Effects of dietary cholesterol, dietary fat, and exercise on mouse plasma cholesterol.
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Animals↗
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Characterization of guinea pig plasma lipoproteins: the appearance of new lipoproteins in response to dietary cholesterol.
Dietary cholesterol induces a hemolytic anemia in guinea pigs, accompanied by changes in the lipid composition of red cells and of plasma lipoproteins. This report presents a characterization of the lipoprotein species present in each main density class in both control and cholesterol-fed guinea pigs. Traces of a typical high density lipoprotein (HDL) were detected in control plasma. HDL from cholesterol-fed, anemic guinea pigs differed from control HDL in electron microscopic appearance and lipid and peptide composition. Long stacks of discs were observed in the electron microscope in addition to smaller, spherical particles characteristic of control HDL. Low density lipoproteins (LDL) from cholesterol-fed, anemic guinea pigs had two main populations, which were separated by gel chromatography. One population appeared in the electron microscope as large transparent discs and contained mainly unesterified cholesterol and phospholipids in a 2:1 molar ratio. The other population resembled control LDL in size and composition except for its high unesterified cholesterol content. Dietary cholesterol also altered the composition and decreased the electrophoretic mobility of very low density lipoproteins. Gel electrophoretic and immunochemical evidence indicates that a peptide (mol wt 35,000) appears in lipoproteins from cholesterol-fed, anemic guinea pigs that is undetectable in those of controls. Similarities between the cholesterol-induced lipoprotein abnormalities in guinea pigs and those reported in patients with obstructive jaundice, biliary cirrhosis, type III hyperlipoproteinemia, or familial lecithin:cholesterol acyltransferase deficiency are discussed.
Animals↗
Endogenous cholesterol synthesis, fecal steroid excretion and serum lanosterol in subjects with high or low response of serum cholesterol to dietary cholesterol.
In this study we addressed the question whether hypo- and hyper-responders to dietary cholesterol differ with regard to the flexibility of endogenous cholesterol synthesis after changes in cholesterol intake. Whole-body cholesterol synthesis was measured as faecal excretion of neutral steroids and bile acids minus cholesterol intake. In addition, we determined serum concentrations of lanosterol, a precursor of cholesterol and a possible indicator of cholesterol biosynthetic activity. The study was carried out with 2 hyper- and 4 hypo-responders; these subjects had shown a consistently high or low response of serum cholesterol to a decrease in dietary cholesterol in two previous experiments. The subjects received controlled high- (on average 697 mg of cholesterol per day) and low-cholesterol (109 mg/day) diets for periods of 4 weeks in succession; cholesterol was the only dietary variable. The two hyper-responders again showed a significant decrease in serum cholesterol. There was essentially no decrease in serum cholesterol in three of the four hypo-responders. The decrease in cholesterol intake caused an increase in cholesterol synthesis in five out of the six subjects. There was no association between the individual change in serum cholesterol and the change in cholesterol synthesis. Transfer from the high- to low-cholesterol diet caused an increase in serum lanosterol in all subjects. The increase was 3- to 4-fold higher in three out of the four hypo-responders than in the two hyper-responders. We tentatively suggest that this study provides some evidence that the flexibility of cholesterol synthesis is involved in the responsiveness to dietary cholesterol.
Journal Article↗
Plasma lipoprotein profiles and arylesterase activities in two inbred strains of rabbits with high or low response of plasma cholesterol to dietary cholesterol.
Cholesterol feeding for 4 weeks of female and male rabbits of two inbred strains increased plasma cholesterol concentrations by about 11 and 48 mmole/1 in the hypo- and hyperresponsive strain, respectively. On the low-cholesterol pre-experimental diet, the hyporesponsive animals had significantly higher plasma HDL (high density protein) cholesterol levels than hyperresponders. In both strains, cholesterol feeding caused elevations of cholesterol in all lipoprotein classes, the difference between the hypo- and hyperresponsive strains in essence only being observed in the VLDL (very low density lipoprotein) fraction. Basal plasma total arylesterase activity was significantly higher in the hypo- than in the hyperresponsive rabbits. Dietary cholesterol caused an increase in plasma esterase activity in both We suggest that in rabbits a low plasma arylesterase activity and a low concentration of HDL cholesterol are associated with an increased sensitivity to dietary cholesterol.
Animals↗
Effects of exercise, dietary cholesterol, and dietary fat on blood lipids.
Exercise, a low fat diet, or a diet low in saturated fat content can each lower plasma total cholesterol and low-density lipoprotein (LDL) cholesterol. We investigated whether these factors together could prevent the lipid-raising effects of dietary cholesterol. Ten healthy, athletic, normolipidemic male volunteers were studied. Two diets of 4 weeks duration each were compared in a randomized, blind crossover design. Diets were identical except for cholesterol content: one contained 600 mg/d; the other 200 mg/d. Both diets contained 15% of calories as protein, 55% as carbohydrate, 30% as fat, and the polyunsaturated fat to saturated fat ratio was 1.5. Exercise level and body weight were kept constant in each subject. As compared with plasma values obtained following the 200-mg/d cholesterol diet, mean values following the 600-mg/d cholesterol diet significantly increased for LDL cholesterol and apolipoprotein B by 10% and 13%, respectively. Mean plasma triglycerides, high-density lipoprotein 2 and 3, and apolipoprotein A-1 levels did not change significantly. Individual responses, however, were highly variable. Three subjects increased LDL cholesterol by more than 25%; 2 subjects increased LDL cholesterol by 10% to 25%; and 5 subjects had 5% or less change in LDL cholesterol. A dietary cholesterol increase can significantly elevate plasma LDL cholesterol and apolipoprotein B in certain normolipidemic, healthy men even when they are exercising regularly and consuming a moderately fat restricted, low saturated fat diet. Dietary cholesterol restriction may therefore be justifiable even when other life-style and dietary measures to minimize blood cholesterol are undertaken.
Adult↗
Treatment of young rats with cholestyramine or a hypercholesterolemic diet does not influence the response of serum cholesterol to dietary cholesterol in later life.
Groups of 10 female Wistar rats (aged 4 weeks) were fed for 29 days either a low-cholesterol commercial diet, a commercial diet containing 2% (w/w) cholesterol, 0.5% cholate and 5% olive oil or a diet containing 2% cholestyramine. The rats were then fed the low-cholesterol commercial diet for the next 91 days and the high-cholesterol diet for another 29 days. There was no significant difference between the groups in the increase of cholesterol in serum and liver during the last period of cholesterol feeding. A fourth group of 10 animals was fed the diet containing cholesterol and cholate during the entire experimental period of 149 days. By the end of the experiment serum cholesterol in these animals was lower and liver cholesterol was higher than in the 3 groups fed the high-cholesterol diet during days 120-149 of the experiment. This study does not present evidence for imprinting effects of early diet manipulation on the later cholesterolemic response to a high cholesterol diet.
Age Factors↗
Plasma and dietary cholesterol in infancy: effects of early low or moderate dietary cholesterol intake on subsequent response to increased dietary cholesterol.
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Aging↗
A new method for assaying rat liver microsomal 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity and its application in a study of the effect of dietary cholesterol on this effect of dietary cholesterol on this enzyme.
A new method suitable for measuring rat liver 3-hydroxy-3-methylglutaryl-CoA reductase activity is described and its advantages over methods previously available are discussed. An accurate time course was measured for the inhibition of liver microsomal 3-hydroxy-3-methylglutaryl-CoA reductase activity by dietary cholesterol; this enzyme was affected 1 1/4 h after the rats began to consume a cholesterol-rich diet. In this experiment there was no correlation between concentrations of microsomal cholesterol ester and the activity of 3-hydroxy-3-methylglutary-CoA reductase.
Alcohol Oxidoreductases↗
U-shape relationship between change in dietary cholesterol absorption and plasma lipoprotein responsiveness and evidence for extreme interindividual variation in dietary cholesterol absorption in humans.
A possible relationship between change in dietary cholesterol absorption and plasma lipoprotein responsiveness was examined in 18 normal subjects fed low fat low cholesterol, high fat low cholesterol, and high fat high cholesterol diets. For the group, neither dietary cholesterol nor dietary fat affected the percentage dietary cholesterol absorption, whereas dietary cholesterol intake raised total and LDL-C and dietary fat raised total, LDL, and HDL-C. On a fixed diet there was approximately a 2-fold variation among subjects in percentage dietary cholesterol absorption. Subjects also varied in response to dietary cholesterol and fat with regard to dietary cholesterol absorption and plasma lipoprotein responsiveness. There was a U-shaped parabolic relationship between dietary cholesterol-induced percent change in LDL-C and the change in percentage dietary cholesterol absorption (R2 = 0.62, P = 0.005). A similar but weaker relationship characterized the responsiveness of HDL-C (R2 = 0.38, P = 0.05). For the group, increased cholesterol intake raised dietary cholesterol mass absorption from 1.6 to 4.6 mg/kg per day, but the range of increase was from 1 to 4.7 mg/kg per day. Increased fat intake also affected dietary cholesterol mass absorption with most subjects displaying a strong inverse relationship between fat intake and mass absorption (r = -0.77, P < 0.003). In summary: i) the percentage change in dietary cholesterol absorption in response to dietary cholesterol does appear to regulate diet responsiveness of LDL and HDL-C, and ii) the large variability in percent absorption and changes in percentage and mass absorption in response to dietary cholesterol suggest the presence of genetically determined differences among individuals in the regulation of dietary cholesterol absorption.
Adult↗
Stimulation of fatty acid biosynthesis by dietary cholesterol and of cholesterol synthesis by dietary fatty acid.
We reported previously that dietary cholesterol produces hypertriglyceridemia in the rat, accompanied by reduced oxidation and increased incorporation of exogenous fatty acid into hepatic triglyceride and increased secretion of very low density lipoprotein. We now report that dietary cholesterol also increases net hepatic fatty acid synthesis and the incorporation of newly synthesized fatty acid into hepatic triglyceride in vivo. Male rats were fed a cholesterol-free, semisynthetic diet (5% [w/w] corn oil) for 7 days, or the same diet supplemented with 0.5% cholesterol. On the day of the experiments, fed animals received 5 mCi 3H2O intraperitoneally (i.p.) either at 1200 h (6 h into the light cycle) or at 2400 h (6 h into the dark cycle). Animals were killed 1 h after receiving the radioisotope. Feeding cholesterol increased hepatic triglyceride and cholesteryl ester concentrations, moderately elevated the content of free cholesterol, but did not affect phospholipid levels. Increased net synthesis of fatty acids by livers of animals receiving cholesterol was observed during the dark period; a similar increase during the light period was also observed for incorporation of newly synthesized fatty acid into hepatic phospholipid and cholesteryl ester, although incorporation into triglyceride was of borderline significance (P < 0.06). In other experiments male rats were fed similar diets for 3, 7, or 21 days. Fed animals received 10 mCi 3H2O, i.p. (900-1000 h), and were killed 24 h later. Duration of feeding did not influence rates of net fatty acid synthesis or the stimulation by cholesterol of incorporation of newly synthesized fatty acid into hepatic triglyceride and cholesteryl ester.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Serum cholesterol response to dietary cholesterol.
Serum cholesterol change, delta Chol mg/dl, from change only in dietary cholesterol, mg/1,000 kcal, x, was analyzed with data from 39 controlled experiments on 64 adults with the model delta Chol = b(x2k-x1k). Values of b were found by iteration for exponents k = 0.3 to k = i.0 yielding eight regression equations to check predicted against observed. The smallest root mean square deviation regression was 7 mg/dl given by delta Chol = 1.5(x2(1/2)-x1(1/2] which predicted an average serum cholesterol change of 18.7 versus 19.9 observed. The relationship pertains to calorie balance on a wide range of nutritionally acceptable diets. A prediction equation proposed from experiments in Massachusetts that took k = 1.0 overpredicted the effect of dietary cholesterol in these experiments by 300%.
Cholesterol↗
THE EFFECT OF DIETARY CHOLESTEROL AND DIFFERENT DIETARY FATS ON CHOLESTEROL CONTENT AND LIPID COMPOSITION OF EGG YOLK AND VARIOUS BODY TISSUES.
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Animals↗
Age-associated reduction of prostacyclin and thromboxane synthesis is inversely related to plasma cholesterol levels: modulation by dietary cholesterol supplementation.
Abnormalities of vasoactive eicosanoid synthesis with age are reported. We observed an age-associated reduction of vascular prostacyclin production and thrombin-stimulated thromboxane A2 production in blood. Amounts of production of these eicosanoids were inversely related to plasma cholesterol levels. However, there were no such relationships in rats supplemented with cholesterol. Dietary cholesterol supplementation induced a reduction of thromboxane A2/prostacyclin ratio regardless of age. These results suggest that age-associated changes of blood cholesterol levels are closely linked with vasoactive eicosanoid synthesis and that excessive consumption of cholesterol may induce a compensatory reaction by reducing the thromboxane A2/prostacyclin ratio.
6-Ketoprostaglandin F1 alpha↗
Effects of dietary cholesterol and type of dietary carbohydrate on hepatic and plasma glycerides and phospholipids in the gerbil.
The influence of dietary cholesterol at levels of 0.01-0.5% (by weight) and carbohydrate type (starch, sucrose or a starch-sucrose mixture) on levels and composition of hepatic and plasma glycerides in the male Mongolian gerbil (Meriones unguiculatus) was studied. Hepatic and plasma triglyceride (TG) levels were generally higher with dietary cholesterol supplementation (0.1 and 0.5%), and animals fed sucrose diets exhibited very low levels of hepatic and plasma TG. The mixed carbohydrate (starch-sucrose) did not affect glycerides in a way that could be interpolated from feeding starch or sucrose diets alone. The percent of 16:0 in liver TG was depressed with cholesterol-feeding (at the 0.5% level only), whereas the percent of 18:1 was elevated. Sucrose diets produced higher percentages of 18:0 in liver TG. Dietary cholesterol elevated concentrations of plasma but not liver phospholipid (PL). Percentages of 20:40 omega 6 and 22:6 omega 3 acids in liver and plasma PL were significantly depressed by cholesterol supplementation, whereas the percent of 18:2 in liver PL was higher when feeding cholesterol and starch (no sucrose). Dietary cholesterol produced higher levels of hepatic 1,2-diglyceride with lower percentages of 18:0 and 20:4 omega 6 and higher percentages of 18:1 and 18:2. Dietary cholesterol may possibly influence fatty acid elongation and desaturation reactions as well as transacylation reactions in phospholipid synthesis. In this regard, compositional data suggested a suppressing effect of dietary cholesterol on 22:6 omega 3 formation as exemplified by a 40% diminution in the docosahexaenate content of hepatic phosphatidylethanolamine in gerbils fed a 0.5% cholesterol diet for only 7 days.
Animals↗
Existence of consistent hypo- and hyperresponders to dietary cholesterol in man.
Hyper- and hyporesponsiveness of serum cholesterol to dietary cholesterol is an established concept in animals but not in man. The authors studied the stability of the individual response of serum cholesterol to dietary cholesterol in three controlled experiments in 1982. The subjects were volunteers from the general population living in or near Wageningen, the Netherlands. Each experiment had a low-cholesterol baseline period (121, 106, and 129 mg/day in experiments 1, 2, and 3, respectively) and a high-cholesterol test period (625, 673, and 989 mg/day). Duplicate portion analysis showed that dietary cholesterol was the only variable. The 94 healthy men and women who completed experiment 1 showed an increase (mean +/- standard deviation (SD] in serum cholesterol of 0.50 +/- 0.39 mmol/liter (19 +/- 15 mg/dl). Seventeen putative hyperresponders, defined by their response in experiment 1, were retested in experiments 2 and 3; they showed responses of 0.28 +/- 0.38 mmol/liter (11 +/- 15 mg/dl) and 0.82 +/- 0.35 mmol/liter (32 +/- 14 mg/dl), respectively. Fifteen hyporesponders, selected in experiment 1, showed responses in experiments 2 and 3 of 0.06 +/- 0.35 mmol/liter (2 +/- 14 mg/dl) and 0.47 +/- 0.26 mmol/liter (18 +/- 10 mg/dl), significantly lower than the corresponding values for hyperresponders. The standardized regression coefficient for individual responses in experiment 2 on those in experiment 1 was beta = 0.34 (p = 0.03, n = 32); the corresponding regression coefficient for experiment 3 and experiment 1 was 0.53 (p less than 0.01). After correction for intraindividual fluctuations the true responsiveness distribution was found to have a between-subject standard deviation of about 0.29 mmol/liter (11 mg/dl). This implies that if the mean response to a certain dietary cholesterol load amounts to e.g., 0.58 mmol/liter (22 mg/dl), then the 16% of subjects least susceptible to diet will experience a rise of only 0.29 mmol/liter (11 mg/dl) or less, while in the 16% of subjects most susceptible to diet, serum cholesterol will rise by 0.87 mmol/liter (34 mg/dl) or more. The authors conclude that modest differences in responsiveness of serum cholesterol to dietary cholesterol do exist in man, and that the wide scatter of responses observed in single experiments is largely due to chance fluctuations.
Adult↗
Dietary cholesterol metabolism in Japanese quail lines selected for plasma cholesterol levels.
Dietary cholesterol metabolism was studied, using a single dose of emulsion, per os (test meal), in lines of Japanese quail that were divergently selected for high (HL) and low (LL) plasma total cholesterol. The meal contained [3H] cholesterol, [14C] beta-sitosterol, unlabeled cholesterol, triolein, and bile salt. Recovery of the nonabsorbable beta-sitosterol in the excreta permitted determination of the percentage of cholesterol absorbed. The amounts of [3H] in the plasma, egg yolks, and the excreta neutral and acid sterols were determined. A line-x-time interaction for [3H] in plasma indicated that the level of plasma cholesterol derived from the test meal declined more rapidly in the LL than in the HL. The higher [3H] detected in the excreta acidic sterols of the LL 12 hr after the test meal indicated that bile acid excretion of cholesterol was greater in the LL than in the HL. There were no differences in cholesterol absorption between lines or sexes. Cumulative [3H] radioactivity in the eggs over 18 days following the test meal was higher in the HL yolks; however, this line effect was due to the greater number of eggs produced by the HL. Thus, one of the mechanisms by which the LL maintains low plasma cholesterol levels is by an enhanced excretion of bile acid compared with the HL. The data also suggest that the more severe atherogenic effect of dietary cholesterol observed in the HL could be, in part, due to the longer residence time of cholesterol in circulation.
Animals↗
Dependence of the effects of dietary cholesterol and experimental conditions on serum lipids in man. I. Effects of dietary cholesterol in a linoleic acid-rich diet.
In this experiment the effect of dietary cholesterol in a linoleic acid-rich diet on serum cholesterol was tested. In a cross-over design 41 young healthy students received a linoleic acid-rich diet for 4 weeks at two levels of dietary cholesterol. The diet contained 14 to 15 energy% linoleic acid. The high cholesterol diet was obtained by adding two egg yolks a day to the rations. Supplementation of the linoleic acid-rich diet with the egg yolk cholesterol caused a significant rise of serum cholesterol of about 11 mg/100 ml (0.29 mmole/liter). The dietary cholesterol did not influence serum triglyceride levels. The influence on serum cholesterol was much less than expected, based on several predictive formulas. It is concluded that the presence of a high content of linoleic acid in the diet reduces the effect of dietary cholesterol on serum cholesterol if the cholesterol is provided as egg yolk.
Adult↗
Hypercholesterolemic effect of dietary cholesterol in diets enriched in polyunsaturated and saturated fat. Dietary cholesterol, fat saturation, and plasma lipids.
Within the context of reduced-fat diets, the effects of incorporating a fat high in stearic acid and adding moderate amounts of dietary cholesterol were examined in 14 middle-aged and elderly women and men (range, 46 to 78 years) with low-density lipoprotein cholesterol (LDL-C) concentrations > 130 mg/dL (range, 133 to 219 mg/dL) at screening. The subjects consumed each of the five diets, which were as follows: (1) a baseline diet (35% fat with 13% saturated fatty acids [SFAs], 12% monounsaturated fatty acids [MUFAs], and 8% polyunsaturated fatty acids [PUFAs], and 128 mg cholesterol/1000 kcal); (2) a reduced-fat diet, in which two thirds of the fat was provided as corn oil (corn oil-enriched diet: 29% fat with 7% SFAs, 9% MUFAs, and 11% PUFAs and 85 mg cholesterol/1000 kcal), which met the National Cholesterol Education Program (NCEP) Step 2 guidelines; (3) a reduced-fat diet, in which two thirds of the fat was provided as beef tallow (beef tallow-enriched diet: 31% fat with 13% SFAs, 11% MUFAs, and 3% PUFAs and 109 mg cholesterol/1000 kcal); and two reduced-fat diets, one (4) enriched in corn oil and the other (5) enriched in beef tallow, to which moderate amounts of cholesterol in the form of egg yolk were incorporated (197 or 226 mg cholesterol/1000 kcal final cholesterol content in corn oil- or beef tallow-enriched diets, respectively). All diets were isocaloric and all food and drink were provided by the metabolic kitchen. Reducing the fat content of the diet resulted in decreased concentrations of LDL-C and high-density lipoprotein cholesterol (HDL-C).(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗