Epidemiological correlates of high density lipoprotein subfractions, apolipoproteins A-I, A-II, and D, and lecithin cholesterol acyltransferase. Effects of smoking, alcohol, and adiposity.

Haffner, Steven M.; Applebaum-Bowden, Deborah; Wahl, Patricia W.; Hoover, Joanne; Warnick, G. Russell; Albers, John J.; Hazzard, William R.

doi:10.1161/01.atv.5.2.169

Cited by 122 publications

(60 citation statements)

References 39 publications

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“…8 Interestingly, a cross-sectional study has demonstrated that smokers have reduced plasma LCAT concentrations (approximately 14%) compared with nonsmokers. 10 We are unaware of any in vivo studies examining the acute effects of cigarette smoke on LCAT activity; studies in this area appear to be warranted.…”

Section: Discussionmentioning

confidence: 99%

“…Epidemiological studies have shown that plasma HDL concentrations are reduced in cigarette smokers. 8 - 10 It has also been shown that acute cigarette smoke exposure in humans results in subtly modified low-density lipoproteins (LDLs) with enhanced atherogenic potential. 11 The mechanism by which cigarette smoke affects plasma LDL and HDL is not known, although it is possible that oxidative damage to protein and/or lipid constituents is involved.…”

mentioning

confidence: 99%

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Modification of LCAT activity and HDL structure. New links between cigarette smoke and coronary heart disease risk.

McCall

Berg

Kuypers

et al. 1994

Arterioscler Thromb

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The mechanism(s) through which smoking influences the progression of atherosclerosis is poorly understood. Recent evidence suggests that oxidants present in the gas phase of cigarette smoke are involved. We exposed human plasma to the filtered gas phase of cigarette smoke to assess its effects on plasma components involved in the antiatherogenic reverse cholesterol transport pathway. In our model, freshly isolated plasma (24 mL) was exposed to filtered air or gasphase cigarette smoke for up to 6 hours at 37°C. Lecithincholesterol acyltransferase (LCAT) activity was dramatically inhibited by cigarette smoke. A single 15-minute exposure to the smoke from an eighth of a cigarette was sufficient to reduce LCAT activity by 7%; additional exposures resulted in further decreases in activity. At 6 hours, only 22% of control LCAT activity remained in plasma exposed to smoke. Compared with control, gas-phase cigarette smoke-exposed plasma possessed high-density lipoprotein (HDL) with increased (16%) negative charge and with cross-linked apolipoproteins AI and AIL These data demonstrate that gas-phase cigarette smoke can inhibit a key enzyme (LCAT) and modify an integral lipid transport particle (HDL) that are essential components for the normal function of the reverse cholesterol transport pathway. Gas-phase cigarette smoke-induced modification of the reverse cholesterol transport pathway may provide a new mechanistic link between cigarette smoke and coronary heart disease risk. plasma high-density lipoprotein (HDL) concentrations are inversely correlated with coronary heart disease risk.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Modification of LCAT activity and HDL structure. New links between cigarette smoke and coronary heart disease risk.

McCall

Berg

Kuypers

et al. 1994

Arterioscler Thromb

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“…Haffner et al 19 studied the effects of smoking, alcohol, and adiposity on HDL subtractions in a group of 33 men and 17 women. They found that HDL 2 correlated much more strongly with BMI and triglycerides than did HDL 3 .…”

Section: Discussionmentioning

confidence: 99%

“…It is hypothesized that HDL 3 assimilates surface components derived from the triglyceride-rich VLDL particles and is thereby converted to HDL 2 . Further support for this concept was provided by the in vivo experimental data of Forte et al 18 A recent paper by Haffner et al 19 found that HDL 3 , rather than HDL 2 , is affected by smoking and alcohol consumption. In this study we have investigated the relationship between…”

Section: T Has Been Known Since the Early 1950smentioning

confidence: 95%

High density lipoprotein subfractions and coronary risk factors in normal men.

Robinson¹,

Ferns²,

Bevan³

et al. 1987

Arteriosclerosis

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Plasma levels of total high density lipoprotein cholesterol (HDL) and Its subtractions (HDL 2 and HDL 3 ) were measured In 366 healthy Caucasian males; these values were related to a number of coronary risk factors. On unlvarlate statistical analysis, total HDL was negatively correlated with cigarette consumption, body mass Index, and serum trlglycerldes, and positively associated with level of physical activity and alcohol consumption. HDL 2 showed an Inverse relationship with cigarette consumption, body mass index, trlglycerldes, and systolic blood pressure and a positive relationship with age. HDL 3 was negatively correlated with cigarette smoking, body mass index, and trlglycerldes and positively associated with exercise level and alcohol consumption. Total HDL and HDL 2 were Inversely related to coronary risk rating, but HDL 3 snowed no significant correlation. Many of these relationships became nonsignificant after allowing for the effects of other variables. In particular, none of the HDL measurements correlated significantly with risk score after allowing for the effect of trlglycerldes. There Is Insufficient evidence at present to recommend the Inclusion of HDL subfractions as routine screening tests for heart disease. HDL subfractions and these and other risk factors in a large group of healthy men. Methods SubjectsThe study population consisted of Caucasian males attending a hearth screening center in north London. Subjects with a medical history of heart disease or diabetes or with a current complaint of angina, and those with an abnormal fasting glucose level were excluded from the study. Also excluded were subjects with electrocardiographic evidence of ischemic heart disease and those taking antihypertensive or lipid-lowering medication. We were left with a final sample of 366 healthy men.The screening process, which has been described in detail elsewhere, 20 ' 21 included a detailed medical history and physical examination, chest x-ray and 12-lead electrocardiogram, and collection of blood for a number of biochemical and hematological measurements. Blood pressure was taken using a random-zero (Gelman Hawksley) sphygmomanometer, the value recorded being the mean of two measurements. Stage V end-point was used for the diastolic pressure. Weight (kg) and height (m) were recorded for each subject, and body mass index (BMI) was calculated as weight/height 2 . Cigarette smoking, alcohol consumption, and exercise level were assessed by a computerized questionnaire. Ex-smokers and those smoking only pipes or cigars were coded as non-cigarette smokers. Teetotalers (10 subjects) were omitted from the alcohol analysis. All procedures were approved by the ethical committee of BUPA Medical Research, and informed consent was obtained from each subject.The subjects fasted overnight for 14 hours.

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“…significantly increase both HDLc and its major apolipoproteins, AI and AII [10][11][12][13][14]. But the dualistic action of alcohol on CHD risk factors complicates the study of the mechanisms, since its negative effects in elevating serum triglycerides [15][16][17] and its close association with cigarette smoking are more related to haemostatic factors and thrombus formation.…”

Section: Introductionmentioning

confidence: 99%

Alcohol and coronary heart disease: the roles of HDL‐cholesterol and smoking

Mänttäri

Tenkanen²,

Alikoski³

et al. 1997

Journal of Internal Medicine

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Abstract. Man$ tta$ ri M, Tenkanen L, Alikoski T, Manninen V (Department of Medicine, Helsinki University and Helsinki Heart Study, Helsinki, Finland). Alcohol and coronary heart disease : the roles of HDL-cholesterol and smoking. J. Intern Med 1997 ; 241 : 157-63. Objectives.To study the role of HDL-cholesterol (HDLc) in the causal pathway mediating the effect of alcohol on coronary heart disease (CHD). Design. Cox proportional hazard models were used to compare the relative CHD risks in various HDLcsmoking categories. Setting. A prospective, multicentre, placebocontrolled, double-blind CHD primary prevention trial with gemfibrozil in primary (occupational) health care units, the Helsinki Heart Study. Subjects. Dyslipidaemic middle-aged men with available alcohol consumption data (1924 of 2035) in the placebo arm of the 5-year study. Main outcome measures. Seventy-seven (of 84) cases of nonfatal myocardial infarction or cardiac death.

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Epidemiological correlates of high density lipoprotein subfractions, apolipoproteins A-I, A-II, and D, and lecithin cholesterol acyltransferase. Effects of smoking, alcohol, and adiposity.

Cited by 122 publications

References 39 publications

Modification of LCAT activity and HDL structure. New links between cigarette smoke and coronary heart disease risk.

Modification of LCAT activity and HDL structure. New links between cigarette smoke and coronary heart disease risk.

High density lipoprotein subfractions and coronary risk factors in normal men.

Alcohol and coronary heart disease: the roles of HDL‐cholesterol and smoking

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