Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cholesterol metabolism”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1979

Changes in cholesterol metabolism with dietary cholesterol in children with familial hypercholesterolaemia.

1. Possible defects in cholesterol metabolism were sought in children with familial hypercholesterolaemia. 2. In nine affected children (eight heterozygotes and one homozygote) and in five healthy children, cholesterol synthesis and bile acid synthesis were determined from the excretion of steroids in the faeces during a low cholesterol diet. Cholesterol synthesis of 10.1 +/- 4.4 mg day-1 kg-1 in the hypercholesterolaemic children was similar to that in these and other normal children. Mean bile acid synthesis of 4.0 +/- 2.1 mg day-1 kg-1 also resembled normal values though three severely affected heterozygotes excreted substantially less. 3. The response to 4 weeks' additional 450 mg of dietary cholesterol/day led to variable changes in the plasma cholesterol and in the sterol balance. On average the affected children showed a rise in plasma cholesterol which resembled that in healthy subjects. The sterol balance fell in most, suggesting a reduction in cholesterol synthesis, which is the normal response to dietary cholesterol. 4. The response to dietary cholesterol was therefore at least qualitatively similar in the hypercholesterolaemic children to that reported in healthy subjects.

Adolescent↗
PubMed1976

Dietary fibre and cholesterol metabolism: effect of fibre rich polysaccharide from blackgram (Phaseolus mungo) on cholesterol metabolism in rats fed normal and atherogenic diet.

The effect of the fibre rich polysaccharide from black gram was studied on the concentration of cholesterol in the tissues, bile salts in the liver and faecal excretion of sterols and bile salts in rats fed normal and high fat cholesterol diet as compared to glucose and sucrose. The binding of bile salts "in vitro" by the polysaccharide was also studied. The rats fed polysaccharide showed the lowest level of cholesterol in the serum, liver and aorta both in normal and high fat -- cholesterol diet groups. Excretion of faecal sterols and bile salts was maximum in the animals fed polysaccharide. The concentration of bile salts in the liver was also maximum in the animals of this group. There was significant binding of bile salts by the polysaccharide when either natural bile or pure bile salt solution was shaken with it. The extent of binding of bile salts was however decreased in the presence of fatty acids, which also released some of the absorbed bile salts from the polysaccharide on subsequent shaking.

Animals↗
PubMed1975

Cholesterol metabolism by Mycobacterium.

Cholesterol metabolism by Mycobacterium species ATCC Number 19652 was studied in defined media. Whole cells were found to take up 91% of the total cholesterol when incubated five days at 34 degrees C in media of pH 6.8-7.4. Uptake of cholesterol by whole cells could be significantly inhibited by 2,4-dinitrophenol and dicyclohexylcarbodiimide. Growth media supernates as well as isolated microbial cell walls were found to contain cholesterol hydrolysing activity. This activity was extractable by Triton X-100 and appeared to have a molecular weight of approximately 100-200,000.

Cell Wall↗
PubMed1978

Multicompartmental analysis of cholesterol metabolism in man. Characterization of the hepatic bile acid and biliary cholesterol precursor sites.

The present report has presented the first clear evidence in man for the existence of specific hepatic cholesterol precursor sites associated with the formation and secretion of bile acids and biliary cholesterol. These hepatic compartments derive virtually all their cholesterol from newly synthesized and lipoprotein free cholesterol. The model which is presented was formulated on current concepts of cholesterol metabolism in man and is concerned, at this initial stage, with the elucidation of the bile acid and biliary cholesterol compartments. The complexity of cholesterol metabolism in man necessitated an initial approach that would minimize the number of inputs of cholesterol into the system, allow for the sampling of several cholesterol compartments, and permit the simultaneous labeling of newly synthesized cholesterol and preformed cholesterol. To achieve these objectives, we studied the patient with a total bile fistula. Six patients were administered simultaneously pulse injections of labeled mevalonic acid and [(14)C]cholesterol. The qualitative features of the specific activity time course curves after labeled mevalonic acid revealed no precursor-product relationship between bile acid, biliary cholesterol, and plasma free cholesterol. The peak specific activity of the bile acids was reached in approximately 100 min and was higher than the biliary cholesterol, which was higher than the plasma free cholesterol. The plasma free cholesterol specific activity became higher than the other lipids after 12 h and remained higher throughout the period of study. Similar related observations were made with [(14)C]cholesterol. The data were then subjected to simulation analysis and modeling using the SAAM-27 computer program. Computer least-square fits of the data were obtained after the model was evolved. During the model development, the least number of compartments and transport pathways were introduced consistent with a good fit of the data. Of particular importance was the constraint that the model fit the data obtained from both [(14)C]cholesterol and labeled mevalonic acid. The same parameter values were used to fit the data from both tracers. The fluxes arrived at in the model indicate that 31% and 20%, respectively, of the cholesterol input into the bile acid and biliary cholesterol precursor sites were derived directly from the newly synthesized hepatic cholesterol. The remainder had its origin predominantly from lipoprotein free cholesterol. Plasma esterified cholesterol (as free) made a small contribution (11%) to the bile acid compartment. Similarly, 10% of the biliary cholesterol arose from an unknown hepatic site. The present report has provided the basis for a new procedure for studying in vivo cholesterol metabolism in man. Examination of the derived cholesterol flux rates between the compartments suggests the presence of an important mechanism regulating the partitioning of lipoprotein free cholesterol between the bile acid and biliary cholesterol precursor sites. Aberrations in the proportioning of precursor cholesterol between these sites could be a causative factor precipitating the excessive secretion of biliary cholesterol and the production of lithogenic bile.

Aged↗
PubMed1979

Effect of contact inhibition on the regulation of cholesterol metabolism in cultured vascular endothelial cells.

Cholesterol synthesis in actively growing bovine vascular endothelial cells is regulated by low density lipoprotein (LDL) at a step prior to mevalonate formation, in a manner comparable to that found in aortic smooth muscle cells. LDL uptake by these cells is associated with induction of cholesterol esterification, an increase in total cell cholesterol, and an inhibition of endogenous sterol synthesis. In contrast, cholesterol metabolism in confluent contact-inhibited endothelial cultures was not significantly affected by LDL even though the cells bind the lipoprotein at high affinity receptor sites. Lysosomal degradation and subsequent regulatory effects on cellular cholesterol metabolism, however, were observed in contact-inhibited endothelial cells incubated with cationized rather than native LDL. Cationized LDL enter the cells independently of the high affinity sites. Therefore, the primary regulation of cholesterol metabolism in these cells is neither through the appropriate intracellular enzymes nor through the high affinity surface receptors, but via an inhibition of LDL internalization. It is suggested that this inhibition is due to a strict contact-inhibited morphology which enables the endothelium of the larger arteries to function as a selective barrier to the high circulating levels of plasma LDL.

Animals↗
PubMed1976

[Effect of nicotinic acid derivatives on the cholesterol metabolism with special regard to biosynthesis, absorption and excretion of cholesterol in the salivary gland (author's transl)].

The cholesterol metabolism of the salivary gland of mice fed on a diet containing 0.5% nicotinic acid derivative, 2, 2, 6, 6, tetrakis--(nicotinoyl-oxymethyl)--cyclohexanol (K-31) was as follows. 1. Total cholesterol level of sublingual and submaxially glands decreased in mice fed on normal diet as well as cholesterol-added diet. 2. The in vivo cholesterol biosynthesis from the acetate-1-14C increased in the sublingual gland, while it was not affected in the submaxillary gland. However, in vitro cholesterol synthesis decreased in both sublingual and submaxillary glands. 3. The disappearance of cholesterol-4-14C injected into the mice was more rapid in the K-31 treated mice than in the control after 30 days. 4. The incorporation of cholesterol-7-3h with a constant specific radioactivity administered orally for 37 days was reduced in the sublingual and submaxillary glands of K-31 treated mice. 5. When the mice were maintained on cholesterol-added diet for 21 days after cholesterol-4-14C injection, the excretion of sterol-14C in the feces was increased in K-31 treated mice. Thus, it was considered that the decrease of the cholesterol level of salivary glands by oral administration of K-31 is due to the increase of the excretion of cholesterol, the decrease of the uptake of the external cholesterol and the increase of excretion of sterol in the feces. These alterations of the cholesterol metabolism appear to induce cholesterol biosynthesis.

Animals↗
PubMed1976

Cholesterol metabolism in groups of rhesus monkeys with high or low response of serum cholesterol to an atherogenic diet.

Cholesterol metabolism has been studied in two groups of five rhesus monkeys each that were selected from the upper and lower sextile in the distribution of serum cholesterol concentration while being fed an atherogenic diet. This diet consisted of a basal commercial monkey food supplemented with saturated fat and cholesterol. To determine differences that might be related to the difference in serum cholesterol concentration, parameters of whole body cholesterol metabolism were measured while the animals were fed the supplemented diet again while they were fed the basal diet. Serum cholesterol and triglyceride concentrations were greater in the high-respoonding (HI) than in the low-responding (LO) groups during both diet periods. Percent of luminal cholesterol absorbed was also greater in the HI than in the LO group during both diet periods. The increase in fecal excretion of endogenous neutral steroids during the period when the atherogenic diet was fed was similar in the two groups; however the increase in excretion of bile acids was greater in the HI than in the LO group. The three-pool model was used for analysis of decay of serum cholesterol specific activity after a tracer pulse dose. The mean size of the total miscible body pool and of pools 1 and 3 (but not pool 2) was greater in both groups when the atherogenic diet was fed than during basal diet feeding. The distribution of the increment in total body pool between pool 1 and the peripheral pools was similar in the two groups. The distribution of the increment in cholesterol of pool 1 between serum and other tissues was also similar for the two groups. There was an indication that a constant cholesterol pool size was not attained even after feeding the atherogenic diet for 8 months. This study indicates that the difference in serum cholesterol concentration between LO and HI responders is, in part, a result of differences in rate of intestinal absorption of cholesterol.

Animals↗
PubMed1977

Cholesterol metabolism in Papua New Guineans.

Cholesterol metabolism has been studied in a group of healthy males drawn from a New Guinea highland population whose plasma cholesterol concentration is low by Western standards and does not rise with age. Mean values from compartmental studies in six subjects were: pool A mass 289 mg/kg; production rate 1069 mg/day or 17.4 mg kg-1 day-1. The average rate of endogenous synthesis measured by sterol balance in twelve men was 751 mg/day or 12.4 mg kg-1 day-1. There was evidence of probable suppression of synthesis by about 500 mg/day when 1 g/day of egg yolk cholesterol was added to the diet of six subjects for 5 weeks. In the latter group, mean cholesterol absorption was 39% (390 mg/day) but the plasma cholesterol concentration did not rise, possibly reflecting compensatory redution in synthesis. It is suggested that these results were unexceptional, except possibly for the failure of the plasma cholesterol concentration to rise when cholesterol was ingested, despite gross differences in diet and many other factors.

Adult↗
PubMed1978

The effect of dietary fat supplements on cholesterol metabolism in ruminants.

The serum cholesterol on ruminant animals rises when supplemental fat is fed in a form that ensures the absorption of long-chain fatty acids. The effects of these fat supplements on cholesterol metabolism have been studied in sheep and goats. The proximal part of the small intestine was the major site of sterol synthesis in sheep. Supplementing the diet with fat significantly enhanced sterolgenesis in the small intestine both in vivo and in vitro, whereas in vitro sterolgenesis appeared to be suppressed in the liver. Increased intestinal sterolgenesis was seen with several varieties of fat, but was greatest when palm oil was fed. The reciprocal findings in the intestine and liver may reflect the increased requirement for cholesterol for the transport of triglyceride in chylomicrons and the secondary inhibiting effect of this cholesterol on sterol synthesis in the liver. Dietary fat supplementation did not alter the excretion of neutral steroids in the feces of goats but did not cause a marked reduction in the excretion of acidic steroids which may have been due to the decreased formation of sterols in the liver. In two lactating goats in which an injection of [14C] cholesterol was followed by daily intraruminal administration of labeled cholesterol, fat supplementation lowered the specific radioactivity of cholesterol in alimentary particles and in milk, being consistent with an increase in intestinally synthesized cholesterol. The hypercholesterolemia that develops in fat-fed ruminants appears to be primarily due to an increased intestinal biosynthesis of cholesterol but may also be partly due to a decreased fecal excretion of bile acids.

Acetates↗
PubMed1978

Cholesterol metabolism in man.

Recent investigations on cholesterol metabolism in man have led to new insights into diseases associated with abnormal accumulations of cholesterol in plasma (hypercholesterolemia), arterial tissues (atherosclerosis) and biliary tract (gallstones). Regulation of cholesterol synthesis under the influence of dietary and plasma cholesterol, may play a crucial role in determining biliary and tissue concentrations of this sterol. Plasma concentrations, on the other hand, appear to be controlled by complex mechanisms for secretion, transformation and removal of plasma lipoproteins. The recent identification of specific cellular receptors for uptake of plasma lipoproteins represents a significant advance for the understanding of regulation of both plasma and tissue concentrations, and possibly of the basic mechanisms underlying accumulation of cholesterol in atherosclerotic plaques.

Absorption↗
PubMed1977

Tissue storage and control of cholesterol metabolism in man on high cholesterol diets.

The possibility of accumulation of tissue cholesterol in human beings submitted to high cholesterol feeding was investigated in liver biopsies and through fecal sterol balance studies. Feeding to 10 individuals 3.1 to 3.4 g/day of cholesterol for 3 weeks raised the mean serum level from 293 to 349 mg/100 ml, namely 19%, whereas the liver cholesterol content was 417 mg/100 g of wet weight. In 10 control cases eating 0.1--0.4 g/day of cholesterol serum cholesterol remained stable throughout the experimental period and the liver cholesterol content was 256 mg/100 g. Difference of liver colesterol level between the two groups was 62%. In 7 patients submitted to two periods of balance investigation on a cholesterol-free synthetic formula diet respectively prior to (PI) and after (PIII) eating the high cholesterol solid food from 4 to 15 weeks (PII), fecal steroid excretion in PIII exceeded PI in 3 patients. Such data are a direct evidence for the existence of an efficient system to release acutely stored cholesterol. In one patient bile acid excretion accounted for the difference between PIII and PI.

Adult↗
PubMed1979

Surfactant cholesterol metabolism of the isolated perfused rat lung.

1. The isolated perfused rat lung was used as the principal model to study surfactant cholesterol metabolism. 2. Cholesterol was found to represent over 50% of the neutral lipid of both the total surfactant and the lamellar body fractions. 3. De novo synthesis of cholesterol from [1-14C]acetate accounted for only 1% of the surfactant cholesterol, the remainder being derived from exogenous cholesterol supplied as serum lipoproteins. 4. Lipoprotein [1,2-3H2]cholesterol was incorporated into the lamellar body and extracellular surfactant fractions. The increase in the cholesterol specific activities of these fractions with time was consistent with a precursor-product relationship between the lamellar body cholesterol and that of the extracellular surfactant. 5. Incorporation of [methyl-14C]choline and [1,2-3H2]cholesterol indicated that the metabolism and secretion of lamellar body and extracellular surfactant cholesterol parallels that of phosphatidylcholine and suggests that most if not all extracellular surfactant cholesterol is derived from the lamellar body. 6. Comparison of the relative specific activities of incorporated [1,2-3H2]-cholesterol indicate that 59% of the total surfactant cholesterol is located extracellularly.

Animals↗
PubMed1979

Cholesterol metabolism in the liver and intestine of the chick: effect of dietary cholesterol, taurocholic acid and cholestyramine.

The effect of feeding cholesterol, taurocholic acid, or cholestyramine to chicks on cholesterogenesis from [1-14C] acetate in liver and intestine was determined in vitro using tissue slices, and in vivo by i.v. injection of [14C] acetate. The conversion of cholesterol to bile acids in liver in vivo was measured in the same treatments after i.v. injection of [3H] cholesterol. Hepatic cholesterogenesis in vitro and in vivo was depressed by dietary cholesterol and taurocholate and enhanced by cholestyramine. Intestinal cholesterogenesis in vivo was depressed only by taurocholate whereas ileal cholesterogenesis in vitro was reduced by dietary cholesterol. Conversion of cholesterol to bile acids was enhanced by dietary cholesterol and cholestyramine and depressed by taurocholate. Hepatic cholesterol metabolism in the chick appears to be regulated by mechanisms similar to those reported for other species.

Acetates↗
PubMed1975

Use of mutant fibroblasts in the analysis of the regulation of cholesterol metabolism in human cells.

Analysis of mutant human fibroblasts deficient in a cell surface receptor for low density lipoproteins (LDL) has led to the delineation of an important, hitherto unrecognized, regulatory process for cholesterol metabolism. On normal cells, binding of LDL to this receptor regulates cholesterol metabolism by two mechanisms: (a) suppression of cholesterol synthesis and (b) facilitation of the rate of proteolytic degradation of the lipoprotein. In cells from homozygotes with the autosomal dominant disorder Familial Hypercholesterolemia, a nearly total reduction in LDL receptors results in two secondary abnormalities: (a) overproduction of cholesterol due to an inability of LDL to suppress the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-controlling enzyme in cholesterol biosynthesis, and (b) impairment in the rate of proteolytic degradation of LDL. Cells from heterozygotes possess about 50 per cent of the normal number of LDL recpetors; this leads to a concentration-dependent defect in regulation, so that attainment of rates of cholesterol synthesis and LDL degradation equal to that in normal cells requires a two to three-fold higher concentration of extracellular LDL in the heterozygote. The identification of this genetic regulatory defect in fibroblasts of heterozygotes with Familial Hypercholesterolemia makes available an in vitro system for studying the molecular mechanism by which a dominant mutation affects gene expression in mammalian cells.

Blood Proteins↗
PubMed1979

Hepatic cholesterol metabolism in normo- and hyperlipidemic patients with cholesterol gallstones.

In vivo studies have shown abnormalities in cholesterol and bile acid metabolism in primary hyperlipoproteinemia (HLP). The aim of the present investigation was to determine if the increased production of cholesterol in HLP type IV can be attributed to a correspondingly high level of the hepatic 3-hydroxy-3-methylglutaryl (HMG) CoA reductase activity and if the low cholic acid: chenodeoxycholic acid synthesis ratio in HLP type II is due to some hydroxylase deficiency. Liver biopsies from 26 normolipidemic and 25 hyperlipidemic (10 type IIa, 6 type IIb, and 9 type IV) patients undergoing elective cholecystectomy were assayed for HMG CoA reductase activity, 12 alpha-hydroxylase activity, and 25-hydroxylase activity. The HMG CoA reductase activity was normal in HLP type IIa and type IIb and was increased about twice HLP type IV (P less than 0.001). The 12 alpha- and 25-hydroxylase activities were normal in all groups of patients. The results are compatible with a normal cholesterol synthesis in the liver in HLP type II. A reduced 12 alpha- or 25-hydroxylase activity cannot explain the low production of cholic acid relative to chenodeoxycholic acid in this type of HLP. The elevated HMG CoA reductase activity found in the liver of type IV patients may, however, be part of the explanation for the elevated synthesis of cholesterol often seen in these patients.

Adult↗
PubMed1979

[Various disorders of cholesterol metabolism and their effect on the development of experimental arteriosclerosis in rats exposed to carbon disulfide].

Basing on the results of the author's own studies performed in a series of experiments in rats, the author discusses the mechanism of the atherosclerotic effect of CS2. The results of the studies carried out by the author indicated that the disturbances of body cholesterol metabolism (especially the increased rate of cholesterol synthesis and decreased rate of its degradation) contribute to elevation of cholesterol level in blood. The above alterations together with the cholesterol metabolism disturbances due to CS2 emerging directly in the aorta wall aggravate the development of the atherosclerotic changes in the vascular wall. The experimental (biochemical and morphological) evidences on the atherosclerotic effect of CS2 have been provided.

Animals↗