Plasma Cholesterol Distribution Research Articles

Lipid Profiles and Prevalence of Dyslipidemia in Korean Adolescents

Background: The aim of this study is to investigate the distribution of plasma cholesterol and triglyceride levels as well as the preva lence of dyslipidemia among Korean adolescents. Methods: We analyzed data for 3,045 adolescents aged 10-18 years (1,622 boys and 1,423 girls) who participated in the Korea National Health and Nutrition Examination Surveys from 2007 to 2010. Results: The mean values of total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), and high-density lipopro tein cholesterol (HDL-C) were 159, 89, 89, and 52 mg/dL, respectively. Plasma cholesterol levels were significantly higher in girls than those in boys (162.1 mg/dL vs. 155.6 mg/dL, P < 0.0001). The 90th percentile values of total cholesterol, triglycerides, and LDLC were 192, 149, 117 mg/dL for boys, and 195, 147, 119 mg/dL for girls. The 10th percentile value of HDL-C was 38 mg/dL for boys and 40 mg/dL for girls. Triglyceride, LDL-C cholesterol levels increased, whereas plasma HDL-C levels decreased with increasing the body mass index (P < 0.0001) in both genders. Total cholesterol levels significantly increased with increasing the body mass in dex, especially in boys (P < 0.0001). The prevalence of dyslipidemia was 25.2% for boys and 21.7% for girls; this value significantly increased with overweight (37-40%) and obesity (53-56%). Independent predictors (odds ratio) of dyslipidemia were age (1.49), overweight (2.06), and obesity (5.11) for boys; overweight (1.95) and obesity (3.22) for girls. Conclusion: Adolescent dyslipidemia is strongly associated with obesity. Lipid screening for overweight or obese youths should be emphasized. Further, longitudinal studies examining the impact of childhood obesity and dyslipidemia on subsequent cardiovascular diseases are needed. (Endocrinol Metab 27:208-216, 2012)

Cholesterol esterification by ACAT2 is essential for efficient intestinal cholesterol absorption: evidence from thoracic lymph duct cannulation

The hypothesis tested in this study was that cholesterol esterification by ACAT2 would increase cholesterol absorption efficiency by providing cholesteryl ester (CE) for incorporation into chylomicrons. The assumption was that absorption would be proportional to Acat2 gene dosage. Male ACAT2⁺/⁺, ACAT2⁺/⁻, and ACAT2⁻/⁻ mice were fed a diet containing 20% of energy as palm oil with 0.2% (w/w) cholesterol. Cholesterol absorption efficiency was measured by fecal dual-isotope and thoracic lymph duct cannulation (TLDC) methods using [³H]sitosterol and [¹⁴C]cholesterol tracers. Excellent agreement among individual mice was found for cholesterol absorption measured by both techniques. Cholesterol absorption efficiency in ACAT2⁻/⁻ mice was 16% compared with 46-47% in ACAT2⁺/⁺ and ACAT2⁺/⁻ mice. Chylomicrons from ACAT2⁺/⁺ and ACAT2⁺/⁻ mice carried ∼80% of total sterol mass as CE, whereas ACAT2⁻/⁻ chylomicrons carried >90% of sterol mass in the unesterified form. The total percentage of chylomicron mass as CE was reduced from 12% in the presence of ACAT2 to ∼1% in ACAT2⁻/⁻ mice. Altogether, the data demonstrate that ACAT2 increases cholesterol absorption efficiency by providing CE for chylomicron transport, but one copy of the Acat2 gene, providing ∼50% of ACAT2 mRNA and enzyme activity, was as effective as two copies in promoting cholesterol absorption.

Effects of Low-Dose Simvastatin on the Distribution of Plasma Cholesterol and Oxidized Low-Density Lipoprotein in Three Ultra-centrifugally Separated Low-Density Lipoprotein Subfractions: 12- Month, Open-Label Trial

The effects of statins on the distribution of oxidized LDL in plasma LDL subfractions have not been well defined. Effects of 12-month treatment with low-dose simvastatin on the distribution of cholesterol and oxidized LDL in 3 ultracentrifugally separated plasma LDL subfractions were compared in patients with hypercholesterolemia. Simvastatin was administered to 30 hypercholesterolemic subjects for 12 months at an initial dose of 5 mg/day, which was increased to 20 mg/day via 10mg/day to decrease plasma LDL-cholesterol (C) lower than 130 mg/dL. Simvastatin dose was fixed after 3 months of treatment. The amounts of cholesterol and oxidized LDL in 3 ultracentrifugally separated plasma LDL subfractions were compared between 0 and 12 months of treatment. The distribution of ox-LDL skewed to denser LDL fractions, compared with cholesterol in plasma LDL subfractions. Plasma cholesterol in low-density LDL, medium-density LDL and high-density LDL decreased significantly by 31%, 30%, and 25%, respectively (p<0.0001) after 12 months of simvastatin treatment. Plasma oxidized LDL was decreased from 70 U/L to 56 U/L in medium-density LDL (p=0.042). Oxidized LDL in low-density LDL and high-density LDL did not change significantly after 12 months of treatment. Treatment with low-dose simvastatin decreased plasma cholesterol in 3 LDL subfractions and oxidized LDL in medium-density LDL. The decrease of oxidized LDL seemed to be not due to the decrease of cholesterol in plasma LDL subfractions because the decreasing patterns of cholesterol and ox-LDL were different in 3 LDL subfractions.

Chlordecone altered hepatic disposition of [ 14C]cholesterol and plasma cholesterol distribution but not SR-BI or ABCG8 proteins in livers of C57BL/6 mice

Organochlorine (OC) insecticides continue to occur in tissues of humans and wildlife throughout the world although they were banned in the United States a few decades ago. Low doses of the OC insecticide chlordecone (CD) alter hepatic disposition of lipophilic xenobiotics and perturb lipid homeostasis in rainbow trout, mice and rats. CD pretreatment altered tissue and hepatic subcellular distribution of exogenous [ 14C]cholesterol (CH) equivalents 4 and 16 h after a bolus intraperitoneal (ip) injection of 5 ml corn oil/kg that contained 10 mg CH/kg. CD pretreatment altered tissue distribution of exogenously administered [ 14C]CH by decreased hepatic and renal accumulation, and increased biliary excretion up to 300%. Biliary excretion of polar [ 14C]CH metabolites was not altered by CD. CD pretreatment decreased subcellular distribution of [ 14C]CH equivalents in hepatic cytosol and microsomes and lipoprotein-rich fraction-to-homogenate ratio. CD pretreatment increased the ratio of [ 14C]CH equivalents in high density lipoprotein (HDL) to that in plasma and reduced [ 14C]CH equivalents in the non-HDL fraction 4 h after a bolus lipid dose. CD pretreatment increased plasma non-HDL total CH by 80% 4 h after a bolus lipid dose. Scavenger receptor class B type I (SR-BI) and ATP-binding cassette transporter G8 (ABCG8) proteins were quantified by western blotting in hepatic membranes from control and CD treated mice. Liver membrane contents of SR-BI and ABCG8 proteins were unchanged by CD pretreatment. The data demonstrated that a single dose of CD altered CH homeostasis and lipoprotein metabolism.

Homozygous disruption of Pctp modulates atherosclerosis in apolipoprotein E-deficient mice

Phosphatidylcholine transfer protein (PC-TP) is a cytosolic phospholipid binding protein and a member of the steroidogenic acute regulatory-related transfer domain superfamily. Its tissue distribution includes liver and macrophages. PC-TP regulates hepatic lipid metabolism, and its absence in cholesterol-loaded macrophages is associated with reduced ATP binding cassette transporter A1-mediated lipid efflux and increased susceptibility to apoptosis induced by unesterified cholesterol. To explore a role for PC-TP in atherosclerosis, we prepared PC-TP-deficient/apolipoprotein E-deficient (Pctp(-/-)/Apoe(-/-)) mice and littermate Apoe(-/-) controls. At 16 weeks, atherosclerosis was increased in chow-fed male, but not female, Pctp(-/-)/Apoe(-/-) mice. This effect was associated with increases in plasma lipid concentrations. By contrast, no differences in atherosclerosis were observed between male or female Pctp(-/-)/Apoe(-/-) mice and Apoe(-/-) controls fed a Western-type diet for 16 weeks. At 24 weeks, atherosclerosis in chow-fed male Pctp(-/-)/Apoe(-/-) mice tended to be reduced in proportion to plasma cholesterol. The attenuation of atherosclerosis in female Pctp(-/-)/Apoe(-/-) mice fed chow or the Western-type diet for 24 weeks was not attributable to changes in plasma cholesterol or triglyceride concentrations. These findings suggest that PC-TP modulates the development of atherosclerosis, in part by regulating plasma lipid concentrations.

Trans Fatty Acids Affect Lipoprotein Metabolism in Rats

This study was designed to investigate the effects of oleic (CIS), palmitic (SAT) and trans fatty acids (TRANS) on cholesterol metabolism. Rats fed the TRANS diet had lower plasma total cholesterol (P < 0.005) and non-HDL-cholesterol (non HDL-C) concentrations (P < 0.005) compared with their CIS-fed counterparts. Plasma HDL-C was highest in rats fed the SAT diet (P = 0.01). An in vivo assay of reverse cholesterol transport (RCT) was performed whereby radiolabeled cholesterol was delivered to the liver as acetylated LDL and the reappearance of label into plasma and HDL was determined. Plasma radioactivity in TRANS-fed rats was lower than in their SAT-fed counterparts (P = 0.01), and consistent with the cholesterol distribution in plasma, the difference was due to lower [(3)H]-cholesterol in lower density lipoproteins. Despite diet-induced differences in the cholesterol and phospholipid concentrations and fatty acid composition of HDL, the amount of label in HDL did not differ among groups, suggesting that consumption of these diets resulted in HDL populations with similar capacity to participate in RCT. The present findings suggest that dietary trans fatty acids regulate the metabolism of apolipoprotein B-containing lipoproteins in rats and that the effect may be masked in species possessing high plasma cholesteryl ester transfer protein (CETP) activity. These results reinforce the important role of CETP activity in determining the distribution of plasma cholesterol in response to dietary trans fatty acids.

Lipoprotein(a), friedewald formula, and NCEP guidelines

The Friedewald low-density lipoprotein cholesterol formula, which is commonly used in clinical chemistry laboratories, comprises both low-density lipoprotein and lipoprotein(a) cholesterol. This confounder must be recognized and appropriately corrected when dealing with subjects with high plasma lipoprotein(a) levels.

Trans fatty acids and cholesterol metabolism: mechanistic studies in rats and rabbits fed semipurified diets

Studies were conducted in rabbits and rats to investigate the effects of diets rich in oleic (CIS diet), palmitic (SAT diet) and trans fatty acids (TRANS diet) on plasma lipids and lipoprotein metabolism. An important difference between these species is that rabbits possess plasma cholesteryl ester transfer protein (CETP) activity while rats are devoid of transfer activity. In the presence of dietary cholesterol (0.2% w/w) the change in plasma low density lipoprotein-cholesterol (LDL-C) concentration from baseline was significantly higher in rabbits fed the TRANS diet compared with those fed the CIS diet (P < 0.01). Despite this difference, the hepatic LDL-receptor activity was similar in all groups. Also, the fatty acid composition of hepatic phospholipids was affected by diet with lower proportion of palmitic (11%) and higher (19%) linoleic acid despite a similar content in the diet. These effects may represent the maintenance of membrane fluidity within narrow limits to ensure optimal function. The studies in rats showed that the plasma total cholesterol concentration was 20% lower (P < 0.01) in TRANS-fed rats compared with those fed the CIS diet. The results of an in vivo assay of reverse cholesterol transport (RCT) suggested that the three diets gave rise to high density lipoprotein (HDL) particles with similar capacity to accept cellular cholesterol. The differential effects of dietary trans fatty acids in these animal models provide another line of evidence that reinforces the significant role of CETP activity in determining the distribution of plasma cholesterol in response to dietary trans fatty acids.

Effect of the antioxidant probucol on transplant arteriosclerosis in aorta-allografted rabbits

The attenuation of atherogenesis by oral probucol treatment, demonstrated in several animal studies, has been attributed to the antioxidative property of probucol. It is thought that probucol, by inhibiting oxidation of low density lipoproteins (LDL) decreases the uptake of LDL into monocytes, and thereby reduces the development of foam cells and fatty streaks. Also, the neointimal proliferation seen after balloon injury has been attenuated by treatment with probucol. Since foam cells and neointimal proliferation are both important elements of transplant arteriosclerosis, we have investigated whether probucol might also retard the development of experimental transplant arteriosclerosis. The thoracic aorta from one rabbit was transplanted as a bypass graft onto the abdominal aorta of another rabbit. Nine rabbits were treated with 1 g probucol per day and seven animals were treated with vehicle. After a recovery period of 2 weeks, all rabbits were clamped at a human level of plasma cholesterol (6 to 7 mmol/l) for a period of 3 weeks. The amount of dietary cholesterol necessary for this clamping tended to be higher in probucol treated than in vehicle-treated rabbits. The distribution of plasma cholesterol between lipoprotein classes was similar in the two groups, except for the concentration of high density lipoproteins (HDL), which was significantly lowered by probucol. Probucol markedly decreased the susceptibility of LDL and intermediate density lipoprotein plus very low density lipoprotein (IDL + VLDL) particles to oxidation, as measured by the production of conjugated dienes when adding Cu2+. Despite this, the development of transplant arteriosclerosis as well as the number of macrophages in the neointima were not significantly different in the aortic allografts from the two groups. These results suggest that antioxidative agents do not retard the development of experimental transplant arteriosclerosis.

Co-expression of cholesteryl ester transfer protein and defective apolipoprotein E in transgenic mice alters plasma cholesterol distribution. Implications for the pathogenesis of type III hyperlipoproteinemia.

Despite the definite etiologic link between apolipoprotein (apo) E mutations and type III hyperlipoproteinemia (HLP), it is not clear what additional factors are involved in the development of florid hyperlipidemia and how to explain the wide variability in the expression of the hyperlipidemic phenotype in carriers of receptor binding-defective apoE variants. The present study was designed to determine whether the overexpression of cholesteryl ester transfer protein (CETP), a plasma protein that transfers cholesteryl esters from the high density lipoproteins (HDL) to the very low density lipoproteins (VLDL) and whose activity is increased in hyperlipidemic states, plays a role in the development of hyperlipidemia and beta-VLDL accumulation in type III HLP. We produced double-transgenic mice that co-expressed high levels of simian CETP and either high or low levels of a human receptor binding-defective apoE variant, apoE(Cys-142). We previously reported that apoE(Cys-142) high-expresser mice showed spontaneous hyperlipidemia and accumulation of beta-VLDL, whereas the low-expresser mice showed only a modest increase in VLDL cholesterol. Co-expression of CETP induced a massive transfer of cholesteryl esters from the HDL to the VLDL in both lines of double-transgenic mice. As a result, HDL cholesterol and apoA-I levels were reduced to about 50% of normal, VLDL cholesterol increased 2.5-fold, and the cholesteryl ester content of VLDL reached values similar to those observed in human beta-VLDL. The ratio of defective to normal apoE in VLDL was unaffected by CETP co-expression and was higher in animals expressing high apoE levels. Finally, in spite of an increased accumulation of beta-VLDL in the high-expresser mice, the VLDL of the low-expresser mice maintained pre-beta mobility upon co-expression of CETP. The results of this study demonstrate that the ratio of defective to normal apoE on the VLDL, rather than the cholesteryl ester content of VLDL, is the major factor determining the development of severe hyperlipidemia and the formation and accumulation of beta-VLDL in type III HLP.

The influence of dietary olive oil and margarine on aortic cholesterol accumulation in cholesterol-fed rabbits maintained at similar plasma cholesterol level.

The present study compares the atherogenicity of a standard diet and diets with 10% olive oil or 10% margarine added, in rabbits maintained at a mean plasma cholesterol level of about 20 mM for 13 weeks. Each group consisted of 15 animals. The distribution of cholesterol in plasma between VLDL, IDL, LDL and HDL was similar in the 3 groups. The thoracic aortic cholesterol accumulation was 16.6 +/- 1.6, 11.4 +/- 1.0 (P < 0.05) and 12.6 +/- 1.7 (P > 0.05) nmol/mg wet weight for the group receiving standard diet, diet with 10% olive oil added and diet with 10% margarine added, respectively. There was no significant difference between groups in the occurrence of the atherosclerotic changes in the proximal and distal parts of coronary arteries, abdominal aorta and renal arteries. The occurrence of atherosclerotic changes in the pulmonary arteries was equal in the groups receiving standard diet and diet with 10% margarine added while it was significantly lower (P < 0.05) in the group receiving diet with 10% olive oil added. The atherosclerotic changes at the aortic orifice of coronary arteries were quanticated morphometrically and were most severe in the group on the standard diet. The results indicate a comparable atherogenic effect of 10% olive oil or margarine addition to standard diet on development of atherosclerosis in rabbits maintained at a similar plasma cholesterol level. The study also suggests that supplementation of olive oil or margarine to standard rabbit diet leads to lower cholesterol accumulation in the thoracic aorta compared with standard diet, an effect not modulated by changes in plasma cholesterol concentrations.

Effects of blocking plasma lipid transfer protein activity in the rabbit

Plasma lipid transfer protein activity was completely blocked in rabbits for up to 48 h by infusion with goat antibody to rabbit lipid transfer protein. Lipid transfer protein activity in plasma of control animals, infused with antibody from a non-immune goat, decreased during the experiment but was never less than 50% of pre-infusion levels. During the period that lipid transfer protein activity was completely blocked, there were changes in high-density lipoprotein composition (expressed as % by weight) with a reduction in triacylglycerol from 8.4 ± 2.4% to 1.0 ± 0.2% ( P < 0.05) and an increase in esterified cholesterol from 10.7 ± 1.7% to 14.5 ± 0.3% ( P < 0.1). In conjunction with the observed changes in high-density lipoprotein composition, there was an increase in high-density lipoprotein particle size from a mean radius of 4.7 to 5.4 nm. The change in composition and particle size was not observed in high-density lipoproteins from control animals. There was a change in the distribution of plasma cholesterol in control animals, with a fall in the proportion of cholesterol in high-density lipoproteins ( P < 0.02) and consequently an increase in the proportion of cholesterol in low-density lipoproteins ( P < 0.02). However, the distribution of plasma cholesterol in animals in which lipid transfer protein activity was inhibited was maintained at original levels during the period of inhibition. Consequently, in these animals, there was a less atherogenic distribution of cholesterol during the period of lipid transfer protein inhibition when compared with control animals. The changes observed in lipoproteins, in the absence of lipid transfer protein activity, demonstrate that lipid transfer protein modifies lipoproteins in vivo and appears to contribute to a more atherogenic lipid profile.

Effect of Animal and Vegetable Fats and Proteins on Distribution of Cholesterol in Plasma and Organs of Young Growing Pigs

Young, growing pigs were fed for 8 wk diets containing either soy protein isolate or ground beef as the main protein source and soybean oil or beef tallow as the main fat source to examine effects of types of dietary protein and fat on cholesterol distribution between blood plasma, plasma lipoproteins and body organs. Type of dietary protein did not influence concentrations of a)cholesterol in plasma,b)low-density-lipoprotein (LDL) cholesterol,c)high-density-lipoprotein (HDL) cholesterol ord)cholesterol in several organs of pigs. Pigs fed tallow had greater concentrations of plasma cholesterol and LDL and HDL cholesterol than did pigs fed soybean oil. Ratios of HDL to LDL were not altered by dietary fat. Cholesterol concentrations were greater in heart, skeletal muscle and viscera of pigs fed soybean oil than in those fed tallow. Plasma cholesterol varied reciprocally with cholesterol in several tissues. Thus, dietary beef and soy protein isolate had similar effects on cholesterol concentrations in plasma, LDL, HDL and organs, whether pigs consumed soybean oil or beef tallow as a major fat source. Soybean oil, however, exerted a hypocholesterolemic effect, irrespective of major source of dietary protein.

Differential involvement of the lipoproteins in cholesterol transport depending on the level of plasma cholesterol. Study in hypercholesterolemic hamsters

FEC hamsters were used to explore to what extent the could maintain an unchanged distribution of plasma cholesterol among the lipoproteins in becoming even more hypercholesterolemic when fed high-cholesterol diets (0.1% or 0.5%). The results showed that the percentage of cholesterol was significantly changed only in the VLDL by cholesterol supplement in the diet. These lipoproteins became already maximally enriched with cholesterol in animals fed the diet with the lower percentage of cholesterol. More interesting were the alterations observed in the distribution of the excess exogenous cholesterol among the lipoproteins. Up to 200 mg/100 ml of total cholesterol in whole plasma, the cholesterol transported in the IDL and HDL fractions increased significantly. Above this concentration, the excess exogenous cholesterol was located only to the VLDL. There was a close correlation between the VLDL cholesterol content and the level of cholesterol in whole plasma. Thus, the involvement of the lipoproteins in cholesterol transport depended on the level of plasma cholesterol which was itself related to the dietary cholesterol intake.

Effects of Dietary Calcium and Fat on Cholesterol in Tissues and Feces of Young Goats

To examine the effects of amount of calcium and type of fat in the diet on distribution of cholesterol in plasma, several tissues and feces, 4-week-old goats (6 females and 18 males) were fed isocaloric diets consisting of goat milk supplemented with cholesterol and 1) soybean oil, 2) tallow, 3) soybean oil and CaCO3 or 4) tallow and CaCO3 for 20 weeks. Plasma cholesterol increased initially in all animals; plasma and lipoprotein cholesterol concentrations, however, were not affected by dietary fat or calcium. Goats fed CaCO3 excreted more calcium and ash in their feces and had greater cholesterol and fat concentrations in their livers. Neutral steroid, but not bile acid, excretion was greater in soybean oil-fed goats than in goats fed tallow. Soybean oil-fed goats had greater cholesterol concentrations in the viscera (minus liver) and tended to have greater cholesterol concentrations in the carcass and whole body. Aortas of soybean oil-fed goats exhibited greater fat deposition. In summary, dietary fat, but not calcium, significantly altered cholesterol disposition in young goats by affecting cholesterol deposition in tissues and excretion in feces, without a concomitant change in plasma cholesterol.

Comparative studies of the circulating lipoproteins in hamster ( Mesocricetus auratus) with a normal or spontaneous high level of cholesterol in the plasma

1. 1. The lipoprotein profile and the distribution of plasma cholesterol were studied comparatively in two strains of hamster, a normal one, and a second, developing spontaneous hypercholesterolemia associated with a high level of cholesterol esters in the liver. 2. 2. In the hypercholesterolemic animals, the amount of cholesterol was increased by 40, 84 and 69% in the circulating VLDL, LDL and HDL respectively. Moreover, the VLDL were particularly rich in cholesterol esters, 21% of their weight in contrast to 11% in controls. 3. 3. A close positive correlation existed between the enrichment of the VLDL with the esters and the accumulation of cholesterol in the hepatic tissue. 4. 4. In the two strains of hamster, there was similar participation of the various classes of lipoprotein in cholesterol transport, that of HDL being particularly high. These lipoproteins carried more than 50% of the circulating cholesterol.

Freeze-fracture images of distribution of filipin- cholesterol complexes in secretory cells of the anterior pituitary and adrenal medulla of mice.

In order to clarify the distribution of cholesterol in plasma- and cytomembranes of secretory cells of the anterior pituitary and adrenal medulla, freeze-fracture images of the filipin-treated tissues were observed.The distribution of cholesterol in all the secretory cells of these organs shows almost the same pattern. The filipin-sterol complexes are distributed somewhat heterogeneously but in moderately high density on the fractured plasma membranes of all the cells examined. The small shallows on the plasma membrane, corresponding to coated pits and showing aggregates of membrane particles (MP), lack the complexes. The limiting membranes of almost all the secretory granules are very rich in complexes.The membranes of rough endoplasmic reticulum, nucleus, mitochondria, and Golgi apparatus, which are considered to contain rich enzymatic protein and have active functional properties, are very poor in distribution of cholesterol, though small clusters consisting of a few complexes are scattered in these organelles except for mitochondria. In the traps-side of the Golgi apparatus, where the immature secretory granules arise, the complexes are relatively denser in distribution as compared with those of the cis-side.

Nutrient intake: Relationships with lipids and lipoproteins in 6–19-year-old children—The Princeton School District study

Relationships between nutrient intakes and plasma lipids and lipoproteins were studied in 949 randomly selected children, ages 6–19, in the biracial, suburban, Princeton School District. While nutrient intake increased with age in males, such age-associated increases in nutrient ingestion were much less consistent or were not significant for females. Primarily in the 6–9 and 10–12 yr age groups, white children ingested more total calories, more saturated fat, and a lower ratio of polyunsaturated to saturated ( P S ) fat, more total carbohydrates, sucrose, starch, and other carbohydrates, and more protein than black children. After adjusting for age, race, sex, weight, and height, several nutrient-lipid and lipoprotein partial correlation coefficients were significant, but of relatively low magnitude. There were weak but significant inverse correlations between dietary P S ratios and dietary carbohydrates with both total ( r = −.07, −0.7) and low-density lipoprotein cholesterol (C-LDL), ( r = −.07, −.08). Plasma high-density lipoprotein cholesterol (C-HDL) was inversely and significantly correlated with dietary sucrose ( r = −.07); plasma triglyceride correlated positively with dietary sucrose ( r = .08). Potential relationships between nutrients and lipids-lipoproteins were also examined in children at the extremes of, and in the middle of, lipid-lipoprotein distributions. After covariance adjustment for age, sex, race, and Quetelet index, children having the highest levels of C-HDL had the lowest intake of dietary carbohydrate and total calories. After further covariance adjustment for total calories, children at the highest end of the plasma cholesterol distribution had a greater intake of cholesterol and total protein than did children in the lowest end of the distribution. Nutrient intake may play a small but significant role relative to lipids and lipoproteins in children, and as such, may have importance relative to pediatric precursors of atherosclerosis.

RELATIVE DISTRIBUTION OF CHOLESTEROL IN PLASMA AND LIVER COMPARTMENTS OF CHICKS FED DIFFERENT FATTY ACIDS.

SummaryGrowing male chicks were fed a fat-free diet or this diet supplemented with stearic, oleic or linoleic acid, with or without added cholesterol. In cholesterol-fed chicks, dietary oleic or linoleic acid increased plasma and liver cholesterol levels and plasma lipid phosphorus levels. Oleic acid-fed chicks had lower plasma and higher liver cholesterol levels than did linoleic acid-fed animals. The total liver-plasma cholesterol pool was higher in oleic than in linoleic acid-fed chicks, but there was a significant difference in distribution of cholesterol between these two compartments. Total liver lipids paralleled liver cholesterol levels. The fatty acids fed had relatively little effect on the plasma and liver cholesterol levels of chicks receiving a cholesterol-free diet.

The relation between inhibition towards clearing, total cholesterol and the distribution of cholesterol in plasma.

The relation between inhibition towards clearing, total cholesterol and the distribution of cholesterol in plasma.