Abstract

The purpose of this study was to evaluate the differences that occur inside the plasma compartment of normolipidemic men, classified on the basis of their response to prolonged consumption of additional dietary cholesterol. Using a crossover design, twoscore men aged 18–57 y were randomly allocated to an egg (640 mg/d additional dietary cholesterol) or placebo group (0 mg/d additional dietary cholesterol), for two 30-d periods, which were separated by a 3-wk washout catamenia. Subjects were classified as hypo- [increase in plasma total cholesterol (TC) of <0.05 mmol/L for each additional 100 mg of dietary cholesterol consumed] or hyperresponders (increase in TC of ≥0.06 mmol/L for each additional 100 mg of dietary cholesterol consumed) on the basis of their plasma reaction to the additional dietary cholesterol provided. Male hyporesponders did non experience an increase in LDL cholesterol (LDL-C) or HDL cholesterol (HDL-C) during the egg catamenia, whereas both lipoproteins were significantly (P < 0.0001 and P < 0.05, respectively) elevated in hyperresponders. Although the LDL/HDL ratio was increased in male hyperresponders after the high cholesterol menstruum, the mean increase experienced by this population was notwithstanding inside National Cholesterol Education Program guidelines. Furthermore, male hyperresponders had higher lecithin cholesterol acyltransferase (P < 0.05) and cholesteryl ester transfer protein (P < 0.05) activities during the egg catamenia, which suggests an increase in reverse cholesterol transport. These information suggest that additional dietary cholesterol does not increase the risk of developing an atherogenic lipoprotein profile in healthy men, regardless of their response classification.

Dietary intake influences lipoprotein concentration, composition and metabolism, which can touch on the development of atherosclerosis and coronary heart disease (CHD). Because CHD is the leading cause of death in the U.s. (one), information technology is important to examine the individual response to certain dietary components that accept been implicated in affliction progression.

Dietary cholesterol, and its human relationship to plasma total cholesterol (TC) and the progression of chronic affliction, has been examined extensively. Early studies (2 ,three) provided testify, which remains consequent today, that increased consumption of dietary cholesterol can elevate TC values to some extent in certain individuals. Considering increases in TC and LDL cholesterol (LDL-C) are established take a chance factors for CHD, recommendations to limit consumption of loftier cholesterol foods accept been implemented in an attempt to foreclose the progression of disease. A recent meta-analysis (4), which examined 17 studies in which experimental diets differed only in the corporeality of dietary cholesterol or the number of eggs consumed, found that ane additional egg per day can increase the TC/HDL cholesterol (HDL-C) ratio by 0.040, causing a two.1% increase in the risk for myocardial infarction. In contrast, a review (5) of multiple instance-controlled studies, which measured intake of cholesterol and disease incidence, found that a relationship could not be conspicuously established between the dietary component and increase in CHD risk. Furthermore, information gathered from the Lipid Research Clinics Prevalence Follow-upwards Report (six), which examined both men and women (due north = 4546), found that no significant relationship existed betwixt deaths owing to CHD and dietary cholesterol intake. Several studies have also failed to find an clan betwixt the incidence of CHD and egg consumption (7 –9). Ane explanation for this failure to connect elevated TC, experienced as a result of boosted egg intake, to CHD incidence is that plasma changes may be due to increases in both LDL-C and HDL-C (10). This simultaneous increment allows for the maintenance of the LDL/HDL ratio, a potent predictor of CHD risk. Furthermore, eggs are a expert source of essential amino acids, folate and other B vitamins, unsaturated fat acids and α-tocopherol, which may offset whatever harmful furnishings of the cholesterol provided (11).

Because individuals do not experience a compatible response to dietary cholesterol, information technology is difficult to accurately predict its effect on plasma TC and lipoprotein concentrations. Factors such as ethnicity, hormonal status, obesity, lipoprotein disorders and genetic predisposition (12 ,xiii) may explain this variation in response. Several meta-analyses (ten ,12 ,14), which examined the bachelor data regarding the plasma lipid and lipoprotein response to dietary cholesterol, provided evidence that a small-scale increase in TC of 0.05–0.06 mmol/L may be predictable in response to a 100-mg increment in dietary cholesterol intake (4 ,15). If this moderate increase is used every bit a reference, those who experience elevations in TC of ≥0.065 mmol/L would exist classified as hyperresponders to dietary cholesterol, whereas hyporesponders would be those who accept no change in TC or experience increases of <0.05 mmol/50 in response to a 100-mg increment in cholesterol intake. A previous test of the plasma response to additional dietary cholesterol feeding in premenopausal women, which utilized this classification, revealed the presence of these ii distinct populations (xvi).

The existence of a hypo- or hyperresponse to dietary cholesterol has been conspicuously established in various creature species (17 –nineteen). The presence of a consistent and reproducible response to dietary cholesterol in men and women has besides been institute (20) and is considered to exist adamant past genetic factors (21 ,22). Mutations of several gene loci, such equally the APOE and APOAIV (23), have been identified that may explain why some individuals are insensitive to dietary cholesterol, whereas others experience significant plasma compartment changes in response to intake. Furthermore, information technology has as well been suggested that hyporesponders may accept the ability to maintain cholesterol homeostasis by decreasing synthesis (24), absorption (25) or increasing biliary excretion (26 ,27) after increased intake of dietary cholesterol.

The primary objective of this study was to further clarify the changes that occur within the plasma compartment of good for you men later prolonged consumption of additional dietary cholesterol. A second objective was to evaluate how those classified as hyperresponders process the excess cholesterol in the plasma compartment. Third, differences betwixt the male person and female response to dietary cholesterol were to be adamant utilizing information previously gathered from an identical report with premenopausal women (16).

SUBJECTS AND METHODS

Materials.

Liquid whole eggs and cholesterol/fat-costless eggs (placebo) were purchased from Better Brands (Windsor, CT). Enzymatic TC and triglyceride (TG) kits were obtained from Roche-Diagnostics (Indianapolis, IN). Apolipoprotein (apo) C-III and apo E kits were ordered from Wako Pure Chemical (Osaka, Japan). Apo B kits, EDTA, aprotinin, sodium azide and phenylmethylsulfonyl fluoride (PMSF) were obtained from Sigma Chemical (St. Louis, MO).

Subjects.

Men (n = 40) betwixt the ages of 20 and 50 y were recruited from the University community. The exclusion criteria for this study included the presence of hypercholesterolemia (TC >five.68 mmol/50), hypertriglyceridemia, hypertension and diabetes. Furthermore, those receiving lipid-lowering drugs were as well excluded. Subjects had TC concentrations within the range of three.62–five.17 mmol/L at baseline.

Experimental protocol.

The experimental protocol was canonical past the University of Connecticut Institutional Review Board, and written informed consent was obtained from each subject. The study utilized a randomized, crossover pattern with subjects initially assigned to an egg or placebo grouping for 30 d, followed by a 3-wk washout menses, subsequently which the second dietary period began. Subjects assigned to the egg group were expected to consume the liquid equivalent of 3 whole eggs/d (∼640 mg/d dietary cholesterol). In contrast, the placebo grouping consumed an identical weight of egg substitutes (0 mg/d dietary cholesterol). The products were identical in terms of color and consistency, and differed only in the fat and cholesterol content. Daily amounts were provided in private containers, and subjects were asked to return any uneaten portion at the stop of the week.

Subjects were expected to adhere to the National Cholesterol Education Programme (NCEP) Footstep I nutrition for the elapsing of the study, and detailed dietary instructions were provided. The NCEP Stride I diet recommends that no >30% of full energy come from fatty, with saturated fat providing only 10% of total fat. In add-on, subjects were instructed to consume no >300 mg/d dietary cholesterol. To ensure compliance with the dietary guidelines, subjects completed vii 24-h dietary records during each treatment period, which included two weekend days. Nutrient intake was adamant using the Diet Data System for Enquiry (NDS-R) software version iv.0, developed by the Nutrition Coordinating Center, University of Minnesota, Minneapolis, MN, Food and Nutrient Database 28.

Two fasting (12 h) blood samples were initially collected, on different days, from each subject into tubes containing 0.10 thousand/100 g EDTA to determine baseline plasma lipids. Plasma was separated by centrifugation at 1500 × k for twenty min at 4°C, and placed into vials containing PMSF (0.05 g/100 g), sodium azide (0.01 one thousand/100 thousand) and aprotinin (0.01 g/100 1000). Two boosted blood samples were collected and processed in the same mode at the end of each diet treatment and washout menstruation. The variables of weight, claret pressure level, level of activity, smoking and alcohol intake were also measured at baseline and after each dietary catamenia to business relationship for the possible influence of these factors on plasma lipid levels and lipoprotein metabolism.

Plasma lipids and apolipoproteins.

Our laboratory has participated in the Centers for Disease Control/National Heart, Lung and Blood Institute (CDC-NHLBI) Lipid Standardization Program since 1989 for quality control and standardization for plasma TC, HDL-C and TG assays. CV assessed past the standardization plan during the report period were 0.76–1.42% for full cholesterol, 1.71–2.72% for HDL-C and 1.64–2.47% for triglycerides.

The effects of dietary cholesterol on TC, LDL-C, HDL-C and TG concentrations and the LDL/HDL ratio were examined. TC was adamant by enzymatic methods using Roche-Diagnostics standards and kits (28). HDL-C was measured in the supernatant after precipitation of apo B-containing lipoproteins (29) and LDL-C was determined using the Friedewald equation (xxx). TG were determined using Roche-Diagnostics kits, which adjust for free glycerol. Means of the two claret draws were used to appraise differences betwixt treatment periods. Kits, which apply an immunoturbidimetric method, were obtained from Sigma for the determination of apo B concentrations. Turbidity was measured in a microplate spectrophotometer at 340 nm (31). Apo C-Three (32) and apo E (33) were measured with a Hitachi Autoanalyzer 740 utilizing kits from Wako.

Classification of hyper- and hyporesponders.

Equally previously mentioned, a pocket-size increment in TC of 0.05–0.06 mmol/Fifty may be considered normal in response to a 100-mg increase in dietary cholesterol. Therefore, for this written report and the previous one conducted in premenopausal women (16), subjects who experienced an increase in total cholesterol ≥0.06 mmol/L for each additional 100 mg of dietary cholesterol were considered hyperresponders. Considering the subjects were fed an additional 640 mg/d of dietary cholesterol, those who experienced an increase in TC of ≥0.41 mmol/50 were considered hyperresponders. The remaining subjects who experienced fluctuations of <0.36 mmol/L (an increase in TC of <0.05 mmol/L for each additional 100 mg of dietary cholesterol consumed) or had no modify in TC were identified equally hyporesponders. The reproducibility of individual differences in response has been documented previously in several controlled and field trials (34).

Plasma CETP and LCAT.

Cholesteryl ester transfer protein (CETP) activity was determined in plasma co-ordinate to the method described past Ogawa and Fielding (35). This method measures the mass transfer of cholesterol ester between HDL and apo B–containing lipoproteins. Thus, physiologic CETP activity was determined through an analysis of the decrease in HDL cholesterol ester mass betwixt 0 and half dozen h, without lecithin:cholesterol acyltransferase (LCAT) inhibition. Samples were incubated at 37°C for half dozen h in a shaking h2o bath. After this menses, total, HDL and plasma free cholesterol were measured, and previously described calculations were performed (36). LCAT activeness was adamant by an endogenous cocky-substrate method, which involves mass analysis of the decrease in plasma costless cholesterol between 0 and 6 h at 37°C. Assays were carried out concurrently with measurements of CETP. Both of these methods have been standardized in our laboratory.

Data assay.

Student's t test was used to compare baseline characteristics of the 2 groups of men. Considering subjects were separated into hyper- and hyporesponders after data collection, a paired t test was used to evaluate the changes in plasma lipids, apoproteins, CETP and LCAT activities that occurred within the response groups during the egg and placebo periods. A paired t test was also used to assess differences in the dietary consumption of macronutrients, dietary cholesterol, alcohol and dietary fiber.

RESULTS

Classification of the men's responses to additional dietary cholesterol resulted in the identification of 25 hypo- and 15 hyperresponders (Fig. 1). Therefore, 62.5% of the men studied exhibited the hyporesponse, whereas only 37.5% were hyperresponders.

Figure i

Changes in plasma total cholesterol in hypo- (n = 25) and hyperresponding (n = 15) men during the egg and placebo intake periods.

Changes in plasma total cholesterol in hypo- (n = 25) and hyperresponding (northward = 15) men during the egg and placebo intake periods.

Figure 1

Changes in plasma total cholesterol in hypo- (n = 25) and hyperresponding (n = 15) men during the egg and placebo intake periods.

Changes in plasma total cholesterol in hypo- (north = 25) and hyperresponding (n = 15) men during the egg and placebo intake periods.

No significant differences were found for age, smoking status, concrete activity, body mass index (BMI) and claret pressure between men classified equally hypo- or hyperresponders at baseline (Table ane). Furthermore, the plasma concentrations of TC, LDL-C, HDL-C and TG were like among men before the dietary treatment, regardless of response. The baseline plasma concentrations of these metabolites were likewise not significantly different from those values obtained after the washout catamenia (data non shown). When the analysis of BMI, weight, claret pressure and hours of physical activity was performed again after the two dietary treatment periods. no significant differences between hypo- and hyperresponders were institute (Table 2).

TABLE 1

Baseline characteristics of men classified as hypo- or hyperresponders1

Parameter Hyper-responders (n = 15) Hypo-responders (n = 25)
Age, y 35.4 ± 11.6 30.ix ± 9.4
Smokers, northward 1 2
Concrete Action, h/wk 5.7 ± v.ane 4.iii ± iv.3
BMI, kg/m 2 24.9 ± three.0 26.1 ± 4.7
Systolic blood pressure, mm Hg 116.9 ± 11.three 123.ane ± 12.two
Diastolic blood pressure, mm Hg 75.1 ± 9.ii 79.9 ± 9.1
Total cholesterol, mmol/L iv.06 ± 0.76 4.00 ± 0.85
LDL cholesterol, mmol/L 2.33 ± 0.66 ii.26 ± 0.073
HDL cholesterol, mmol/50 1.14 ± 0.eighteen 1.17 ± 0.21
Triglycerides, mmol/Fifty ane.31 ± 0.85 ane.19 ± 0.69
Parameter Hyper-responders (n = fifteen) Hypo-responders (n = 25)
Age, y 35.4 ± eleven.six 30.nine ± nine.4
Smokers, n ane ii
Physical Activity, h/wk 5.7 ± five.ane iv.3 ± four.three
BMI, kg/m 2 24.nine ± three.0 26.1 ± iv.vii
Systolic claret force per unit area, mm Hg 116.9 ± 11.3 123.1 ± 12.2
Diastolic blood pressure level, mm Hg 75.1 ± nine.2 79.9 ± 9.1
Total cholesterol, mmol/L 4.06 ± 0.76 4.00 ± 0.85
LDL cholesterol, mmol/L 2.33 ± 0.66 ii.26 ± 0.073
HDL cholesterol, mmol/L 1.14 ± 0.18 1.17 ± 0.21
Triglycerides, mmol/L ane.31 ± 0.85 1.19 ± 0.69

one

Data are presented as hateful ± SD.

Tabular array one

Baseline characteristics of men classified equally hypo- or hyperresponders1

Parameter Hyper-responders (northward = fifteen) Hypo-responders (n = 25)
Age, y 35.4 ± xi.half-dozen 30.nine ± ix.4
Smokers, n 1 2
Physical Activity, h/wk v.vii ± v.1 iv.three ± iv.3
BMI, kg/m 2 24.nine ± 3.0 26.1 ± 4.7
Systolic blood pressure level, mm Hg 116.9 ± eleven.three 123.one ± 12.2
Diastolic blood pressure, mm Hg 75.1 ± nine.ii 79.9 ± 9.1
Full cholesterol, mmol/L 4.06 ± 0.76 4.00 ± 0.85
LDL cholesterol, mmol/Fifty ii.33 ± 0.66 2.26 ± 0.073
HDL cholesterol, mmol/L 1.14 ± 0.18 ane.17 ± 0.21
Triglycerides, mmol/L i.31 ± 0.85 ane.19 ± 0.69
Parameter Hyper-responders (n = 15) Hypo-responders (northward = 25)
Age, y 35.4 ± 11.6 30.9 ± 9.4
Smokers, north 1 2
Physical Activity, h/wk five.7 ± five.1 4.3 ± four.3
BMI, kg/yard 2 24.9 ± iii.0 26.ane ± 4.vii
Systolic claret pressure, mm Hg 116.9 ± 11.iii 123.1 ± 12.2
Diastolic blood pressure level, mm Hg 75.1 ± nine.2 79.9 ± 9.1
Total cholesterol, mmol/50 4.06 ± 0.76 4.00 ± 0.85
LDL cholesterol, mmol/Fifty two.33 ± 0.66 2.26 ± 0.073
HDL cholesterol, mmol/Fifty ane.14 ± 0.18 1.17 ± 0.21
Triglycerides, mmol/L one.31 ± 0.85 1.19 ± 0.69

1

Information are presented as mean ± SD.

TABLE 2

Trunk mass index, weight, blood pressure level and hours of physical activity of hypo- and hyperresponders during the egg and placebo periods1

BMI Weight SBP DBP Physical activity
kg/m2 kg mm Hg h/wk
Hyperresponders
 Egg 24.9 ± 3.2 78.2 ± 13.2 118.two ± eight.half dozen 76.ix ± 6.6 4.vii ± 4.7
 Placebo 25.0 ± iii.1 77.3 ± xiii.5 117.6 ± eleven.6 76.2 ± 7.0 5.two ± iv.8
Hyporesponders
 Egg 26.1 ± 4.9 82.nine ± 18.0 120.2 ± ten.0 78.6 ± 7.0 4.4 ± 3.iii
 Placebo 26.1 ± five.1 82.8 ± eighteen.viii 119.5 ± 10.4 78.2 ± 7.8 4.2 ± 3.vii
BMI Weight SBP DBP Physical activity
kg/mtwo kg mm Hg h/wk
Hyperresponders
 Egg 24.ix ± 3.2 78.2 ± thirteen.2 118.2 ± 8.half-dozen 76.9 ± half-dozen.vi iv.7 ± 4.seven
 Placebo 25.0 ± 3.1 77.3 ± 13.five 117.half dozen ± xi.6 76.2 ± vii.0 5.2 ± 4.8
Hyporesponders
 Egg 26.one ± 4.nine 82.nine ± 18.0 120.2 ± ten.0 78.6 ± 7.0 4.4 ± 3.3
 Placebo 26.1 ± 5.one 82.8 ± xviii.8 119.5 ± ten.4 78.two ± 7.8 iv.2 ± 3.7

1

Values represent hateful ± sd for north = fifteen hyper- and 25 hyporesponders. BMI, body mass index; SBP = systolic claret pressure level; DBP = diastolic blood pressure.

TABLE ii

Body mass index, weight, blood pressure and hours of physical activity of hypo- and hyperresponders during the egg and placebo periodsone

BMI Weight SBP DBP Physical activity
kg/yardtwo kg mm Hg h/wk
Hyperresponders
 Egg 24.9 ± 3.ii 78.2 ± 13.2 118.2 ± 8.6 76.9 ± vi.6 4.7 ± four.vii
 Placebo 25.0 ± 3.i 77.3 ± 13.5 117.half dozen ± eleven.6 76.ii ± 7.0 v.ii ± 4.8
Hyporesponders
 Egg 26.1 ± 4.9 82.9 ± eighteen.0 120.2 ± x.0 78.vi ± 7.0 4.four ± 3.3
 Placebo 26.1 ± v.1 82.viii ± eighteen.8 119.5 ± 10.4 78.two ± 7.viii 4.2 ± 3.7
BMI Weight SBP DBP Physical action
kg/k2 kg mm Hg h/wk
Hyperresponders
 Egg 24.9 ± three.2 78.2 ± 13.two 118.2 ± viii.6 76.9 ± 6.6 4.7 ± four.vii
 Placebo 25.0 ± iii.1 77.3 ± 13.5 117.half-dozen ± 11.6 76.2 ± 7.0 5.2 ± 4.viii
Hyporesponders
 Egg 26.1 ± 4.9 82.9 ± 18.0 120.2 ± ten.0 78.half-dozen ± 7.0 4.iv ± 3.3
 Placebo 26.i ± 5.one 82.8 ± xviii.8 119.5 ± 10.four 78.2 ± seven.8 four.2 ± 3.7

i

Values represent hateful ± sd for due north = 15 hyper- and 25 hyporesponders. BMI, body mass alphabetize; SBP = systolic claret pressure; DBP = diastolic claret pressure level.

Dietary intake analysis (Table three) indicated that both hypo- and hyperresponders reported significantly higher consumption of total fatty and cholesterol during the egg period. Hyperresponders reported a iii.7% higher percentage of energy obtained from full fatty during the egg period. Similarly, hyporesponders reported a three.ix% increment in the per centum of energy caused from total fatty. Furthermore, hyperresponders reported elevated intakes of MUFA during the egg flow (P < 0.05), whereas intake did not change significantly between dietary periods for hyporesponders. In dissimilarity, hyporesponders were the but grouping to report a pregnant increase in the percentage of energy obtained from saturated fatty acids (SFA) during the egg consumption period compared with the placebo. In add-on, no differences in the percentage of energy obtained from fiber were reported in either response grouping regardless of dietary treatment (data not shown).

TABLE 3

Percent of free energy intake from total fat, saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fat of hypo- and hyperresponders during the egg and placebo periods1

Energy total Fat Energy SFA Energy MUFA Energy PUFA Dietary cholesterol
% mg/d
Hyperresponders
 Egg 34.3 ± 6.0 ten.7 ± 2.v 13.v ± 3.0 7.3 ± 2.six 831.nine ± 79.4
 Placebo 30.half-dozen ± 8.7 9.6 ± ii.9 11.7 ± 3.ix 7.0 ± 2.4 179.7 ± 79.7
 Paired t test P < 0.05 NS2 P < 0.05 NS P < 0.0001
Hyporesponders
 Egg 34.85 ± 4.9 11.5 ± 2.iii 13.5 ± 2.4 6.5 ± 1.4 810.four ± 134.1
 Placebo 30.9 ± 7.four 10.1 ± 3.0 12.4 ± 3.7 6.2 ± 1.8 185.0 ± 86.four
 Paired t test P < 0.01 P < 0.01 NS NS P < 0.0001
Free energy full Fatty Energy SFA Free energy MUFA Energy PUFA Dietary cholesterol
% mg/d
Hyperresponders
 Egg 34.iii ± 6.0 x.vii ± 2.five thirteen.v ± 3.0 7.3 ± ii.6 831.9 ± 79.four
 Placebo 30.6 ± 8.7 9.vi ± 2.9 11.7 ± iii.9 vii.0 ± 2.iv 179.vii ± 79.vii
 Paired t examination P < 0.05 NS2 P < 0.05 NS P < 0.0001
Hyporesponders
 Egg 34.85 ± 4.9 11.5 ± ii.3 13.5 ± 2.four 6.5 ± 1.iv 810.4 ± 134.1
 Placebo 30.9 ± 7.four 10.ane ± iii.0 12.4 ± three.7 6.two ± one.8 185.0 ± 86.4
 Paired t test P < 0.01 P < 0.01 NS NS P < 0.0001

1

Values are expressed as hateful ± sd, n = 15 hyper- and due north = 25 hyporesponders.

ii

NS, P > 0.05.

TABLE 3

Per centum of energy intake from full fat, saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fat of hypo- and hyperresponders during the egg and placebo periods1

Energy total FAT Energy SFA Free energy MUFA Energy PUFA Dietary cholesterol
% mg/d
Hyperresponders
 Egg 34.3 ± 6.0 10.7 ± 2.5 xiii.five ± three.0 vii.3 ± 2.half-dozen 831.9 ± 79.iv
 Placebo 30.6 ± 8.7 9.half-dozen ± 2.9 11.7 ± 3.ix 7.0 ± 2.4 179.7 ± 79.7
 Paired t test P < 0.05 NStwo P < 0.05 NS P < 0.0001
Hyporesponders
 Egg 34.85 ± iv.nine 11.5 ± two.3 13.5 ± two.iv 6.5 ± i.4 810.4 ± 134.ane
 Placebo 30.ix ± 7.4 10.1 ± iii.0 12.iv ± three.vii 6.2 ± 1.viii 185.0 ± 86.4
 Paired t test P < 0.01 P < 0.01 NS NS P < 0.0001
Free energy total Fatty Energy SFA Energy MUFA Energy PUFA Dietary cholesterol
% mg/d
Hyperresponders
 Egg 34.3 ± half dozen.0 10.7 ± 2.5 13.v ± 3.0 seven.iii ± 2.half dozen 831.ix ± 79.four
 Placebo 30.six ± viii.7 nine.six ± 2.9 11.seven ± 3.9 7.0 ± 2.iv 179.seven ± 79.7
 Paired t test P < 0.05 NS2 P < 0.05 NS P < 0.0001
Hyporesponders
 Egg 34.85 ± 4.9 11.5 ± 2.3 13.5 ± ii.4 half dozen.five ± ane.four 810.four ± 134.i
 Placebo thirty.9 ± 7.4 10.1 ± 3.0 12.four ± 3.7 vi.ii ± ane.8 185.0 ± 86.iv
 Paired t exam P < 0.01 P < 0.01 NS NS P < 0.0001

1

Values are expressed as mean ± sd, n = xv hyper- and n = 25 hyporesponders.

ii

NS, P > 0.05.

Hyporesponders did not have any meaning changes in the levels of LDL-C, HDL-C, TG or the LDL/HDL ratio during either treatment period (Tabular array 4). In dissimilarity, hyperresponders did accept significant increases in LDL-C (P < 0.0001), HDL-C (P < 0.05) and the LDL/HDL ratio (P < 0.05) during the egg period, just no changes were seen in plasma TG concentration.

TABLE 4

Plasma lipids and lipoprotein ratios of hypo- and hyperresponders during the egg and placebo periodsi

TC LDL-C HDL-C Triglycerides LDL/HDL
mmol/Fifty
Hyperresponders
 Egg 4.88 ± 0.86 two.87 ± 0.82 i.29 ± 0.23 i.56 ± 0.75 2.33 ± 0.lxxx
 Placebo four.13 ± 0.71 2.21 ± 0.60 one.19 ± 0.19 ane.50 ± 0.93 1.91 ± 0.70
 Paired t exam P < 0.0001 P < 0.0001 P < 0.05 NS P < 0.05
Hyporesponders
 Egg 4.33 ± 0.80 two.44 ± 0.71 ane.24 ± 0.24 one.37 ± 0.72 2.07 ± 0.lxxx
 Placebo four.38 ± 0.76 2.48 ± 0.69 1.25 ± 0.23 1.33 ± 0.72 2.08 ± 0.80
 Paired t test NS NS NS NS NS
TC LDL-C HDL-C Triglycerides LDL/HDL
mmol/Fifty
Hyperresponders
 Egg four.88 ± 0.86 2.87 ± 0.82 1.29 ± 0.23 1.56 ± 0.75 ii.33 ± 0.80
 Placebo iv.13 ± 0.71 2.21 ± 0.60 1.19 ± 0.19 1.50 ± 0.93 1.91 ± 0.70
 Paired t test P < 0.0001 P < 0.0001 P < 0.05 NS P < 0.05
Hyporesponders
 Egg iv.33 ± 0.80 2.44 ± 0.71 one.24 ± 0.24 1.37 ± 0.72 2.07 ± 0.80
 Placebo iv.38 ± 0.76 2.48 ± 0.69 i.25 ± 0.23 ane.33 ± 0.72 ii.08 ± 0.80
 Paired t test NS NS NS NS NS

1

Values are expressed as mean ± sd. n = xv hyper- and north = 25 hyporesponders. NS, P > 0.05.

Table 4

Plasma lipids and lipoprotein ratios of hypo- and hyperresponders during the egg and placebo periods1

TC LDL-C HDL-C Triglycerides LDL/HDL
mmol/Fifty
Hyperresponders
 Egg 4.88 ± 0.86 2.87 ± 0.82 1.29 ± 0.23 1.56 ± 0.75 two.33 ± 0.80
 Placebo iv.13 ± 0.71 two.21 ± 0.60 i.xix ± 0.19 i.50 ± 0.93 1.91 ± 0.70
 Paired t test P < 0.0001 P < 0.0001 P < 0.05 NS P < 0.05
Hyporesponders
 Egg four.33 ± 0.80 2.44 ± 0.71 1.24 ± 0.24 1.37 ± 0.72 2.07 ± 0.lxxx
 Placebo iv.38 ± 0.76 2.48 ± 0.69 1.25 ± 0.23 one.33 ± 0.72 2.08 ± 0.80
 Paired t test NS NS NS NS NS
TC LDL-C HDL-C Triglycerides LDL/HDL
mmol/L
Hyperresponders
 Egg iv.88 ± 0.86 2.87 ± 0.82 1.29 ± 0.23 1.56 ± 0.75 ii.33 ± 0.eighty
 Placebo 4.thirteen ± 0.71 two.21 ± 0.lx ane.19 ± 0.19 1.fifty ± 0.93 one.91 ± 0.70
 Paired t test P < 0.0001 P < 0.0001 P < 0.05 NS P < 0.05
Hyporesponders
 Egg 4.33 ± 0.80 ii.44 ± 0.71 1.24 ± 0.24 1.37 ± 0.72 2.07 ± 0.80
 Placebo 4.38 ± 0.76 2.48 ± 0.69 1.25 ± 0.23 i.33 ± 0.72 2.08 ± 0.80
 Paired t test NS NS NS NS NS

ane

Values are expressed as mean ± sd. northward = xv hyper- and n = 25 hyporesponders. NS, P > 0.05.

Although hyperresponders had increases in LDL-C after the dietary cholesterol challenge, no significant alter was found in the concentration of apo B (Table v). In improver, dietary handling did not touch on apo Eastward and C-Iii in either response grouping. Nevertheless, hyperresponders did have pregnant (P < 0.05) changes in the activities of LCAT and CETP after the dietary cholesterol challenge. LCAT was elevated from 17.7 ± 4.2 to 20.6 ± 6.seven μmol/(h · L plasma) after egg consumption. Furthermore, CETP activity was 14.three ± 9.i and xviii.6 ± ix.9 μmol/(h · Fifty plasma) during the placebo and egg periods, respectively. However, no significant differences in action were detected for hyporesponders, regardless of treatment period. There was a correlation (P < 0.05, r = 0.53) between changes in HDL-C after egg consumption and CETP activeness changes for the aforementioned flow.

TABLE 5

Plasma apoproteins and LCAT and CETP activities in hypo- and hyperresponders during the egg and placebo periods1

Apo B Apo E Apo C-III Plasma
LCAT CETP
yard/L μmol/(h · 50)
Hyperresponders
 Egg 756 ± 100 38 ± 11 146 ± 62 20.vi ± vi.7 18.6 ± 9.ix
 Placebo 734 ± 100 36 ± 11 140 ± 64 17.7 ± iv.2 14.iii ± nine.1
 Paired t test NS NS NS P < 0.05 P < 0.05
Hyporesponders
 Egg 713 ± 108 34 ± 9 13.three ± 50 16.9 ± three.seven 12.five ± 7.4
 Placebo 731 ± 90 35 ± 8 13.4 ± 50 18.five ± 5.7 xv.4 ± 7.2
 Paired t exam NS NS NS NS NS
Apo B Apo E Apo C-Three Plasma
LCAT CETP
g/Fifty μmol/(h · Fifty)
Hyperresponders
 Egg 756 ± 100 38 ± eleven 146 ± 62 xx.vi ± 6.7 18.half dozen ± 9.ix
 Placebo 734 ± 100 36 ± eleven 140 ± 64 17.7 ± four.2 fourteen.three ± 9.ane
 Paired t test NS NS NS P < 0.05 P < 0.05
Hyporesponders
 Egg 713 ± 108 34 ± nine xiii.3 ± 50 xvi.ix ± 3.7 12.5 ± vii.4
 Placebo 731 ± 90 35 ± 8 xiii.4 ± 50 18.5 ± 5.7 15.four ± 7.2
 Paired t test NS NS NS NS NS

ane

Values are expressed as hateful ± sd. north = 15 hyper- and n = 25 hyporesponders. NS, P > 0.05.

TABLE 5

Plasma apoproteins and LCAT and CETP activities in hypo- and hyperresponders during the egg and placebo periods1

Apo B Apo Due east Apo C-3 Plasma
LCAT CETP
k/L μmol/(h · L)
Hyperresponders
 Egg 756 ± 100 38 ± xi 146 ± 62 20.6 ± 6.vii eighteen.6 ± 9.9
 Placebo 734 ± 100 36 ± 11 140 ± 64 17.7 ± 4.2 14.3 ± 9.one
 Paired t test NS NS NS P < 0.05 P < 0.05
Hyporesponders
 Egg 713 ± 108 34 ± 9 13.3 ± 50 16.ix ± 3.seven 12.5 ± 7.4
 Placebo 731 ± xc 35 ± 8 thirteen.iv ± 50 xviii.five ± 5.7 15.4 ± seven.2
 Paired t test NS NS NS NS NS
Apo B Apo E Apo C-Three Plasma
LCAT CETP
thousand/L μmol/(h · Fifty)
Hyperresponders
 Egg 756 ± 100 38 ± 11 146 ± 62 20.6 ± half dozen.7 eighteen.6 ± 9.9
 Placebo 734 ± 100 36 ± 11 140 ± 64 17.7 ± 4.2 fourteen.3 ± 9.i
 Paired t test NS NS NS P < 0.05 P < 0.05
Hyporesponders
 Egg 713 ± 108 34 ± 9 13.three ± 50 16.9 ± three.vii 12.5 ± vii.4
 Placebo 731 ± 90 35 ± 8 13.iv ± l 18.5 ± v.7 15.4 ± 7.ii
 Paired t exam NS NS NS NS NS

one

Values are expressed equally mean ± sd. n = fifteen hyper- and north = 25 hyporesponders. NS, P > 0.05.

Because the same experimental conditions were used previously to examine the response of premenopausal women to a dietary cholesterol challenge (16), a comparing of the data obtained for the two gender groups was conducted. No changes in LDL-C, HDL-C or the LDL/HDL ratio were found in men and women classified as hyporesponders. All the same, hyperresponders of both genders had significant increases in LDL-C and HDL-C levels after the dietary cholesterol claiming (Fig. 2). Male hyperresponders had an LDL-C concentration of 2.two ± 0.59 mmol/L during the placebo period and 2.viii ± 0.81 mmol/Fifty afterward egg intake. Female hyperresponders had LDL-C levels of two.51 ± 0.70 mmol/L and 3.01 ± 0.71 mmol/L during the placebo and egg periods, respectively. HDL-C levels during the placebo flow were i.57 ± 0.27 mmol/L and 1.19 ± 0.19 mmol/L for female and male hyperresponders, respectively. HDL-C levels in female hyperresponders increased to 1.76 ± 0.twoscore mmol/Fifty after egg consumption. Male hyperresponders experienced a smaller alter in HDL-C after the dietary cholesterol challenge, achieving a mean concentration of 1.28 ± 0.22 mmol/L. Male hyperresponders likewise experienced an increment in the LDL/HDL ratio from one.91 ± 0.70 (placebo) to 2.33 ± 0.fourscore after egg intake, whereas female hyperresponders did not exhibit ratio changes (Fig. 3).

FIGURE 2

Plasma LDL and HDL cholesterol concentrations in men and premenopausal women during egg and placebo periods. Values are means ± sd for male hyperresponders (n = 15) and hyporesponders (n = 25) and female hyperresponders (north = xx) and hyporesponders (n = 31).**Significantly dissimilar from the placebo menstruation (P < 0.001). NS, P > 0.05. Female data were adapted from Herron et al. (16).

Plasma LDL and HDL cholesterol concentrations in men and premenopausal women during egg and placebo periods. Values are means ± sd for male person hyperresponders (n = 15) and hyporesponders (due north = 25) and female hyperresponders (n = 20) and hyporesponders (north = 31).**Significantly different from the placebo period (P < 0.001). NS, P > 0.05. Female data were adapted from Herron et al. (16).

Effigy 2

Plasma LDL and HDL cholesterol concentrations in men and premenopausal women during egg and placebo periods. Values are means ± sd for male hyperresponders (n = 15) and hyporesponders (n = 25) and female hyperresponders (n = 20) and hyporesponders (n = 31).**Significantly different from the placebo menstruum (P < 0.001). NS, P > 0.05. Female data were adapted from Herron et al. (16).

Plasma LDL and HDL cholesterol concentrations in men and premenopausal women during egg and placebo periods. Values are means ± sd for male hyperresponders (n = fifteen) and hyporesponders (n = 25) and female hyperresponders (n = twenty) and hyporesponders (n = 31).**Significantly different from the placebo catamenia (P < 0.001). NS, P > 0.05. Female data were adapted from Herron et al. (sixteen).

FIGURE 3

Plasma LDL/HDL ratios in men and premenopausal women during egg and placebo periods. Values are means ± sd for male hyperresponders (n = xv) and hyporesponders (n = 25) and female hyperresponders (n = 20) and hyporesponders (due north = 31).**Significantly different from the placebo menstruation (P < 0.05). NS, P > 0.05. Female data were adapted from Herron et al. (16).

Plasma LDL/HDL ratios in men and premenopausal women during egg and placebo periods. Values are means ± sd for male person hyperresponders (n = 15) and hyporesponders (n = 25) and female person hyperresponders (n = 20) and hyporesponders (n = 31).**Significantly different from the placebo period (P < 0.05). NS, P > 0.05. Female data were adapted from Herron et al. (16).

Effigy 3

Plasma LDL/HDL ratios in men and premenopausal women during egg and placebo periods. Values are means ± sd for male person hyperresponders (n = 15) and hyporesponders (due north = 25) and female person hyperresponders (n = 20) and hyporesponders (n = 31).**Significantly different from the placebo period (P < 0.05). NS, P > 0.05. Female data were adapted from Herron et al. (16).

Plasma LDL/HDL ratios in men and premenopausal women during egg and placebo periods. Values are means ± sd for male hyperresponders (n = 15) and hyporesponders (n = 25) and female hyperresponders (due north = 20) and hyporesponders (northward = 31).**Significantly different from the placebo period (P < 0.05). NS, P > 0.05. Female data were adapted from Herron et al. (16).

DISCUSSION

Diets high in cholesterol tin can be associated with an increase in consumption of animal products and a decrease in the selection of fruits, vegetables and foods high in fiber (xv). Therefore, to examine the male response to a prolonged exposure to boosted dietary cholesterol consumption, we must offset business relationship for any possible furnishings of dietary fat on plasma lipid concentrations.

Dietary intake analysis.

The analysis of the cocky-reported dietary intake information indicated that both response groups complied with the NCEP step I diet requirements regarding cholesterol and fat intake during both treatment periods. The egg substitute given in this study, although it did contain the same quality and amount of poly peptide, contained no fat or cholesterol. Therefore, the dietary variations observed can exist attributed primarily to the eggs consumed. One whole egg provides 313.5 kJ, i.5 k of SFA, 1.nine k of MUFA and 0.682 yard of PUFA (37). Consequently, both hypo- and hyperresponders reported a pregnant elevation in the pct of energy obtained from total fatty during the egg period, with hyporesponders recording the greatest increment in consumption. Epidemiologic data clearly indicate that a strong positive relationship exists between the pct of energy obtained from SFA and CHD incidence (38). It has been determined that a fluctuation in LDL-C of 0.120 mmol/50 (4.6 mg/dL) can exist expected for every 1% alter in SFA intake with relation to the percentage of total free energy consumed (12). Interestingly, hyporesponders were the but group that reported a meaning increase (1.iv% modify) in the percent of energy obtained from SFA during the egg period. Even so, their mean LDL-C level actually decreased, although non significantly, by 0.04 mmol/L (1.5 mg/dL). It has as well been adamant previously that diets that supercede SFA with MUFA and PUFA result in a decrease in plasma LDL-C concentrations (39). Ane study (40) found that replacing SFA with MUFA resulted in decreases of 12% in TC and 15% in LDL-C levels. In improver, MUFA-rich LDL particles have been shown to be less susceptible to oxidation than those enriched with PUFA (41). In this study, hyperresponders were the only group that reported a significant (P < 0.05) increment in MUFA intake during the egg period. These findings suggest that the fluctuations seen in the plasma compartment are independently driven past the egg's contribution of cholesterol to the diet.

Plasma compartment changes.

It has been reported that gender does not impact the plasma response to dietary cholesterol consumption (xx). Therefore, the men in this study were expected to feel changes in the plasma compartment like to those examined previously in premenopausal women subjected to the same experimental conditions (sixteen). During the high cholesterol period, male person hyperresponders experienced significant increases in LDL-C, HDL-C and the activities of LCAT and CETP. Female hyperresponders also experienced significant increases in LDL-C, HDL-C and CETP activeness after the dietary cholesterol challenge. Furthermore, female hyperresponders had elevated LCAT activity, regardless of dietary treatment. The higher concentrations and action levels of these variables suggest that hyperresponders, regardless of gender, enhance the opposite cholesterol transport pathway to mobilize the excess cholesterol to the liver, the major site of cholesterol elimination from the body.

Peripheral cells cannot degrade sterols; therefore, they rely on the transfer of neutral lipids to lipoproteins. Excess free cholesterol, collected by HDL, must be esterified immediately by LCAT to preserve the hydrophilic nature of the particle and to maintain the concentration gradient for further intake (42). The cholesteryl ester (CE) in the HDL particle has an alternate fate too. CE tin be transferred to the apo B–containing lipoproteins in exchange for triglycerides. This transfer is mediated by CETP. Because increased CETP activeness promotes this enrichment of circulating apo B–containing lipoproteins with CE, and is usually associated with a decrease in HDL-C, information technology is regarded every bit proatherogenic (43). However, if an increment in CETP is not related to a decrease in HDL-C, the protein appears to office in an antiatherogenic fashion by enhancing the enrichment of LDL particles that tin be taken upwardly by the liver, where the cholesterol ester components are metabolized (44). This process represents an indirect pathway of contrary cholesterol send that may be enhanced in some individuals in response to increased dietary cholesterol intake. Other studies (45) have provided evidence suggesting that dietary cholesterol consumption does not inhibit the reverse cholesterol ship pathway, simply in fact enhances cholesterol efflux from cells.

Of particular business organization in the nowadays written report was that the male population had elevations in LDL-C after egg intake that were not offset by the college HDL-C concentrations, and therefore the LDL/HDL ratio was increased. Several previous studies (46 –50) found that a beneficial LDL/HDL ratio tin be maintained after egg consumption. Although this was not the case in the men in this report, the mean was still <3.25, which is considered to be correlated with depression run a risk for CHD according to the updated clinical guidelines of the NCEP adult treatment panel III (51).

The atherogenicity of the LDL particle is too an important indicator of CHD take a chance. LDL particles are heterogeneous with regard to size, density, limerick, charge and atherogenicity (52). Small, dense LDL particles, identified every bit the pattern B bracket, are considered to exist more atherogenic than the larger CE-enriched fraction (53). A predominance of LDL particles in this pattern B bracket has been shown to be associated with a threefold increase in CHD adventure (54 ,55), which may be due to the easy entry of the particle into the arterial wall and its high susceptibility to oxidation. We speculated that because the increase in LDL-C in hyperresponders was not accompanied by an elevation in the measured plasma apo B concentration, this population may have a predominance of the larger, less atherogenic lipoprotein particles subsequently the dietary cholesterol challenge. This is based on the agreement that one apo B is present on each particle, and therefore maintenance of the apoprotein concentration indicates that the increase in LDL-C may not be due to an increase in the number of circulating particles, but to an increment in the size of the lipoprotein.

These results indicate that premenopausal women and men with initial plasma cholesterol concentrations that identify them at a low take chances for CHD do not develop an atherogenic lipoprotein profile after the consumption of additional dietary cholesterol, regardless of their response classification. Information technology is important to notation that the men who participated in this study happened to have low baseline TC values, and therefore were not a representative sample of the overall male person population of the U.s.. This was a random occurrence in that the men were recruited from the University community and no subjects who volunteered were ineligible for participation. Information technology is possible that individuals with college TC concentrations may respond differently to the same dietary handling.

Special thanks are extended to Dolores Silbart, our phlebotomist, for her fourth dimension and effort.

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Abbreviations

  • apo

  • BMI

  • CE

  • CETP

    cholesteryl ester transfer protein

  • CHD

  • HDL-C

  • LCAT

    lecithin:cholesterol acyltransferase

  • LDL-C

  • NCEP

    National Cholesterol Education Program

  • PMSF

    phenylmethylsulfonyl fluoride

  • SFA

  • TC

  • TG

Author notes

1

K.L.H. is the 2002 recipient of the American Egg Board Egg Diet Center Dissertation Fellowship in Diet.

© 2003 The American Social club for Nutritional Sciences