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Biomedical subjects

J Jimenez-Pereperez

Publications and source records attributed to J Jimenez-Pereperez.

6 recordsLinked to original sources
PubMed2000

The effect of apolipoprotein B xbaI polymorphism on plasma lipid response to dietary fat.

BACKGROUND AND AIMS: Lipid response to dietary fat and cholesterol is, to a large extent, genetically controlled. Apolipoprotein B (apo B) plays a dominant role in cholesterol homeostasis. Several polymorphic sites within or adjacent to the gene locus for apo B have been detected. The X+ allele of the XbaI restriction fragment polymorphism of the apo B gene has been found to be associated with higher serum cholesterol and/or triglyceride levels. In order to study the influence of this mutation on the plasma lipid response in diets of varying fat content, 72 healthy male subjects were studied, 21 X- X- (X-) and 51 X+ (X+ X- or X+ X+). METHODS AND RESULTS: These subjects followed three consecutive 28-day diet periods: one rich in saturated fats (SAT diet; 38% fat, 20% saturated); a National Cholesterol Education Program type I diet (NCEP-I diet) (28% fats, < 10% saturated); and a third monounsaturated (MUFA diet) (38% fats, 22% monounsaturated). The different genotypes can be observed to have significant effects on total and LDL cholesterol concentrations (P < 0.017). X+ individuals had higher levels of total and LDL cholesterol after the consumption of a SAT diet (P < 0.012; P < 0.006, respectively), NCEP diet (P < 0.060; P < 0.054, respectively) and MUFA diet (P < 0.022; P < 0.042, respectively) in comparison with X- individuals. A significant interaction between genotypes and dietary effects was observed for diet-induced changes in plasma triglycerides (P < 0.032). Significant decreases in the absolute values of triglyceride concentrations (-0.18 mmol L(-1), P < 0.024) were noted in the X- subjects after the high intake of a MUFA diet, while no significant differences were observed in the X+ individuals (0.006 mmol L(-1), P < 0.858). CONCLUSIONS: Our results suggest that the total triglyceride response to diet is influenced by the apo B XbaI polymorphism.

Adult↗
PubMed1998

Dietary fat clearance is modulated by genetic variation in apolipoprotein A-IV gene locus.

Previous studies have shown that the A-IV-347Ser polymorphism is associated with the variability in low density lipoprotein (LDL)-cholesterol response to dietary therapy. The present study was designed to evaluate the association of this polymorphism with the individual variability observed in postprandial lipemic response. This polymorphism was characterized in 50 healthy male subjects homozygous for the apolipoprotein (apo)E3 allele. All subjects were subjected to a vitamin A-fat load test. Blood was drawn at time 0 and every hour over a period of 11 hours. Cholesterol and triglycerides (TG) in plasma and lipoprotein fractions of CH, TG, and retinyl palmitate (RP) were determined. Data from the postprandial lipemia revealed that subjects with the A-IV-347Ser allele (n = 14) have a lower postprandial response in total TG (P < 0.025), large triglyceride rich lipoproteins (TRL) TG (P < 0.02), and small-TRL TG levels (P < 0.007), and a higher postprandial response in large-TRL apoA-IV (P < 0.006) and apoB-100 (P < 0.041) levels than subjects homozygous for the A-IV-347Thr subjects (n = 36). In conclusion, the modifications observed in postprandial lipoprotein metabolism associated with this polymorphism within the apoA-IV gene locus may be involved in the variability in LDL-CH response observed in subjects consuming high saturated fat diets.

Adolescent↗
PubMed1996

Monounsaturated fatty acid-enriched diet decreases plasma plasminogen activator inhibitor type 1.

An increase in levels of plasma plasminogen activator inhibitor type 1 (PAI-1) is one of the main hemostatic alterations in patients with coronary heart disease. Despite growing interest in the fibrinolytic system, few studies have been undertaken to determine the effect exerted on it by the different dietary fatty acids. We investigated the effect of a monounsaturated fat (MUFA)-rich diet in comparison with a low-fat diet (National Cholesterol Education Program step 1 diet) (NCEP-1) on factors involved in blood coagulation and fibrinolysis. We also determined the effect of dietary cholesterol on these blood parameters. Twenty-one young, male, healthy volunteers followed two low-fat/high-carbohydrate diets (< 30% fat, < 10% saturated fat, 14% MUFA) for 24 days each, with 115 or 280 mg of cholesterol per 1000 kcal per day, and two oleic acid-enriched diets (38% fat, 24% MUFA) with the same dietary cholesterol as the low-fat/high-carbohydrate diets. Plasma levels of fibrinogen, thrombin-antithrombin complexes, prothrombin fragments 1+2, plasminogen, alpha 2 antiplasmin, and tissue plasminogen activator were not significantly different among the experimental diets used in this study. Consumption of the diet rich in MUFA resulted in a significant decrease in both PAI-1 plasma activity (P < .005) and antigenic PAI-1 (P < .04) compared with the carbohydrate-rich diet (NCEP-1). The addition of dietary cholesterol to each of these diets did not result in any significant additional effect. Changes in insulin levels and PAI-1 activity were positively correlated (r = .425; P < .02). In conclusion, consumption of diets rich in MUFAs decreases PAI-1 plasma activity, which is accompanied by a parallel decrease in plasma insulin levels.

Adult↗
PubMed1995

Lipoprotein concentrations in normolipidemic males consuming oleic acid-rich diets from two different sources: olive oil and oleic acid-rich sunflower oil.

The effects on plasma lipid concentrations of two oleic acid-rich diets, prepared with two different plant oils--olive oil and sunflower oil high in monounsaturated fatty acids (MUFAs)-- were compared with a National Cholesterol Education Program (NCEP) I diet. Twenty-one healthy, normolipidemic, young males consumed an NCEP-I diet (30% of energy as fat) during a 25-d period. Subjects were then assigned to two 4-wk study periods, according to a randomized, crossover design. Group one was placed on an olive oil-enriched diet (40% fat, 22% MUFAs), followed by a 4-wk period of a sunflower oil-enriched diet (40% fat, 22% MUFAs). In group two, the order of the diets was reversed. Both MUFA dietary periods resulted in an increase in high-density-lipoprotein (HDL) cholesterol (7% for the olive oil diet and 4% for the sunflower oil diet) and in apolipoprotein (apo) A-I (9% for both) compared with the NCEP-I diet. Low-density-lipoprotein (LDL) cholesterol and apo B concentrations (x +/- SEM) were lower (P < 0.05) during the sunflower oil diet (2.40 +/- 0.11 mmol/L, 0.85 +/- 0.04 mg/L) than during the olive oil diet (2.64 +/- 0.15 mmol/L, 0.93 +/- 0.05 mg/L). No significant differences were observed in these variables between the sunflower oil and NCEP-I (2.48 +/- 0.13 mmol/L, 0.89 +/- 0.04 mg/L) diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Influence of mutation in human apolipoprotein A-1 gene promoter on plasma LDL cholesterol response to dietary fat.

The plasma lipid response to changes in dietary fat and cholesterol can vary between individuals. At present, responders cannot be identified in advance. An adenine to guanine (A-->G) mutation in the promoter of the apolipoprotein A1 gene (apoA-1) has been suggested as affecting plasma high-density lipoprotein cholesterol. In 50 young men we examined the effect of the same mutation on the responses of both high and low density lipoprotein cholesterol to low-fat diet. The frequency for the A allele was 0.14. Subjects were fed a low-fat diet for 25 days, followed by a diet rich in monounsaturated fatty acid (MUFA, 22% out of 40% fat) for 28 days and lipoproteins were measured at the end of each diet. There were no differences in initial total cholesterol between subjects with the G/G mutation (170 mg/dL: 100 mg/dL = 2.59 mmol/L) and the G/A mutation (169 mg/dL) genotypes. After consumption of the high monounsaturated fat diet, significant increases were noted in plasma LDL cholesterol (10 mg/dL, p = 0.035) in the G/A subjects but not in the G/G subjects (1 mg/dL, p = 0.996). These differences showed that a significant diet-gene interaction (p = 0.015) existed. No differences were observed on HDL cholesterol between groups. Plasma low-density lipoprotein cholesterol responsiveness to diet may be explained by variation at the apoA-I gene locus.

Adult↗