the dynamic equilibrium of cholesterol.
The effects of ingestion of an unsaponifiable avocado and soya extract (P.I.A.S.) on the rates of cholesterol turnover were studied in the Rat smaller than in toto greater than. The balance is the same as in control rats, but fecal and urinary excretions of cholesterol are well enhanced and transformation into bile acids is consequently reduced. The absorption coefficient of cholesterol is unchanged in spite of the presence of phytosterols in the extract. The extract having been said to have a beneficial effect on scleroderma a special study was undertaken of the skin. The GLC analysis of sterols show the very probable presence of phytosterols and a richer proportion of cholesterol, precursors particularly methostenol in the skin of rats fed on P.I.A.S. than in that of the controls. These modifications do not produce any variations in the rate of cholesterol synthesis as measured in vitro.
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The genetically hypercholesterolemic RICO rat: a good model for testing a food substance or a drug specific for a key enzyme involved in cholesterol metabolism? The genetically hypercholesterolemic RICO rat, whose cholesterolemia is situated between 1.3 and 1.5 mg x mL(-1), possibly reaching 2 mg x mL(-1), after the addition of cholesterol to its food, possesses a different lipoprotein spectrum than man, because approximatively 70% of the plasma cholesterol is carried by HDL (28% of which are carried by the light HDL1 subfraction, rich in apolipoproteinE (apoE). The effects of certain substances in food (carbohydrates, cholesterol, allyldisulfide, etc.) or drugs (ethinylestradiol, streptozotocin, statins, inhibitors of ACAT, etc.) on the cholesterolemia of the rat were studied, in relation to certain important parameters of cholesterol metabolism (LDLr, VLDL liver secretion, activities of lipolytic enzymes: LPL, HL, etc.). The increase in a number of LDL receptors (LDLr) in the RICO rat, induced by ethinylestradiol, streptozotocin, etc., provokes an important decrease in the apoE-rich HDL concentration, filtered out by its receptors. This decrease is observed in man for LDL. Simvastatin, which stimulates LDLr in man and not in rat, lowers the level of LDL in man and has no effect on the cholesterolemia of the RICO rat. In rat and man, the concentration of plasma cholesterol is inversely proportional to the rate of cholesterol synthesis in the organism and to its plasma turnover rate. The concentration of cholesterol in the plasma carried by the HDL1 of the rat, is however, proportional to hepatic cholesterogenesis. This fraction is positively correlated to the activity of hepatic lipase (HL) and negatively to the activity of lipoprotein lipase (LPL), released by heparin. These data demonstrate the importance of the liver and lipolytic enzymes in the intraplasmatic hydrolysis of HDL3 (precursors of HDL1), murine particles that can be considered similar to human LDL.
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