Biomedical subjects

Carmen Marín

Publications and source records attributed to Carmen Marín.

18 recordsLinked to original sources

PubMed2006

The Mediterranean and CHO diets decrease VCAM-1 and E-selectin expression induced by modified low-density lipoprotein in HUVECs.

BACKGROUND AND AIM: The oxidative modifications of low-density lipoprotein (LDL) are crucial for the atherosclerosis process. The aim of this study was to determine if the minimally modified LDL, obtained after the ingestion of three different diets, produce differential effects on the vascular cell adhesion molecule-1 (VCAM-1) and E-selectin expression in human umbilical endothelial cells (HUVECs). METHODS AND RESULTS: Twenty healthy young males were exposed to three dietary periods. Each period lasted four weeks. During the first period, all subjects consumed a saturated fat (SFA) enriched diet (38% fat, 20% SFA). The second and third dietary periods were administered following a randomized crossover design: a low fat high carbohydrates diet (CHO diet) and a Mediterranean diet. LDL particles, isolated during each dietary period, were oxidized by exposure to UV light and incubated for 48 h with HUVEC. Thereafter, 100 U/mL of TNF-alpha was added and incubation continued for 6 h. Cellular ELISA determined adhesion molecules expression. Lag time, propagation rate and total amounts of formed conjugated dienes were calculated in LDL incubated with 10mumol/L Cu(2+). When compared to the SFA diet, LDL isolated from the Mediterranean and CHO diets induced a lower expression of VCAM-1 and E-selectin in HUVECS (P<0.007). There were no differences between both lipid lowering diets. However, lag time of LDL from the Mediterranean diet was higher than with the CHO diet (P<0.042). This parameter was inversely correlated with E-selectin expression (r=-0.497; P<0.04). CONCLUSION: Our results suggest that both the Mediterranean and CHO diets may decrease the pro-inflammatory environment induced by modified LDL in endothelial cells.

Adult↗

PubMed2006

Postprandial lipoprotein metabolism, genes and risk of cardiovascular disease.

PURPOSE OF REVIEW: Several lines of evidence suggest that postprandial lipemia increases the risk of atherogenesis, and in each of the systems involved in postprandial metabolism the roles of many genes have been explored in order to establish the possible implications of their variability in coronary heart disease risk. RECENT FINDINGS: This report focuses on recent results pertaining to postprandial lipoprotein metabolism and genes, their variability and their relationship with intermediate phenotypes and coronary heart disease. The postprandial lipid response was modified by polymorphisms within the genes for apolipoprotein AI, apolipoprotein E, apolipoprotein B, apolipoprotein CI, apolipoprotein CIII, apolipoprotein AIV, apolipoprotein AV, lipoprotein lipase, hepatic lipase, fatty acid-binding protein-2, the fatty acid transport proteins, microsomal triglyceride transfer protein and scavenger receptor class B type I. We also discuss recent advances in the effects of gene regulation using knockdown animal models on postprandial lipoprotein metabolism. SUMMARY: The review discusses several of these factors as well as the potential impact of gene polymorphism on the variability of postprandial lipoprotein metabolism as intermediate phenotypes for coronary heart disease. The variability in postprandial lipid response is highly complex. Future studies will need to be large if they are to assess the effects of multiple polymorphisms.

Cardiovascular Diseases↗

PubMed2005

A polymorphism exon 1 variant at the locus of the scavenger receptor class B type I (SCARB1) gene is associated with differences in insulin sensitivity in healthy people during the consumption of an olive oil-rich diet.

UNLABELLED: Scavenger receptor class B type I (SCARB1) was described as the first high-density lipoprotein receptor. Increasing evidence indicates that SCARB1 plays additional roles particularly in type 2 diabetes mellitus. Our aim was to determine whether the presence of an exon 1 (G-->A) polymorphism at the SCARB1 gene modifies the insulin sensitivity to dietary fat. METHODS: We studied 59 healthy volunteers (30 men and 29 women, 42 G/G homozygous and 17 G/A heterozygous). Subjects consumed three diets for 4 wk each: a saturated fatty acid (SFA)-rich diet (38% fat, 20% SFA), followed by a carbohydrate (CHO)-rich diet (30% fat, 55% CHO) or a monounsaturated fatty acid (MUFA)-rich diet (38% fat, 22% MUFA) after a randomized crossover design. For each diet, we investigated peripheral insulin sensitivity with the insulin suppression test. RESULTS: Steady-state plasma glucose after the MUFA diet was lower in G/A compared with G/G subjects (P = 0.030). This effect was not observed after CHO and SFA diets (P = 0.177 and 0.957, respectively). Plasma nonesterified free fatty acid values were lower in subjects carrying the A allele for all the diet periods. CONCLUSIONS: Our findings show that carriers of the G/A genotype have significant increases in insulin sensitivity after a MUFA-rich diet compared with G/G individuals.

Adult↗

PubMed2005

The Ala54Thr polymorphism of the fatty acid-binding protein 2 gene is associated with a change in insulin sensitivity after a change in the type of dietary fat.

BACKGROUND: Insulin resistance, a condition associated with type 2 diabetes, results from the interaction of environmental and genetic factors. OBJECTIVE: We examined the influence of the intestinal fatty acid-binding protein 2 (FABP2) Ala54Thr polymorphism on insulin sensitivity. DESIGN: Fifty-nine healthy young subjects (28 were Ala54/Ala54, 27 were Ala54/Thr54, and 4 were Thr54/Thr54) completed 3 diets, each of which lasted 4 wk. The first diet, which all subjects consumed, was a high-saturated fatty acid (SFA) diet (38% of energy as fat and 20% of energy as SFAs). The second and third diets were administered according to a randomized crossover design, and they consisted of a low-fat and high-carbohydrate diet (CHO diet; 28% of energy from fat and <10% of energy from SFAs) and a high-monounsaturated fatty acid (MUFA) diet (called the Mediterranean diet; 38% of energy from fat and 22% of energy from MUFAs). All food and drinks were prepared and provided in the research kitchen. We determined in vivo insulin resistance by using the insulin suppression test with somatostatin. RESULTS: Steady state plasma glucose concentrations were significantly higher in Ala54Thr subjects after the SFA diet than after the CHO diet or the Mediterranean diet. The plasma free fatty acid concentrations in these subjects were significantly lower after the CHO and Mediterranean diets than after the SFA diet. However, no significant differences between the 3 diets were observed in the Ala54 allele homozygotes. CONCLUSION: Insulin sensitivity decreased in subjects with the Thr54 allele of the FABP2 polymorphism when SFAs were replaced by MUFAs and carbohydrates.

Adult↗

PubMed2005

The apolipoprotein E gene promoter (-219G/T) polymorphism determines insulin sensitivity in response to dietary fat in healthy young adults.

Insulin sensitivity (IS) is determined by genetic and environmental factors, including diet. The apoE gene promoter -219G/T polymorphism is associated with coronary heart disease and increased postprandial triacylglycerol-rich lipoprotein concentration, circumstances related to insulin resistance. Thus, our aim was to determine whether this polymorphism modified the IS response to dietary fat in healthy young adults. Volunteers (n = 43) with the apoE3/E3 genotype (8 GG, 25 GT and 10 TT) completed 3 dietary periods, each lasting 4 wk. They first consumed a SFA-rich diet [38% fat (% of energy in the total diet), 20% SFA (% of energy in the total diet)], and then, in a randomized, crossover design, a carbohydrate (CHO)-rich diet (30% fat, 55% CHO) or a monounsaturated fatty acid (MUFA)-rich diet (38% fat, 22% MUFA). After each diet period, we investigated peripheral IS using the insulin suppression test. The steady-state plasma glucose (SSPG) concentration was lower (P < 0.05) in GG subjects than in GT and TT individuals, regardless of the diet consumed. Significant diet x genotype interactions were found for SSPG and plasma nonesterified FFA (NEFA) concentrations. Thus, the shift from the SFA-rich diet to the MUFA- or CHO-rich diets decreased (P < 0.05) the SSPG and NEFA concentrations in GG and GT, but not in TT subjects. In conclusion, carriers of the -219T allele are less insulin sensitive than GG individuals. Furthermore, only carriers of the -219G allele have improved IS when MUFA- or CHO-rich diets are consumed instead of a SFA-rich diet.

Adult↗

PubMed2005

The -514 C/T polymorphism in the hepatic lipase gene promoter is associated with insulin sensitivity in a healthy young population.

Impaired insulin action has been associated with diabetes, dyslipidemia and atherosclerotic vascular disease. The expression of insulin resistance results from the interaction of environmental and genetic factors. Human hepatic lipase (HL) is a lipolytic enzyme that plays a role in the metabolism of several lipoproteins, while insulin up-regulates the activity of HL via insulin-responsive elements in the HL promoter. We have examined the influence of -514 C/T polymorphism in the hepatic lipase gene promoter on insulin sensitivity in 59 healthy young subjects (30 males and 29 females). The volunteers were subjected to three dietary periods, each lasting four weeks. During the first period all subjects consumed a saturated fat (SFA)-enriched diet with 38% as fat (20% SFA, 12% monounsaturated fatty acids (MUFA) and 6% polyunsaturated fatty acids (PUFA)). In the second and third dietary periods, a randomized crossover design was used, consisting of a low fat, high carbohydrate diet (CHO diet) (< 10% SFA, 12% MUFA and 6% PUFA) and a high-MUFA, or Mediterranean diet, with < 10% SFA, 22% MUFA and 6% PUFA. We determined the in vivo insulin resistance using the insulin suppression test with somatostatin. Steady-state plasma glucose (SSPG) concentrations (a measure of insulin sensitivity) were significantly higher in men carriers of the -514T allele after the consumption of the SFA diet than after the CHO diet and the Mediterranean diet. This effect was not observed in women. Moreover, there were no significant differences in insulin sensitivity after the three diets in men and women with the CC genotype. In summary, our results show an improvement in insulin sensitivity in men with the -514T allele of the HL promoter polymorphism, when MUFA and carbohydrates are consumed instead of SFA fat.

Adult↗

PubMed2005

[Effect of the Mediterranean diet on fasting concentrations of activated factor VII in healthy persons].

INTRODUCTION AND OBJECTIVES: Many clinical and epidemiologic studies suggest that activated factor VII may be involved in the pathogenesis of coronary heart disease. Our objective was to determine the effect of a Mediterranean diet on plasma levels of activated factor VII in comparison to a low-fat diet and a diet rich in saturated fat. PATIENTS AND METHOD: The study population comprised 16 healthy normolipemic men who consumed 3 different diets in consecutive 28-day periods. The first diet was rich in saturated fat (38% calories as fat, 20% saturated fat), the second was a low-fat, high-carbohydrate diet (28% calories as fat, 10% saturated fat), and the third was enriched in monounsaturated fatty acids (38% calories as fat, 22% monounsaturated fat). At the end of each period, plasma concentrations of total cholesterol, HDL cholesterol, LDL cholesterol, total triglycerides, apolipoprotein A-I, apolipoprotein B, and glucose were measured. Activated factor VII was determined with a coagulation assay. RESULTS: The diet rich in saturated fat was associated with a significant increase in total cholesterol, LDL cholesterol, apolipoprotein AI, and apolipoprotein B in comparison to the other 2 diets. There were no significant differences between the carbohydrate-rich diet and the Mediterranean diet in any of the lipid parameters. The Mediterranean diet decreased plasma levels of factor VIIa in comparison to the diet rich in saturated fat (34.6+/-15.3 mU/mL vs 101.5+/-19.2 mU/mL; P<.05). CONCLUSIONS: In comparison to the diet rich in saturated fat or the high-carbohydrates diet, the Mediterranean diet decreased plasma concentrations of activated factor VII in healthy young men. This phenomenon may constitute another protective mechanism of the Mediterranean diet in reducing cardiovascular risk.

Adult↗

PubMed2004

Effect of simvastatin in familial hypercholesterolemia on the affinity of electronegative low-density lipoprotein subfractions to the low-density lipoprotein receptor.

The effect of simvastatin therapy on the biologic characteristics of the electronegative low-density lipoprotein (LDL) subfraction of patients with familial hypercholesterolemia (FH) was studied. Total LDL, isolated from FH plasma at 0, 3 and 6 months of simvastatin treatment, was subfractionated into electropositive LDL (LDL[+]) and electronegative LDL (LDL[-]) by anion exchange chromatography. LDL isolated from healthy normolipemic (NL) subjects was used as a control. The LDL(-) proportion was twofold higher in patients with FH than in NL subjects (17.6 +/- 1.6% vs 7.8 +/- 1.5%, respectively; p <0.05) and was progressively reduced by simvastatin therapy (15.7 +/- 1.6% at 3 months; 13.8 +/- 2.5% at 6 months; p <0.05). Both LDL subfractions from patients with FH had a higher relative cholesterol content and decreased apolipoprotein B and triglycerides than NL subfractions. Simvastatin progressively induced changes in lipid content of both LDL subfractions in patients with FH, and lipid composition was closer to these subfractions in NL subjects after 6 months of therapy. Binding displacement experiments in human fibroblasts demonstrated that LDL(-) from both groups of subjects had a lower affinity of binding to the LDL receptor that LDL(+). In addition, LDL(+) in patients with FH presented an intermediate binding affinity between LDL(-) and LDL(+) in NL subjects. Simvastatin-induced changes in LDL composition were accompanied by a progressive increase in affinity of LDL(+) and LDL(-) in patients with FH. After 6 months of therapy, LDL(+) in FH had an affinity similar to that of LDL(+) in NL subjects. The LDL(-)-induced release of chemokines interleukin-8 and monocyte chemotactic protein-1 from cultured endothelial cells was twofold higher compared with that of LDL(+). No difference in chemokine release between patients with FH and NL subjects or the effect of simvastatin were observed. We conclude that simvastatin therapy was able to modify LDL subfraction composition in subjects with FH and increase their affinity to the LDL receptor. This improvement could contribute to the observed reduction in LDL(-) proportion induced by simvastatin.

Adult↗

PubMed2004

Influence of the -514C/T polymorphism in the promoter of the hepatic lipase gene on postprandial lipoprotein metabolism.

The -514C/T polymorphism located in the promoter region of the hepatic lipase gene mediates changes in the plasma levels of the enzyme. The aim of this study was to determine whether the presence of this polymorphism modifies the postprandial clearance of lipoproteins of intestinal origin. 51 normolipemic volunteers, homozygotes for the allele E3 of the apo E were selected (26 homozygotes for the C allele and 25 carriers of the T allele in both homozygote and heterozygote form). The subjects underwent a Vitamin A fat-loading test. Blood was drawn every hour until the 6th hour and every 2 h and 30 min until the 11th hour to determine cholesterol and plasma triglycerides as well as cholesterol, triglycerides (TG) and retinyl palmitate in triacylglycerol-rich lipoproteins (chylomicrons and chylomicron remnants). Carriers of the T allele showed significantly lower postprandial levels of apolipoprotein B (P < 0.01), total TG in plasma (P < 0.05), small TRL-TG (P < 0.04), large TRL-TG (P < 0.04) and small TRL-cholesterol (P < 0.04) when compared to subjects homozygous for the C allele. Our data suggest that the T allele of the -514C/T polymorphism in the promoter region of the hepatic lipase gene is associated with a lower postprandial lipemic response.

Adult↗

PubMed2004

Apolipoprotein E gene promoter -219G->T polymorphism increases LDL-cholesterol concentrations and susceptibility to oxidation in response to a diet rich in saturated fat.

BACKGROUND: The apolipoprotein E (APOE) gene promoter polymorphism (-219G-->T) has been associated with increased risk of myocardial infarction, premature coronary artery disease, and decreased plasma apolipoprotein E concentrations. OBJECTIVE: We aimed to determine in healthy subjects whether this polymorphism modifies the susceptibility of LDL to oxidation and the lipid response to the content and quality of dietary fat. DESIGN: Fifty-five healthy men with the APOE3/E3 genotype (7 GG, 38 GT, and 10 TT) completed 3 dietary periods, each lasting 4 wk. The first was a saturated fatty acid (SFA)-rich diet [38% fat-20% SFA and 12% monounsaturated fatty acid (MUFA)-and 47% carbohydrates (CHO)], which was followed by a CHO-rich diet (30% fat-<10% SFA and 12% MUFA-and 55% CHO) or a MUFA-rich diet (38% fat-<10% SFA and 22% MUFA-and 47% CHO) in a randomized crossover design. At the end of each dietary period, LDL oxidation susceptibility, lipids, and lipoproteins were measured. RESULTS: Compared with carriers of the G allele, TT subjects had a significantly (P < 0.05) shorter lag time after the SFA diet. The replacement of the SFA diet by the CHO or MUFA diet induced a greater increase (P < 0.05) in lag time in the TT subjects than in the GG or GT subjects. Carriers of the T allele had higher LDL-cholesterol (P < 0.05) and apolipoprotein B (P < 0.05) plasma concentrations after the SFA diet than did GG subjects. Compared with GG subjects, carriers of the T allele had a significantly (P < 0.05) greater decrease in LDL cholesterol and apolipoprotein B when they changed from the SFA to the CHO diet. CONCLUSION: The -219G-->T polymorphism may partially explain differences in individual responses to diet.

Apolipoprotein E3↗

PubMed2004

Butter and walnuts, but not olive oil, elicit postprandial activation of nuclear transcription factor kappaB in peripheral blood mononuclear cells from healthy men.

BACKGROUND: Nuclear transcription factor kappaB (NF-kappaB) plays an important role in atherosclerosis by modulating gene expression. Postprandial lipemia has been correlated with an increase in NF-kappaB activation in vascular cells and it is associated with an increase in postprandial triacylglycerol-rich lipoproteins, which are involved in the development of atherosclerotic plaque. OBJECTIVE: The objective of this study was to determine the effect of the intakes of 3 different foods with different fat compositions on the postprandial activation of monocyte NF-kappaB. DESIGN: Eight healthy men followed a 4-wk baseline diet and then consumed 3 fat-load meals consisting of 1 g fat/kg body wt (65% fat) according to a randomized crossover design. Each meal had a different fatty acid composition, and the consumption of each meal was separated by 1 wk. The compositions of the 3 test meals were as follows: olive oil meal [22% saturated fatty acids (SFAs), 38% monounsaturated fatty acids (MUFAs), 4% polyunsaturated fatty acids (PUFAs), and 0.7% alpha-linolenic acid], butter meal (38% SFAs, 22% MUFAs, 4% PUFAs, and 0.7% alpha-linolenic acid), and walnut meal (20% SFAs, 24% MUFAs, 16% PUFAs, and 4% alpha-linolenic acid). RESULTS: Ingestion of the olive oil meal did not elicit NF-kappaB activation compared with ingestion of either the butter meal at 3 h (P <0.05) or the walnut meal at 9 h (P <0.05). There was no significant difference in the postprandial triacylglycerol response between the 3 meals. CONCLUSIONS: Consumption of an olive oil-enriched meal does not activate NF-kappaB in monocytes as do butter and walnut-enriched meals. This effect could enhance the cardioprotective effect of olive oil-enriched diets.

Arteriosclerosis↗

PubMed2004

The effect of dietary fat on LDL size is influenced by apolipoprotein E genotype in healthy subjects.

LDL particle size is dependent on both genetic factors and environmental factors such as dietary fat composition. The apolipoprotein E (apoE) genotype is a major genetic determinant of LDL size. Thus, the aim of this work was to study whether the apoE genotype interacts with the quantity and quality of dietary fat, modifying LDL size in young healthy subjects. Healthy subjects (n = 84; 66 apoE 3/3, 8 apoE 4/3, 10 apoE 3/2) were subjected to 3 dietary periods, each lasting 4 wk. The first was an SFA-enriched diet (38% fat, 20% SFA), which was followed by a carbohydrate (CHO)-rich diet (30% fat, < 10% SFA, 55% carbohydrate) or a monounsaturated fatty acid (MUFA) olive oil-rich diet (38% fat, 22% MUFA) following a randomized crossover design. At the end of each diet period, LDL particle size and plasma levels of total cholesterol, LDL cholesterol (LDL-C), HDL-C, apoB, apoA-I, and triacylglycerols were determined. LDL particle size was significantly higher (P < 0.04) in subjects with the apoE 4/3 genotype compared with those with apoE 3/3 and apoE 3/2 in the basal state. LDL size was smaller (P < 0.02) after the CHO diet than after the MUFA or SFA diets. After the CHO diet, a significant increase in LDL particle size (P < 0.035) was noted with respect to the MUFA diet in apoE 4/3 subjects, whereas a significant decrease was observed in the apoE 3/3 individuals (P < 0.043). In conclusion, a Mediterranean diet, high in MUFA-fat increases LDL particle size compared with a CHO diet, and this effect is dependent of apoE genotypes.

Adult↗

PubMed2004

The influence of lipoprotein lipase gene variation on postprandial lipoprotein metabolism.

Lipoprotein lipase (LPL) is one of the key enzymes in the metabolism of triacylglycerol-rich lipoproteins (TRL). We evaluated whether the association of LPL HindIII (H1/H2) and Serine447-Stop (S447X) polymorphisms may explain the interindividual variability observed during postprandial lipemia. Fifty-one healthy male volunteers (26 with the H2S447 genotype, 15 with the H1X447 genotype, and 10 with the H1S447 genotype) were subjected to a vitamin A-fat load test consisting of 1 g fat/kg body weight and 60,000 IU vitamin A. Blood was drawn every hour until the 6th hour and every 2 h and 30 min until the 11th hour. Data revealed that subjects that are homozygous for the H2 allele (H2H2) showed a higher postprandial response for small TRL, retinyl palmitate (RP), large TRL-RP, large TRL-B48, and small TRL-B48 levels. Furthermore, in the case of the S447X polymorphism, 447Ter carriers had a lower postprandial response for small TRL-RP, large TRL-B48, and small TRL-RP. Subjects with the LPL H2S447 genotype had higher plasma triacylglycerol, large TRL-triacylglycerol, large TRL-RP, small TRL-RP, and large TRL-B48 (P < 0.037) than H1X447 subjects. The modifications observed in postprandial lipoprotein metabolism in young normolipemic males with LPL polymorphism could be involved in the lower risk of coronary artery disease associated with the H1X447 genotype.

Adolescent↗

PubMed2003

The influence of the apolipoprotein E gene promoter (-219G/ T) polymorphism on postprandial lipoprotein metabolism in young normolipemic males.

The apolipoprotein E (apoE) gene promoter (-219G/T) polymorphism has been associated with increased risk of myocardial infarction, premature coronary heart disease, and decreased plasma apoE concentrations. We examined whether the -219G/T polymorphism could modify the postprandial response of triacylglycerol-rich lipoproteins (TRLs). Fifty-one healthy apoE 3/3 male volunteers (14GG, 29GT, and 8TT) were given a vitamin A fat-loading test consisting of 1 g of fat/kg body weight and 60,000 IU of vitamin A per m2 of body surface area. Blood samples were taken at time 0 and every hour until the sixth hour, and every 2 hours and 30 minutes until the eleventh hour. Cholesterol, triacylglycerols (TGs), and apoE were determined in plasma; and cholesterol, TG, apoB-100, apoB-48, and retinyl palmitate (RP) were analyzed in lipoprotein fractions. Postprandial lipemia data revealed that subjects with the -219TT genotype had a higher postprandial response of large TRL-cholesterol (P < 0.03), large TRL-triacylglycerols (P < 0.001), large TRL-RP (P < 0.004), and small TRL-apoB-48 (P < 0.03) than carriers of the -219G allele. Moreover, the -219TT subjects had the lowest postprandial levels of serum apoE (P < 0.05). In conclusion, the -219G/T polymorphism may influence TRL metabolism during the postprandial period, thus prolonging postprandial lipemia in subjects with the TT genotype.

Adolescent↗

PubMed2003

The apo A-I gene promoter region polymorphism determines the severity of hyperlipidemia after heart transplantation.

BACKGROUND: To study whether the Apolipoprotein A-I (apo A-I) promoter region gene polymorphism produces changes in the lipid profile of heart transplant recipients. METHODS: One hundred and three heart transplant recipients (93 men and 10 women, with a mean age of 47 +/- 13 yr) receiving triple immunosuppressive therapy were submitted to a genetic study of the apo A-I gene promoter region. Anthropometric and analytical data, including lipid profile, arterial blood pressure, were collected prior to transplantation and 3, 6, 12, and 24 months after transplantation. RESULTS: Sixty-three subjects had the GG genotype and 40 the GA genotype. Carriers of the GA genotype had higher triglyceride levels at 6 months and 2 yr (2.50 +/- 1.20 versus 1.93 +/- 0.98 mmol/L and 2.46 +/- 1.58 versus 1.60 +/- 0.68 mmol/L, respectively, p < 0.001), and a greater rise in LDL-cholesterol at 1 yr than the GG subjects (4.57 +/- 1.16 versus 4.16 +/- 1.18 mmol/L, p < 0.05). Multiple regression analyses showed that genetic variants at the apo A-I promoter region are responsible for 11% of the variability in triglyceride levels at 6 months (p = 0.005). CONCLUSIONS: The GA genotype of the apo A-I promoter region produces a greater rise in plasma triglyceride and LDL-cholesterol levels in heart transplant patients.

Apolipoprotein A-I↗

PubMed2003

Polymorphism exon 1 variant at the locus of the scavenger receptor class B type I gene: influence on plasma LDL cholesterol in healthy subjects during the consumption of diets with different fat contents.

BACKGROUND: The association between polymorphisms in the scavenger receptor class B type I (SRB-I) gene and variations in basal plasma concentrations of cholesterol in humans has recently been described. OBJECTIVE: The objective of the study was to determine whether the exon 1 variant (G-->A) at the SRB-I gene is associated with the lipid response to the content and quality of dietary fat in healthy subjects. DESIGN: We studied 97 healthy volunteers with exon 1 polymorphism [65 homozygous for allele 1 (1/1) and 32 heterozygous for allele 2 (1/2)]. Both groups consumed 3 diets lasting 4 wk each. The first was a saturated fatty acid (SFA)-rich diet (38% fat, 20% SFA), which was followed by a carbohydrate (Cho)-rich diet (30% fat, < 10% SFA, 55% carbohydrate) or a monounsaturated fatty acid (MUFA), olive oil-rich diet (38% fat, 22% MUFA) according to a randomized crossover design. At the end of each dietary period, plasma concentrations of triacylglycerol and of total, LDL, and HDL cholesterol were measured. RESULTS: Carriers of the 1/2 genotype had a trend toward higher concentrations of LDL cholesterol (P < 0.11) after the SFA-rich diet than did those who were homozygous for 1/1. Carriers of the mutation showed a significantly greater (P = 0.007) decrease in LDL-cholesterol concentrations (-23%) in changing from an SFA-rich diet to a Cho-rich diet than did noncarriers of the mutation (-16%). CONCLUSION: Carriers of the minority allele, 1/2, are more susceptible to the presence of SFA in the diet because of a greater increase in LDL cholesterol.

Alleles↗

PubMed2002

[Response degree of cholesterol LDL to feeding in males with hypercholesterolemia according to baseline value].

BACKGROUND: The response of plasma cholesterol to diet is modulated by endogenous and exogenous factors such as body mass, tobacco consumption, gender and the genetic background. Our purpose was to know whether the response degree depends on the concentration of cholesterol prior to the intervention and whether several polymorphisms modulating the cholesterol response to diet are actually involved in such response. PATIENTS AND METHOD: Seventy two males with hypercholesterolemia were administered three different 4-weeks duration diets. The first one was a saturated fat-enriched (SAT) diet. Then, in a randomized and crossed manner, subjects were categorized in two groups: one group received a diet with low fat but high complex carbohydrates contents (HCO); the another group received a monounsaturated fat-enriched diet (Mediterranean diet). In the third period, we inverted the diets of the previous period. We determined the prevalent genotypes of the following apoproteins: E, CIII, A-IV, A-I, B, A-IV 360. RESULTS: The diet with low fat contents and the Mediterranean diet led to a significant decrease of total cholesterol, LDL-c and HDL-c. Those at the upper LDL-c tertile, after the SAT diet, were found to have statistically significant greater decreases (absolute and relative values) with the Mediterranean and HCO diet. In the multivariate analysis, the only variable with an effect on the modification of LDL-c, after shifting a SAT to any hypolipidemic diet, were the levels of LDL-c at the end of a SAT diet. The allelic frequency of different apoproteins in the hyper-respondent group was not different from that in the hypo-respondent group (response displayed when going from a SAT period to any hypolipidemic diet). CONCLUSIONS: The decrease of LDL-c observed with hypolipidemic diets (low in fat contents or Mediterranean) was more significant in those individuals with hypercholesterolemia who had higher levels of LDL-c at the onset.

Adolescent↗

PubMed2002

Effects of the human apolipoprotein A-I promoter G-A mutation on postprandial lipoprotein metabolism.

BACKGROUND: There is considerable interindividual variability in the postprandial lipid response to a fat-rich meal, and genetic factors have been considered to account for some of these effects. We previously showed that the G-A mutation 5' to the apolipoprotein (apo) A-I gene was significantly associated with the LDL-cholesterol response to diet. OBJECTIVE: We evaluated whether this effect is mediated by mechanisms involving postprandial lipoprotein metabolism. DESIGN: Twenty-eight G/G and 23 G/A healthy male subjects, homozygotes for the apo E3 allele, were subjected to a vitamin A fat-loading test. Blood was drawn at time 0 and every hour for 11 h. RESULTS: There was a significant postprandial decrease in plasma cholesterol, LDL cholesterol, and apo B in G/G subjects but not in G/A subjects. A greater postprandial response in large triacylglycerol-rich lipoproteins (TRLs) and a smaller postprandial response in large TRL apo A-IV was observed in G/A than in G/G subjects. Retinyl palmitate in large and small TRL concentrations was similar for both genotypes. No significant genotype effects were detected for triacylglycerol concentrations in plasma, small TRL fraction, and apo A-I and HDL-cholesterol concentrations. CONCLUSION: Our data suggest that the G-A mutation affects the LDL-cholesterol response to diet by mechanisms involving postprandial lipoprotein cholesterol metabolism.

Adult↗