Browsing by Author "DELPOZO, R"

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    INFLUENCE OF LEGUME INTAKE ON BILIARY LIPIDS AND CHOLESTEROL SATURATION IN YOUNG CHILEAN MEN - IDENTIFICATION OF A DIETARY RISK FACTOR FOR CHOLESTEROL GALLSTONE FORMATION IN A HIGHLY PREVALENT AREA
    (1989) NERVI, F; COVARRUBIAS, C; BRAVO, P; VELASCO, N; ULLOA, N; CRUZ, F; FAVA, M; SEVERIN, C; DELPOZO, R; ANTEZANA, C; VALDIVIESO, V; ARTEAGA, A
    Chileans and North American Indians have one of the highest prevalence rates of cholesterol gallstones in the world. The most common theory to explain this has been the operation of some as yet undefined genetic risk factor in these populations. Searching for some common environmental factor for gallstones in Chileans and North American Indians, we found that beans and other legumes are common foods consumed by both populations. In this study we tested the hypothesis that legume intake may favor the production of biliary cholesterol supersaturation. We studied 20 young men subjected to a diet containing 120 g/day of legumes and a control diet without legumes for a period of 1 mo each. Both diets supplied identical quantities of energy, carbohydrates, protein, total fat, fiber, and cholesterol. Low-density lipoprotein cholesterol concentration decreased by 16% (p < 0.001) after the legume diet. Biliary cholesterol saturation increased in 19 of the 20 subjects; the mean of the group markedly increased from 110% to 169% (p < 0.001) after the legume diet. These results are consistent with the hypothesis that legume intake is a potential risk factor for cholesterol gallstone disease.
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    REGULATION OF BILIARY CHOLESTEROL SECRETION IN THE RAT - ROLE OF HEPATIC CHOLESTEROL ESTERIFICATION
    (1984) NERVI, F; BRONFMAN, M; ALLALON, W; DEPIEREUX, E; DELPOZO, R
    Although the significance of the enterohepatic circulation of bile salts in the solubilization and biliary excretion of cholesterol is well established, little is known about the intrahepatic determinants of biliary cholesterol output. Studies were undertaken to elucidate some of these determinants in the rat. Feeding 1% diosgenin for 1 wk increased biliary cholesterol output and saturation by 400%. Bile flow, biliary bile salt, phospholipid and protein outputs remained in the normal range. When ethynyl estradiol (EE) was injected into these animals, biliary cholesterol output decreased to almost normal levels under circumstances of minor changes in the rates of biliary bile salt and phospholipid outputs. Similarly, when chylomicron cholesterol was i.v. injected into diosgenin-fed animals, biliary cholesterol output significantly decreased as a function of the dose of chylomicron cholesterol administered. Relative rates of hepatic cholesterol synthesis and esterification were measured in isolated hepatocytes. Although, hepatic cholesterogenesis increased 300% in diosgenin-fed animals, the contribution of newly synthesized cholesterol to total biliary cholesterol output was only 19 .+-. 9%, compared with 12 .+-. 6% in control and 15 .+-. 5% in diosgenin-fed and EE-injected rats. The rate of oleate incorporation into hepatocytic cholesterol esters was 30% inhibited in diosgenin-fed rats. When EE was injected into these animals, the rate of cholesterol esterification increased to almost 300%. To investigate further the interrelationship between hepatic cholesterol esterification and biliary cholesterol output, 21 diosgenin-fed rats were studied. Six of them received in addition EE and 10 received chylomicron cholesterol. The relationships between biliary cholesterol output as a function of both microsomal acyl-CoA:cholesterol acyltransferase (ACAT) activity and hepatic cholesterol ester concentration were significantly correlated in a reciprocal manner. The size of the biliary cholesterol precursor pool can be rapidly modified through changes in the activity of the hepatic ACAT. [Implications with respect to the role of high cholesterol secretion to gallstone disease were presented.].
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    SUB-CELLULAR DISTRIBUTION OF CHOLESTEROL ESTER HYDROLASE IN HUMAN-LIVER
    (1981) DELPOZO, R; BRONFMAN, M; BULL, P; NERVI, F
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    THE EFFECT OF PROGESTERONE ON THE REGULATORY MECHANISMS OF BILIARY CHOLESTEROL SECRETION IN THE RAT
    (1983) NERVI, FO; DELPOZO, R; COVARRUBIAS, CF; RONCO, BO
    The hypothesis was tested that progesterone [P4], an inhibitor of cholesterol esterification in liver microsomes, increases biliary cholesterol output by increasing the availability of cholesterol. Initial bile samples of 20 min were obtained from acute bile fistula rats after 7 daily doses of P4 (5-55 mg per kg of body wt). Biliary cholesterol output correlated with the doses of P4 r = 0.64 (P < 0.005). A 100% increment in biliary cholesterol output was obtained with P4 doses of 30-55 mg/kg of body wt. Under these conditions, biliary phospholipid output increased 50% (P < 0.02), but bile salt output remained normal. The relationship between biliary cholesterol and phospholipids as a function of bile salt output was studied after acute depletion of the bile salt pool. A rectangular hyperbola was the best curve fitting for the experimental data in control and P4 injected rats. In the physiological range of bile salt output, between 60 and 120 nmol/g per min, P4-injected rats secreted 100% more biliary cholesterol than did controls. The calculated theoretical maximal cholesterol and phospholipid outputs were significantly increased in P4-injected animals. Serum and hepatic cholesterol pool, free and ester fractions, remained normal. The acyl-CoA:cholesterol acyltransferase reaction was 30% inhibited in hepatic microsomes of P4-injected rats, (P < 0.05). The changes in biliary phospholipids and cholesterol output produced by P4 were rapidly reversed by either 0.5% cholesterol feeding or 2 mg/kg of body wt ethynylestradiol injection. These manipulations simultaneously produced a 100% increment in the microsomal acyl-CoA:cholesterol acyltransferase activity (P < 0.005) and increased 4-fold the concentration of hepatic cholesterol esters. This experimental model suggests a functional interrelationship between biliary cholesterol output and the rate at which the liver esterifies cholesterol.