PubMed Health⌕ Search

Biomedical subjects

G Zylberberg

Publications and source records attributed to G Zylberberg.

16 recordsLinked to original sources
PubMed1997

Effect of smoking cessation on lipoprotein A-I and lipoprotein A-I:A-II levels.

Cigarette smoking is associated with low plasma high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) A-I levels, which may explain, in part, its deleterious effects on coronary heart disease (CHD). In a group of ex-smokers, we assessed the influence of smoking cessation on apo A-I particle levels. Plasma lipid, apolipoprotein, and lipoparticle concentrations of 58 subjects who had completely stopped smoking (ex-smokers) were compared with those of 37 subjects who had continued smoking (smokers) before and after a smoking cessation counseling program. Nutritional intake was recorded before and after the program to adjust for potential interaction with plasma lipid variables. Smokers and ex-smokers were similar in gender distribution, age, body mass index (BMI), social status, and nutrient intake. There were significantly greater increases in total cholesterol (P < .04), HDL-C (P < .005), HDL2-C (P < .008), and lipoprotein (Lp) A-I:A-II (P < .04) in ex-smokers than in smokers. After smoking cessation, ex-smokers consumed more vegetable protein (P < .02) and polysaccharides (P < .04) and had higher plasma levels of HDL-C (P < .0004), apo A-I (P < .001), Lp A-I (P < .007), and Lp A-I:A-II (P < .01) than smokers. Adjustments on nutritional variables did not show any additional difference between ex-smokers and smokers, suggesting that smoking per se effects Lp A-I and Lp A-I:A-II levels. In conclusion, HDL particles including Lp A-I and Lp A-I:A-II are higher in ex-smokers than in smokers.

Adult↗
PubMed1996

Cigarette smoking is associated with differences in nutritional habits and related to lipoprotein alterations independently of food and alcohol intake.

OBJECTIVE: To assess the effects of smoking on serum lipoprotein levels taking into account current nutritional intakes. DESIGN: Case-control study comparing smokers and non-smokers. SETTING: Ambulatory subjects of the Urban Community of Lille examined at home or at the Health Care Center. SUBJECTS: Men, between 45 and 65 years of age; n = 89 smokers (cases) and n = 91 non-smokers (controls); non-smokers were randomly selected from the voter's registration lists, 7 smokers and 2 non-smokers were excluded for hyperlipidemia. INTERVENTIONS: Blood sampling, medical examination and three-day food records validated by a registered dietician. RESULTS: Smokers were younger (P < 0.001) and thinner (P = 0.003), chose more frequently visible fats of animal origin (P = 0.03) and reported significantly larger daily meat servings (P = 0.01) than non-smokers. Smokers had a significantly higher intake of non-alcoholic energy (P < 0.05), lipids of animal origin (P = 0.003), saturated fat (P < 0.01) and monounsaturated fat (P < 0.01) and a lower P/S ratio (P = 0.02) than non-smokers. After adjustment on age and body mass index, smokers had significantly higher levels of mean serum triglycerides (P = 0.03), VLDL-cholesterol (P = 0.0003) and systolic blood pressure (P = 0.02) and lower values of HDL-cholesterol (P = 0.02) than non-smokers. Additional adjustment for alcohol consumption showed significantly lower apo A-I values (P = 0.03) in smokers than non-smokers. Further adjustment for the intake of lipids of animal origin revealed higher apo B values (P = 0.04) in smokers than non-smokers. CONCLUSIONS: (1) Smoking is associated with serum lipid and lipoprotein alterations independently of nutritional factors, (2) Nutritional habits of smokers are less 'healthy' than those of non-smokers (3) Smokers is a group of particular importance in terms of multifactorial public health intervention.

Aged↗
PubMed1993

Parental history of early myocardial infarction is associated with decreased levels of lipoparticle AI in adolescents.

A family history of coronary heart disease (CHD) is a known risk factor for CHD. To investigate the possible role of lipoprotein particles in the relationship between family history of CHD and risk of CHD, we performed a case-control study in a sample of adolescents. The case group consisted of 97 adolescents whose parents had suffered a verified myocardial infarction before the age of 55 years. The control group was composed of 194 subjects without any family history of CHD. One case patient was matched to two control subjects for gender, age, and body mass index. In both groups, plasma lipid variables were measured, including total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C) low-density lipoprotein cholesterol, apolipoprotein (apo)AI, apoB, apoAI-containing lipoprotein particles without apoAII (LpAI) and with apoAII, and apoB-containing lipoprotein particles with apoE and with apoCIII. Adolescents with a family history of early myocardial infarction had lower plasma levels of HDL-C (P < .0001), apoAI (P < .01), and LpAI (P < .0001) than control subjects (adjusted for gender, age, body mass index, smoking habits, and oral contraceptive use). No other differences were statistically significant between case and control subjects. The analysis was repeated separately for male and female subjects. In young men, the best predictor of family history of early myocardial infarction was the LpAI plasma level, whereas in young women it was the HDL-C plasma level. Decreased levels of HDL-C and LpAI lipoprotein particles explain part of the relationship between parental history of early myocardial infarction and CHD risk.

Adolescent↗
PubMed1991

Plasma concentrations of apolipoprotein A-I containing particles in normolipidaemic young men.

Low levels of plasma high-density lipoprotein (HDL)-cholesterol and apolipoprotein (apo)-A-I are associated with premature coronary heart disease. However, particles in the density range of HDL are heterogeneous. Two main types of apo A-I-containing particles can be identified, one species containing both apo A-I and apo A-II (Lp A-I:A-II) and the other apo A-I but no apo-A-II (Lp A-I). This study was designed to measure HDL cholesterol, apo A-I, and, using a new procedure, Lp A-I in 233 healthy normolipidaemic young men (cholesterol less than 250 mg dl-1 and triglycerides less than 200 mg dl-1). Among these subjects, the composition of HDL was very variable as indicated by the 10th and the 90th percentiles of the HDL-cholesterol/apo A-I ratios which were 0.32 and 0.49, respectively. The 10th and 90th percentiles of apo A-I and Lp A-I:A-II were 126 and 167 mg dl-1 and 83 and 116 mg dl-1, respectively. On the other hand, Lp A-I showed a much larger variation, the 10th and 90th percentiles being at 33 and 62 mg dl-1, respectively. The distribution of individual values of Lp A-I showed that this fraction of apo A-I-containing particles was very variable among subjects, the Lp A-I/apo A-I ratio extending from 0.18 to 0.58. Triglycerides, Lp A-I and Lp A-I:A-II were correlated with HDL cholesterol, but no correlation between apo A-I containing subfractions and plasma triglycerides was noticed. Since preliminary results from angiographic and clinical studies show that Lp A-I could exert a protective role for atherosclerosis, it would seem that the measurement of Lp A-I might help in the future to characterize better the individual's risk for atherosclerosis.

Adolescent↗
PubMed1990

Effect of alcohol intake on human apolipoprotein A-I-containing lipoprotein subfractions.

High-density lipoprotein comprises two main types of lipoprotein particles: (1) those that contain apolipoproteins A-I and A-II, designated LpA-I:A-II, and (2) those that contain apolipoprotein A-I but not apolipoprotein A-II, designated LpA-I. Both have been extensively studied and are believed to represent distinct metabolic entities that may confer differing protection against coronary artery disease risk. We have previously suggested that LpA-I might represent the antiatherogenic effect, which has been ascribed mainly to its effect on high-density lipoprotein cholesterol; we set out to investigate, in 344 men, the relation between LpA-I:A-II and LpA-I levels and alcohol consumption. As the alcohol intake rose, LpA-I:A-II levels increased, while LpA-I levels fell. On the assumption that LpA-I is the antiatherogenic fraction of high-density lipoprotein, the putative protective action of alcohol consumption against coronary artery disease should be reconsidered.

Adult↗