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J Dallongeville

Publications and source records attributed to J Dallongeville.

At least 55 records · Page 3Linked to original sources
PubMed1999

Lipid and lipoprotein analysis of cats with lipoprotein lipase deficiency.

BACKGROUND: We have previously described a colony of domestic cats with a naturally occurring mutation in the lipoprotein lipase (LPL) gene. We have now further characterized cats homozygous for LPL deficiency (LPL -/-, homozygotes), and have contrasted these with heterozygotes (LPL +/-) and normal cats (LPL +/+). MATERIALS AND METHODS: Density gradient ultracentrifugation with subsequent lipid analysis, agarose and polyacrylamide gel electrophoresis was used to examine detailed liproprotein differences between the genotypes. Oral fat loading studies and breast milk fatty acid analysis were also performed to further characterize the phenotypic expression of LPL deficiency in this model system. RESULTS: Several lipid abnormalities associated with homozygosity for LPL deficiency were evident. Triglyceride-rich lipoprotein-triglycerides (TRL-TG) and cholesterol (TRL-C) were higher (TRL-TG 2.09 +/- 1.14 vs. 0.15 +/- 0.04 mmol L-1, P < 0.001; TRL-C 0.42 +/- 0.30 vs. 0.11 +/- 0.16 mmol L-1, P < 0.05) in male -/- than in male +/+ cats, as was HDL-cholesterol (HDL-C, 1.75 +/- 0.24 vs. 1.41 +/- 0.14 mmol L-1, P < 0.05). LDL-C levels were lower in homozygous cats than in control cats, similar to what is seen in human LPL deficiency. Oral fat loading studies revealed that homozygous cats have a marked reduced ability to clear plasma TGs in terms of peak time (7 h vs. 3 h), peak height (9.36 vs. 1.1 mmol L-1), area under the TG clearance curve (AUC, 280.3 vs. 2.2 h mmol L-1) and time to return to baseline. Fasting lipid and lipoprotein levels were not significantly different between heterozygous and normal cats. However, oral fat loading in heterozygotes revealed an intermediate phenotype (peak of 2.35 mmol L-1 at 5 h, AUC 13.1 h mmol L-1), highlighting the impaired TG clearance in these animals. CONCLUSION: Thus, LPL deficiency in the cat results in a lipid and lipoprotein phenotype that predominantly parallels human LPL deficiency, further validating the use of these animals in studies on the pathobiology of LPL.

Animals↗
PubMed1999

Influence of mental stress and circadian cycle on postprandial lipemia.

BACKGROUND: Mental stress produces alterations in serum lipids and lipoproteins. OBJECTIVE: The objective was to assess the effect of mental stress during the day and night on postprandial lipoproteins. DESIGN: Fourteen healthy subjects aged 26.6 +/- 5.0 y were given randomly the same meal either at night (0100) or during the day (1300), with or without (control session) a mental stress challenge. The meal contained 40% of estimated daily energy needs. The mental task was performed on a computer and consisted of a task of choice reaction. Blood samples were drawn at baseline and hourly for 7 h after the meal. RESULTS: Urinary epinephrine concentrations were higher (P < 0.012) during the mental task than during the control sessions. Repeated-measures analysis of variance showed that mean postprandial triacylglycerol concentrations were significantly higher (P < 0.02) and total cholesterol (P < 0.0001) and HDL-cholesterol concentrations were significantly lower (P < 0.0001) at night than during the day. The mean postprandial VLDL-triacylglycerol concentration was significantly higher (P < 0.04) during the mental task than during the control sessions. Similarly, the VLDL-cholesterol response, calculated as the area under the postprandial curve, was significantly greater (P < 0.02) during the mental task than during the control sessions. There was no interaction between mental stress and nyctohemeral cycle on postprandial lipoprotein responses, suggesting that both indexes act independently on postprandial lipid metabolism. CONCLUSIONS: Mental stress is associated with increased concentrations of postprandial triacylglycerol-rich lipoprotein fractions. Therefore, postprandial hyperlipidemia is one possible mechanism contributing to the higher risk of ischemic heart disease in stressed people.

Adult↗
PubMed1999

Pinus pinaster oil affects lipoprotein metabolism in apolipoprotein E-deficient mice.

The aim of the present study was to assess the antiatherogenic properties of Pinus pinaster (maritime pine) seed oil. To this end, the effects of P. pinaster oil supplementation on lipoprotein levels and atherosclerotic lesions were compared to those of lard or sunflower oil in apolipoprotein E-deficient mice. Plasma total cholesterol (P < 0.0001) and VLDL + intermediary density lipoprotein (IDL)-cholesterol (P < 0.0001) levels were lower in mice fed P. pinaster and sunflower oil than in those fed the lard diet. In contrast, triglycerides (P < 0.0001) and VLDL + IDL-triglycerides (P < 0.0001) levels were higher in mice fed P. pinaster oil than sunflower oil or lard. The VLDL + IDL lipid composition of apolipoprotein E-deficient mice fed P. pinaster oil was intermediate between that of lard-fed transgenic mice and that of wild-type mice fed nonpurified diet. Using the Triton WR1339 method, the fractional catabolic rate of plasma triglycerides was found to be lower in mice fed P. pinaster oil (P < 0.0001) than sunflower oil or lard diet, suggesting a defective clearance of triglycerides in the P. pinaster group. Finally, the susceptibility of triglyceride-rich lipoproteins to in vitro lipoprotein lipase-mediated lipolysis was lower in the P. pinaster oil-fed group than in the lard-fed group. Despite the differences in VLDL + IDL level and lipid composition, the surface areas of aortic atherosclerotic lesions were not significantly different among mice fed P. pinaster, sunflower or lard diets. In conclusion, the results of the present study indicated that feeding P. pinaster oil had no better preventive effect on aortic atherosclerotic lesion extension in apolipoprotein E-deficient mice than other saturated or polyunsaturated fats.

Animals↗
PubMed1999

Leptin response to carbohydrate or fat meal and association with subsequent satiety and energy intake.

To assess the impact of the macronutrient content of a meal on the postprandial leptin response and its relationship with postprandial satiety, 22 young healthy subjects (11 men and 11 women) were given, in a randomized order, an isoenergetic meal [carbohydrate (81%) or fat (79%)] or remained fasting. Blood sampling and hunger and satiety scores were collected hourly during 9 h after the meal. Spontaneous intake was measured at a buffet meal at 9 h postprandially. In both genders, leptin response was higher after the carbohydrate meal than after the fat meal and while fasting. In women, leptin levels were higher after the fat meal than while fasting. Leptin response was significantly correlated to insulin response (r = 0.51, P < 0.0001). Hunger and satiety ratings and subsequent energy intake were not different after carbohydrate or fat intake. In conclusion, a carbohydrate meal induces higher postprandial leptin levels than an isoenergetic fat meal. Short-term regulation of postprandial satiety and food intake is not influenced by circulating leptin.

Adult↗
PubMed1999

Cell culture conditions determine apolipoprotein CIII secretion and regulation by fibrates in human hepatoma HepG2 cells.

Fibrates are widely used drugs which lower triglycerides and increase HDL concentrations in serum. Recent findings from our laboratory have shown that fibrates repress apolipoprotein (apo) CIII gene expression, an effect that explains partially the triglyceride-lowering activity of these drugs. The goal of the present study was to compare the effect of various fibrates on apo CIII gene expression in the human hepatoblastoma cell line HepG2. First, we demonstrate that the level of apo CIII secretion by HepG2 cells is controlled by serum factors whereas apo CIII mRNA levels are not and even increase under conditions when apo CIII secretion dramatically decreases. Twelve different fetal calf serum batches were tested during this study and apo CIII secretion in cell medium could only be detected with three of them. The effect of serum on apolipoprotein secretion was more pronounced for apo CIII whereas other apolipoproteins (apo E, apo B, apo AII and apo AI) were affected to a lesser extent. Under serum conditions allowing apo CIII secretion, treatment with the peroxisome-proliferator activated receptor (PPAR)alpha activators fenofibrate, gemfibrozil and Wy-14643 result in a marked lowering of apo CIII secretion and gene expression, this effect being most pronounced with Wy-14643. Comparison of the activity of a PPARgamma-specific ligand, the antidiabetic thiazolidinedione, BRL-49653 and a PPARalpha ligand Wy-14643 showed a marked decrease of apo CIII secretion and gene expression after activation of PPARalpha but not PPARgamma. In conclusion, fibrates down-regulate apo CIII gene expression in human HepG2 cells, most likely via PPARalpha but not via PPARgamma. However, these effects are only observed in HepG2 cells cultured under appropriate conditions.

Animals↗
PubMed1999

The T allele of the hepatic lipase promoter variant C-480T is associated with increased fasting lipids and HDL and increased preprandial and postprandial LpCIII:B : European Atherosclerosis Research Study (EARS) II.

The common C-480T transition in the hepatic lipase (HL) promoter has been shown to be associated with lower HL activity and increased high density lipoprotein (HDL) cholesterol. We examined the frequency and lipid associations of this HL polymorphism in 385 healthy, young (18- to 28-year-old) men whose fathers had had a premature myocardial infarction (designated cases) and 405 age-matched controls. These individuals were participants in the European Atherosclerosis Research Study II postprandial trial, who had been recruited from 11 European countries in 4 regions (the Baltic; United Kingdom; and central and southern Europe). Overall, the frequency of the T allele was 0.207 in controls and 0.244 in cases (P=0.08). The T allele was associated with higher fasting plasma total cholesterol (P<0.01), triglycerides (P<0.01), and HDL cholesterol (P<0.01). The strongest association was found with apolipoprotein (apo) A-I concentration, which was 10% higher in individuals homozygous for the T allele compared with those homozygous for the C allele (P<0.001). This polymorphism had no effect on the rise in plasma triglyceride levels after a fatty meal. However, before and after the fat load was ingested, levels of particles containing both apoC-III and apoB (LpC-III:B) were higher in carriers of the T allele, with homozygotes having 23% and 27% higher levels preprandially and postprandially, respectively, than those homozygous for the C allele (P<0.05). Thus, our results demonstrate that the C-480T polymorphism in the HL promoter is associated with alterations in plasma lipids and lipoproteins and the accumulation of atherogenic LpC-III:B particles.

Adolescent↗
PubMed1999

Modulation of rat liver apolipoprotein gene expression and serum lipid levels by tetradecylthioacetic acid (TTA) via PPARalpha activation.

3-Thia fatty acids are modified fatty acids that promote hepatic peroxisome proliferation and decrease serum triacylglycerol, cholesterol and free fatty acid levels in rats. In vivo administration of tetradecylthioacetic acid (TTA) to rats led to a significant decrease in liver apolipoproteins apoA-I, A-II, A-IV, and C-III mRNA levels, and to an increase of liver acyl-CoA oxidase (ACO), carnitine palmitoyltransferase-II, and 3-hydroxy-3-methylglutaryl coenzyme A synthase (HMG-CoA synthase) mRNA levels and activities. By contrast, no significant changes of lipoprotein lipase (LPL) mRNA levels were detected in rat epididymal adipose tissue. Liver carnitine palmitoyltransferase-I, apoB, apoE, and LDL receptor mRNA levels were not significantly affected. When tested in vitro, TTA increased rat ACO and carnitine palmitoyltransferase-I mRNA levels in primary rat hepatocytes and also LPL mRNA levels in 3T3-L1 preadipocytes. TTA also enhanced the transcriptional activity of chimeras containing the DNA binding domain of the yeast transcription factor Gal4 fused to the ligand binding domain of either human PPARalpha or human PPARgamma. The effect depended on the concentration tested and the cell type. In conclusion, our data suggest that in vitro, TTA activates both PPARalpha and PPARgamma, but the latter with much lower affinity. TTA affects serum lipid levels in vivo in rats by acting mainly on the liver via PPARalpha where it decreases the liver expression of genes involved in vascular lipid transport and increases the expression of genes involved in intracellular fatty acid metabolism. -Raspé, E., L. Madsen, A-M. Lefebvre, I. Leitersdorf, L. Gelman, J. Peinado-Onsurbe, J. Dallongeville, J-C. Fruchart, R. Berge, and B. Staels. Modulation of rat liver apolipoprotein gene expression and serum lipid levels by tetradecylthioacetic acid (TTA) via PPARalpha activation.

3T3 Cells↗
PubMed1998

Mechanism of action of fibrates on lipid and lipoprotein metabolism.

Treatment with fibrates, a widely used class of lipid-modifying agents, results in a substantial decrease in plasma triglycerides and is usually associated with a moderate decrease in LDL cholesterol and an increase in HDL cholesterol concentrations. Recent investigations indicate that the effects of fibrates are mediated, at least in part, through alterations in transcription of genes encoding for proteins that control lipoprotein metabolism. Fibrates activate specific transcription factors belonging to the nuclear hormone receptor superfamily, termed peroxisome proliferator-activated receptors (PPARs). The PPAR-alpha form mediates fibrate action on HDL cholesterol levels via transcriptional induction of synthesis of the major HDL apolipoproteins, apoA-I and apoA-II. Fibrates lower hepatic apoC-III production and increase lipoprotein lipase--mediated lipolysis via PPAR. Fibrates stimulate cellular fatty acid uptake, conversion to acyl-CoA derivatives, and catabolism by the beta-oxidation pathways, which, combined with a reduction in fatty acid and triglyceride synthesis, results in a decrease in VLDL production. In summary, both enhanced catabolism of triglyceride-rich particles and reduced secretion of VLDL underlie the hypotriglyceridemic effect of fibrates, whereas their effect on HDL metabolism is associated with changes in HDL apolipoprotein expression.

Humans↗
PubMed1998

Retinoids increase human apo C-III expression at the transcriptional level via the retinoid X receptor. Contribution to the hypertriglyceridemic action of retinoids.

Hypertriglyceridemia is a metabolic complication of retinoid therapy. In this study, we analyzed whether retinoids increase the expression of apo C-III, an antagonist of plasma triglyceride catabolism. In men, isotretinoin treatment (80 mg/d; 5 d) resulted in elevated plasma apo C-III, but not apo E concentrations. In human hepatoma HepG2 cells, retinoids increased apo C-III mRNA and protein production. Transient transfection experiments indicated that retinoids increase apo C-III expression at the transcriptional level. This increased apo C-III transcription is mediated by the retinoid X receptor (RXR), since LG1069 (4-[1-(5,6,7,8-tetrahydro-3,5,5,8, 8-pentamethyl-2-naphtalenyl)ethenyl]benzoic acid), a RXR-specific agonist, but not TTNPB ((E)- 4-[2-(5,6,7,8-tetrahydro-5,5,8, 8-tetramethyl-2-naphtalenyl)propenyl]benzoic acid), a retinoic acid receptor (RAR)-specific agonist, induced apo C-III mRNA in HepG2 cells and primary human hepatocytes. Mutagenesis experiments localized the retinoid responsiveness to a cis-element consisting of two imperfect AGGTCA sequences spaced by one oligonucleotide (DR-1), within the previously identified C3P footprint site. Cotransfection assays showed that RXR, but not RAR, activates apo C-III transcription through this element either as a homo- or as a heterodimer with the peroxisome proliferator-activated receptor. Thus, apo C-III is a target gene for retinoids acting via RXR. Increased apo C-III expression may contribute to the hypertriglyceridemia and atherogenic lipoprotein profile observed after retinoid therapy.

Adult↗
PubMed1998

Characterization of two HDL subfractions and LpA-I, LpA-I:A-II distribution profiles and clinical characteristics of hyperalphalipoproteinemic subjects without cholesterol ester transfer protein deficiency.

The aims of the present study were (i) to characterize the HDL2, HDL3 and the LpA-I, LpA-I:A-II distribution, (ii) to investigate the prevalence of atherosclerotic lesions and (iii) to assess the activity of cholesteryl ester transfer protein (CETP) in 29 hyperalphalipoproteinemic (HALP) patients (HDL-C=90+/-11 mg/dl) with combined hypercholesterolemia (LDL-C=180+/-16 mg/dl). According to the HDL2/HDL3 and LpA-I/LpA-I:A-II ratios, two HALP profiles (A and B) were defined: in 22 patients (HALP profile A) these ratios were increased compared to the normolipidemic control subjects (1.19+/-0.11 versus 0.53+/-0.19, P < 0.001 and 1.01+/-0.2 versus 0.51+/-0.25, P < 0.001, respectively) and in seven patients (HALP profile B) these ratios were within the normal range (0.64+/-0.20 and 0.69+/-0.2, respectively). The atherosclerotic lesions were assessed by ultrasonography of the carotid arteries. Amongst patients with HALP profile A, 17 were free from lesions, five had intimal wall thickening and none displayed plaques, whereas for patients within the HALP profile B, only one was free from lesions, two had intimal wall thickening and four displayed plaques. CETP activities (348+/-116 versus 371+/-75%/ml/h) and CETP concentrations (2.4+/-0.5 versus 2.5+/-0.6 microg/ml) were similar in HALP profiles A and B, however these values were both higher than in control subjects (190+/-40%/ml/h, P < 0.001 and 1.8+/-0.3 microg/ml, P < 0.001, respectively). Hence the hyperalphalipoproteinemic profiles (A and B) described here were not related to CETP deficiency. In conclusion, the HALP profile A was characterized by both increased HDL2/HDL3 and LpA-I/LpA-I:A-II ratios and was associated with a low prevalence of atherosclerosis, whereas the HALP profile B, characterized by HDL2/HDL3 and LpA-I/LpA-I:A-II ratios within the normal range, was less cardioprotective.

Adult↗
PubMed1998

Short term response of circulating leptin to feeding and fasting in man: influence of circadian cycle.

OBJECTIVE: To investigate whether acute feeding induces changes in circulating leptin levels in humans and whether these changes vary according to nycthemeral cycle. METHODS: First experiment. Eighteen male subjects were given a fatty meal at 08.00 h. Blood sampling was performed for 10 h following this meal. Second experiment. Thirteen male subjects were given either a mixed meal or remained fasting either at night (starting at 01.00 h) or during the day (starting at 13.00 h). Blood samples were drawn every hour for a period of 8 h. RESULTS: First experiment. Serum leptin levels increased progressively from a mean (s.d.) baseline of 3.8 +/- 2.2 ng/ml to a value of 4.5 +/- 2.7 ng/ml (P < 0.01) 8 h after the fatty meal. Second experiment. During the day, serum leptin levels increased progressively from 2.65 +/- 1.7 to 3.34 +/- 2.2 ng/ml (P < 0.001) 6 h after the test-meal and decreased from 2.68 +/- 1.5 to 1.9 +/- 1.1 ng/ml (P < 0.001) 8 h after the beginning of the fasting experiment. Similar results were obtained at night. No statistically significant differences in leptin levels were observed between day and night sessions in response to feeding (mean area under the curve: 3.0 +/- 4.1 vs 4.1 +/- 4.1 ng/ml) and fasting (-2.9 +/- 2.2 vs -1.5 +/- 2.2 ng/ml). CONCLUSION: In two independent experiments, human serum leptin levels increase following food intake. This response is not influenced by nycthemeral cycle.

Adult↗
PubMed1998

Influence of alcohol consumption and various beverages on waist girth and waist-to-hip ratio in a sample of French men and women.

OBJECTIVE: The goal of the present study was to assess the association between alcohol consumption and abdominal fat deposition in France, a country where wine is the most commonly consumed alcoholic beverage. METHODS: We analyzed the association between alcohol consumption and various markers of body weight, in a population sample recruited in three distinct geographical areas of France (MONICA centers). This sample included men (n = 1778) and women (n = 1730) aged 35- 64 y, randomly selected from electoral rolls. Alcohol consumption was assessed with a quantitative frequency questionnaire. RESULTS: Alcohol intake ranged from 0-1655 ml of alcohol per week. Wine was the main source of alcohol, representing 67% of total alcohol intake in both genders. In men, there was no association between alcohol intake and body mass index (BMI) or body weight, whereas in women, alcohol consumption was inversely correlated with BMI (P < 0.0001) and body weight (P < 0.0002). In men, total alcohol consumption was positively associated with waist-to-hip ratio (WHR, P < 0.0002) and waist girth (P < 0.004), independently of BMI. Similarly, in women, positive associations were found between alcohol intake and WHR (P < 0.0001) as well as waist girth (P < 0.0001), independently of BMI. In a linear regression model including types of beverages and usual confounders, reporting consumption of either wine, beer or spirit was poorly associated with WHR in men, whereas wine (P < 0.0008) and beer (P < 0.0001) consumptions were both positively associated with WHR in women. However, there was no evidence of a statistically significant heterogeneous effect of wine, beer and spirits on WHR in both genders. CONCLUSION: In a sample of representative French people, in whom wine is the most common alcoholic beverage, alcohol consumption is associated with greater WHR independently of BMI in both men and women.

Adult↗
PubMed1998

A genetic polymorphism of the peroxisome proliferator-activated receptor gamma gene influences plasma leptin levels in obese humans.

Peroxisome proliferator-activated receptor gamma (PPARgamma) is a transcription factor implicated in adipocyte differentiation, lipid and glucose metabolism. A polymorphism corresponding to a silent C-->T substitution was detected in exon 6 of the PPAR gamma gene. We analysed the relationships between this genetic polymorphism and various markers of the obesity phenotype (body weight, body mass index, waist:hip ratio and plasma leptin levels) in a representative sample of 820 men and women living in northern France. The frequencies of the C and T alleles were 0.860 and 0.140 respectively. In the whole sample no association of the polymorphism with the markers tested was observed but a statistically significant interaction ( P < 0.03) existed between this polymorphism and body mass index for plasma leptin levels. This result suggested that the impact of the PPAR gamma gene polymorphism on plasma leptin levels differed according to the BMI of the subjects. Indeed, obese subjects (BMI >30 kg/m2) bearing at least one T allele ( CT + TT ) had higher plasma leptin levels than subjects who did not (35.0 +/- 17.4 ng/ml versus 28.3 +/- 14.8 ng/ml respectively; P < 0.001). This effect existed in both genders, despite the higher plasma leptin levels observed in women. The plasma leptin level increase was not associated with elevation of body mass index, even though these two variables were highly correlated. Thus for a given leptin level the BMI was relatively lower in obese subjects carrying at least one T allele than in obese CC homozygotes. Our results show that in obese subjects variability within the PPAR gamma gene locus is associated with circulating leptin levels and may modify the relationship between leptin levels and adipose tissue mass.

Adult↗
PubMed1998

Cigarette smoking is associated with unhealthy patterns of nutrient intake: a meta-analysis.

The aim of this investigation was to assess the relationship between smoking status and nutrient intakes using a meta-analysis. Publications in English were sought through a Medline search using the following key words: food habits, eating, feeding behavior, diet, food, nutrition, nutritional status or assessment, tobacco use disorder, tobacco, nicotine and smoking. Scanning relevant reference lists of articles and hand searching completed the data collection. No attempt was made to search for unpublished results. Paper selection was based on nutritional surveys including comparisons of smokers with nonsmokers. Fifty-one published nutritional surveys from 15 different countries with 47,250 nonsmokers and 35,870 smokers were used in the analysis. The estimates of size effects were calculated with the mean and variance values of each nutrient intake and the size of the sample. Smokers declared significantly (all P < 10(-5)) higher intakes of energy (+4.9%), total fat (+3.5%), saturated fat (+8.9%), cholesterol (+10.8%) and alcohol (+77.5%) and lower intakes of polyunsaturated fat (-6.5%), fiber (-12.4%), vitamin C (-16.5%), vitamin E (-10.8%) and beta-carotene (-11.8%) than nonsmokers. Protein and carbohydrate intakes did not differ between smokers and nonsmokers. There was no evidence of heterogeneity among studies. In conclusion, the nutrient intakes of smokers differ substantially from those of nonsmokers. Some of these differences may exacerbate the deleterious effects of smoke components on cancer and coronary heart disease risk.

Adolescent↗
PubMed1998

Double-Blind Comparison of Apolipoprotein and Lipoprotein Particle Lowering Effects of Atorvastatin and Pravastatin Monotherapy in Patients With Primary Hypercholesterolemia.

METHODS AND RESULTS: A total of 305 subjects with primary hypercholesterolemia were randomized in a 3:1 ratio to receive either atorvastatin 10 mg daily or pravastatin 20 mg daily according to a 16-week double-blind comparative study of the effect on apolipoprotein and lipoprotein particle levels. All patients had low-density lipoprotein (LDL)-cholesterol levels between 4.2 and 6.6 mM and triglyceride concentrations below 4.5 mM at baseline. After 16 weeks of treatment, apoB (-27% and -16%; P <.001), apoE (-13.3% and -5.6%; P <.05) and the triglyceride-rich LpC-III:B particle (-33% and -26%; P <.05) levels were reduced to a significantly greater extent in the atorvastatin than in the pravastatin treatment group. Both atorvastatin and pravastatin increased apoA-I levels, an effect that was more pronounced in the pravastatin group (+7% and +11%; P <.002). The increased apoA-I levels predominated on LpA-I in the atorvastatin group (+11%) and on LpA-I:A-II in the pravastatin group (+13%). ApoA-II levels were decreased with atorvastatin to a greater extent than with pravastatin (-1% and +2.8%; P <.05). CONCLUSIONS: Although atorvastatin and pravastatin belong to the same therapeutic family, they produce different effects in apoliprotein concentrations in hypercholesterolemic patients. Atorvastatin, an agent of the new generation, appears to efficiently reduce apoB-containing lipoprotein particles containing apoC-III.

Journal Article↗