Human apolipoprotein A-I gene promoter mutation influences plasma low density lipoprotein cholesterol response to dietary fat saturation

1998 ◽  
Vol 137 (2) ◽  
pp. 367-376 ◽  
Author(s):  
Pedro Mata ◽  
Jose Lopez-Miranda ◽  
Miguel Pocovi ◽  
Rodrigo Alonso ◽  
Carlos Lahoz ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Zaza Makaridze ◽  
Elene Giorgadze ◽  
Ketevan Asatiani

The study was designed to assess the association between insulin resistance (IR) and apolipoprotein B/apolipoprotein A-I ratio (ApoB/ApoA-I ratio), metabolic syndrome (MetS) components, total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) in the nondiabetic population of Georgia. The subjects were 1522 Georgians of Caucasian origin (mean age = 45 years, 653 women) without diabetes who had visited the clinics for a related health checkup between 2012 and 2013. IR was calculated using the computer homeostasis model assessment (HOMA2-IR) and was defined as the upper quartile. MetS was diagnosed using the updated ATP-III definition of the metabolic syndrome. Logistic and multiple regression models were used to estimate the association between IR and other components. IR was positively correlated with age, ApoB, ApoB/ApoA-I ratio, MetS components (excluding high-density lipoprotein cholesterol—HDL-C), LDL-C, fasting insulin, and TC and negatively correlated with HDL-C and ApoA-I in both sexes (allP<0.001). In the logistic regression models, gender, age, ApoB/ApoA-I ratio, diastolic pressure, HDL-C, LDL-C, fasting glucose, and triglycerides were the covariates significantly associated with IR (OR: 8.64, 1.03, 17.95, 1.06, 0.13, 1.17, 3.75, and 2.29, resp.; allP<0.05). Multiple regression models demonstrated that these components (except for HDL-C) made an independent contribution to the prediction of HOMA2 (allP<0.05).


1994 ◽  
Vol 87 (1) ◽  
pp. 61-67 ◽  
Author(s):  
H. T. Vanhanen ◽  
J. Kajander ◽  
H. Lehtovirta ◽  
T. A. Miettinen

1. Serum cholesterol reduction and changes in cholesterol metabolism were studied during rapeseed oil feeding without and with increasing amounts of sitostanol trans-esterified with rapeseed oil fatty acids and dissolved in rapeseed oil mayonnaise. Fifteen mildly hypercholesterolaemic subjects replaced 50 g of their usual dietary fat by 50 g of rapeseed oil fat mayonnaise for 6 weeks followed by randomization so that eight subjects continued on rapeseed oil mayonnaise alone (control group) for 15 weeks and seven on rapeseed oil mayonnaise with a small dose of sitostanol ester (800 mg/day of sitostanol) for 9 weeks followed by 6 weeks with higher dose of sitostanol ester (2000 mg/day of sitostanol). 2. During the rapeseed oil period the reduction in serum low-density lipoprotein cholesterol was 14% from the home diet. The control-adjusted reduction by the low sitostanol ester dose was 7.4% (not significant) and by the higher dose it was 15.7%. 3. The low dose of sitostanol ester had no consistent effect on cholesterol precursors or cholestanol in serum, reduced serum levels of campesterol and sitosterol by 28.2% and 23.6%, respectively, and reduced cholesterol absorption efficiency significantly from 28.7% to 23.4%. In accordance, faecal excretion of neutral and particularly endogenous neutral sterols increased (16.7% and 19.7%, respectively), but faecal cholesterol elimination and cholesterol synthesis were only insignificantly increased. 4. During the high dose of sitostanol ester the high-density lipoprotein- to low-density lipoprotein-cholesterol ratio increased. Serum levels of cholesterol precursor sterols, indicators of cholesterol synthesis, increased up to 12%, whereas those of cholestanol were slightly decreased and those of campesterol and sitosterol values were further reduced by 30% and 25.6%, respectively. 5. Associations of serum plant sterols and cholesterol precursors with cholesterol absorption efficiency and synthesis and the sitostanol-ester-induced changes in serum campesterol and lathosterol proportions with those in serum low-density lipoprotein-cholesterol suggest that reduced cholesterol absorption efficiency was the main reason for cholesterol reduction and that there was a compensatory increase in cholesterol synthesis. 6. The findings indicate that sitostanol ester dissolved in dietary fat is apparently unabsorbable and interferes with sterol absorption so that the serum levels of cholesterol and low-density lipoprotein-cholesterol are reduced to the extent that sitostanol ester-fat mixture in reasonable daily amounts can be recommended to replace dietary fat for lowering of serum cholesterol.


Author(s):  
Simone C. Sorkin ◽  
Francisco J. Forestiero ◽  
Mario H. Hirata ◽  
Elizabeth C. R. Guzmán ◽  
Selma A. Cavalli ◽  
...  

AbstractBackground: Apolipoprotein A-I gene (Methods:Results: G–75A polymorphism was associated with differences in serum concentrations of triglyceride and very low-density lipoprotein (VLDL)-cholesterol (p=0.026) in HC men. After atorvastatin treatment, women carrying theConclusion: Our data suggest that


1999 ◽  
Vol 274 (17) ◽  
pp. 11564-11572 ◽  
Author(s):  
Elisabeth Boisfer ◽  
Gilles Lambert ◽  
Véronique Atger ◽  
Nhuan Quang Tran ◽  
Danièle Pastier ◽  
...  

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