1/5
Repletion of the plasma pool of nutrient transport proteins occurs at different rates during the nutritional rehabilitation of severely malnourished children / JF Morlese; T Forrester; M Del Rosario; M Frazer; F Jahoor.-- p.214-219.-- En: The Journal of Nutrition.-- 128, 2 (1998)
APOLIPOPROTEINA A-I   LACTANTE   LEUCINA   PREALBUMINA   DESNUTRICION PROTEICO-ENERGETICA   PROTEINAS DE ENLACE DE RETINOL
Ubicación: Centro de Información y Documentación (CANIA)   
Solicite el material por este código: AS-4623
Tipo de Material:
Separata

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2/5
Lowering of HDL2-cholesterol and lipoprotein A-I particle levels by increasing the ratio of polyunsaturated to saturated fatty acids / F Fumeron; L Brigant; HJ Parra; JM Bard; JC Fruchart.-- pp. 655-9.-- En: American Journal of Clinical Nutrition.-- 53, 3 (1991)
ADULTO   ANALISIS DE VARIANZA   APOLIPOPROTEINA A-I   APOLIPOPROTEINAS A   APOLIPOPROTEINAS B   CORONARIOPATIA   GRASAS EN LA DIETA   GRASAS NO SATURADAS EN LA DIETA   LIPOPROTEINAS HDL   LIPOPROTEINAS DEL COLESTEROL HDL
Ubicación: Centro de Información y Documentación (CANIA)   
Solicite el material por este código: AS-5689
Tipo de Material:
Separata

    The protective role of high-density lipoproteins (HDLs) has been attributed to the subfractions HDL2 (according to the density) and lipoprotein A-I (LpA-I) (according to the composition in apolipoproteins). We investigated the effect of a high ratio of polyunsaturated to saturated fatty acids (P:S) on these subfractions in a homogeneous group of young adult males. Two prescribed diets were consumed successively at the subjects' homes for 3 wk each in a random order; one diet contained 70 g butter (P:S 0.2, diet B), the other contained 70 g sunflower margarine (P:S 1.1, diet M). Total calorie, fat, and cholesterol intakes were similar for the two diets. Cholesterol and apolipoprotein B in serum and in low-density lipoproteins (LDLs) were lower with diet M than with diet B. However, significant decreases in protective subfractions of HDL, HDL2, and LpA-I were observed. This undesirable effect of the diet with a high P:S could cancel the benefits of lowering the LDL-cholesterol concentrations.




3/5
Lipid, lipoprotein, and apolipoprotein assessment during an 8-wk very-low-calorie diet / M Parenti; AC Babini; ME Cecchetto; P Di Bartolo; et.al..-- pp. 268S-70S.-- En: American Journal of Clinical Nutrition.-- 56, 1 Suppl (1992)
ADULTO   APOLIPOPROTEINA A-I   APOLIPOPROTEINAS   APOLIPOPROTEINAS B   INDICE DE MASA CORPORAL   COLESTEROL   DIETA REDUCTORA   INGESTION DE ENERGIA   FEMENINO   LIPIDOS   LIPOPROTEINAS   LIPOPROTEINAS DEL COLESTEROL HDL   LIPOPROTEINAS DEL COLESTEROL LDL   OBESIDAD MORBIDA   TRIGLICERIDOS
Ubicación: Centro de Información y Documentación (CANIA)   
Solicite el material por este código: AS-5691
Tipo de Material:
Separata

    The influence of a very-low-calorie diet (VLCD) on lipid pattern is controversial. To evaluate the long-term effect of semistarvation on lipid patterns, a group of severely obese patients [aged 37 +/- 12 y, body mass index (BMI) 40.0 +/- 0.9] underwent a VLCD for 8 wk. Total cholesterol (TC), LDL cholesterol (LDL-C), and HDL cholesterol (HDL-C), triglycerides (TGs), apolipoproteins A1 (apo A1) and B (apo B) were analyzed every week. TC (6.07 +/- 0.23 vs 5.53 +/- 0.25 mmol/L, P less than 0.0008), HDL-C (mmol/L 1.26 +/- 0.06 vs 1.04 +/- 0.05 mmol/L, P less than 0.0001), TGs (1.46 +/- 0.19 vs 1.06 +/- 0.10 mmol/L, P less than 0.0008), and apo A1 (1.57 +/- 0.06 vs 1.32 +/- 0.06 g/L, P less than 0.0002) decreased, whereas LDL-C and apo B showed a biphasic behavior: they significantly fell during the first 3 wk, but during the last weeks returned to their initial values.




4/5
Dietary treatment for familial hypercholesterolemia--differential effects of dietary soy protein according to the apolipoprotein E phenotypes / A Gaddi; A Ciarrocchi; A Matteucci; et.al..-- pp. 1191-6.-- En: American Journal of Clinical Nutrition.-- 53, 5 (1991)
ADULTO   APOLIPOPROTEINA A-I   APOLIPOPROTEINAS A   APOLIPOPROTEINAS B   APOLIPOPROTEINAS E   COLESTEROL   PROTEINAS EN LA DIETA   HUMANO   HIPERCOLESTEROLEMIA FAMILIAR   LIPOPROTEINAS HDL   LIPOPROTEINAS DEL COLESTEROL HDL   LIPOPROTEINAS DEL COLESTEROL LDL   PROTEINAS DE SOYA   SOYA   PROTEINAS VEGETALES
Ubicación: Centro de Información y Documentación (CANIA)   
Solicite el material por este código: AS-5695
Tipo de Material:
Separata

    Familial hypercholesterolemia, one form of type IIa hyperlipidemia, usually responds poorly to standard low-lipid diets. To define the responsiveness to a soy-protein diet in this disease, one homozygous and twenty heterozygous type IIa patients were submitted to a 4-wk traditional hypocholesterolemic diet followed by 4 wk in which animal protein was substituted with texturized soy protein. Soy was then withdrawn for a further 4 wk. No significant changes in plasma lipids were observed during low-lipid diets. The soy diet, however, caused a marked decrease in total (-20.8%) and low-density-lipoprotein (-25.8%) cholesterol and in apolipoprotein B (-14.1%). The plasma cholesterol reduction was higher in patients with apolipoprotein E3/E3 or E3/E4 vs an almost negligible effect on E3/E2. These results confirm that soy-protein diets can lower cholesterol in type IIa patients with familial disease. Data on the sensitivity of patients with different apo-E isoforms agree with recent hypotheses suggesting that soy proteins may activate B,E receptors.




5/5
High density lipoproteins, reverse transport of cholesterol, and coronary artery disease. Insights from mutations / G Assmann; A von Eckardstein; H Funke.-- p. III28-34.-- En: Circulation.-- 87, 4 Suppl (1993)
APOLIPOPROTEINA A-I   APOLIPOPROTEINAS   TRANSPORTE BIOLOGICO   PROTEINAS PORTADORAS   CORONARIOPATIA   HUMANO   LIPOPROTEINAS DEL COLESTEROL HDL   MUTACION   FACTORES DE RIESGO
Ubicación: Centro de Información y Documentación (CANIA)   
Solicite el material por este código: AS-5915
Tipo de Material:
Separata

    The reverse cholesterol transport model is most widely used to explain both the role of high density lipoproteins (HDL) in lipid metabolism and the inverse association between HDL cholesterol plasma concentration and the risk for coronary artery disease (CAD). As familial HDL cholesterol deficiency is frequently paralleled with a family history of premature CAD, much interest has been directed toward the molecular defects in apolipoproteins and lipid-transfer enzymes involved in the formation and metabolism of HDL. Knowledge of the basic defects in rare HDL-deficiency syndromes and apolipoprotein variants provides genetic markers of whether the presence of these molecular defects accounts for low HDL cholesterol levels and the accompanying coronary risk. METHODS AND RESULTS. Sequence analysis of proteins or DNA from patients with HDL deficiency or hyperalphalipoproteinemia as well as from randomly screened probands has helped to identify a series of molecular defects in the genes of apolipoprotein (apo) A-I, apo A-II, apo A-IV, apo C-III, lecithin cholesterol acyltransferase, and cholesterol ester-transfer protein. Some of these mutations were associated with absent and low levels of HDL cholesterol in homozygous and heterozygous carries, respectively, but only a few homozygotes were at an increased risk of CAD. These mutations were invaluable for gaining insight into structural-functional relations in HDL metabolism. CONCLUSIONS. Mutations in the genes of apo A-I, apo A-II, apo A-IV, apo C-III, lecithin cholesterol acyltransferase, and cholesterol ester-transfer protein can influence HDL cholesterol plasma concentrations but do not account for the coronary risk associated with low HDL cholesterol levels. In general, these observations suggest that the low HDL concentrations in CAD patients are not a reflection of impaired reverse cholesterol transport but rather of some other metabolic disturbances, such as catabolism of triglyceride-rich particles.





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