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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum lipid, lipoproteins, apolipoproteins and plasma insulin and glucose were studied in rhesus monkeys (Macaca mulatta) fed high sucrose diets (69%, w/w), with and without added cholesterol. When compared to basal diet, a high sucrose diet with no added cholesterol fed for 6 weeks increased serum total cholesterol and triglycerides by factors of 1.2 and 2.8, respectively. Cholesterol supplementation of sucrose diets increased the serum total cholesterol levels by a factor of 2.2 and decreased the serum triglycerides by 0.47. The serum cholesterol response to experimental diets was reflected predominantly in beta-lipoprotein and to a lesser extent in alpha-lipoprotein. Sucrose diets without cholesterol enriched the beta- and pre-beta-lipoproteins with triglycerides and protein at the expense of cholesterol. On the same diet, the protein content of alpha-lipoprotein increased at the expense of cholesterol and triglycerides. In contrast, dietary cholesterol decreased the triglyceride content and increased the cholesterol content of all the lipoprotein classes. Sucrose feeding seems to increase ApoB more than non-ApoB proteins. The proportion of ApoC-II relative to ApcoC-III increased in each animal on a sucrose diet; exogenous cholesterol further increased this trend. While sucrose diet decreased ApoA-I/ApoA-II ratios, cholesterol supplementation reversed this trend. Dietary sucrose increased the plasma glucose, insulin, and insulin-glucose ratios. The addition of cholesterol also tended to decrease plasma glucose and insulin levels. These observations indicate varied responses of serum lipoproteins and apoproteins to dietary sucrose with and without cholesterol supplementation.
Atherosclerosis 1979 Jul
PMID:Varied effects of dietary sucrose and cholesterol on serum lipids, lipoproteins and apolipoproteins in rhesus monkeys. 11 94

Apolipoproteins from human plasma high density (HDL), low density (LDL) and very low density lipoproteins (VLDL) were visualized in human arteries employing immunofluorescence techniques. Comparison between the localization patterns in extracranial and intracranial arteries and those in coronary arteries and the aorta was made. ApoA-I from HDL, apoB from LDL, and apoC-III from VLDL, as well as neutral lipid, were all localized to connective tissue and extracellular lipid pools in atherosclerotic lesions, and only to areas of intimal thickening in grossly "uninvolved" arteries. The degree of superposition of localizations was similiar in each vascular bed, and within the error resulting from the structural changes due to the focal nature of the atherosclerotic process. These results suggest a broad specificity in localization of apolipoproteins in most arterial lesions, and suggest that no differences in apolipoprotein accumulation exist between extracranial and intracranial arteries, coronary arteries, or the aorta. Variations in prevalence for atherosclerosis in each arterial bed must be accounted for on other bases.
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PMID:Apolipoprotein localization in human cranial arteries, coronary arteries, and the aorta. 78 16

Apoproteins from plasma lipoproteins were localized by immunofluorescence techniques in human carotid artery atherosclerotic lesions. These studies were performed in light of the possible importance of these apoproteins in both lipid metabolism and the pathogenesis of atherosclerosis. ApoA-I from high density lipoproteins, apoB from low density lipoproteins, and apoC-III from very low density lipoproteins were localized also as markers for their respective lipoproteins, since the latter cross-react immunologically. The three apoproteins were localized to the same regions of lesions as neutral lipids and, to some extent, fibrinogen. These regions consisted of bands of collagen fibers, usually deeper within the lesion, and the lipid core or atheroma of such advanced lesions. Although the superposition of localization for the three apoproteins and lipid was only 53%, it was suggested that deviation from complete superposition was due to the abrupt changes in lesion structure resulting from the focal nature of the atherosclerotic process. These results suggest that there is a broader specificity than previously implied of the interaction between such lesion components as connective tissue and extracellular lipid accumulations, and apoproteins from plasma lipoproteins. This interaction is believed to result in a net retention within atherosclerotic lesions of human extracranial arteries of these plasma-derived factors, either as free apoproteins or as native lipoproteins.
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PMID:Localization of apo-lipoproteins in human carotid artery plaques. 117 63

This study determined the effect of pinacidil on the concentration of plasma lipids and apolipoproteins in male patients previously equilibrated with 25 mg hydrochlorothiazide twice daily. Pinacidil therapy given to 52 hypertensives at 25 to 100 mg daily for 8 weeks resulted in a reduction of systolic and diastolic blood pressure concurrently to reductions in plasma cholesterol and triglycerides with no change in low density lipoprotein-cholesterol (LDL-C) and high density lipoprotein-cholesterol (HDL-C). There was an associated decrease in apolipoproteins (Apo)B, C-III and E and elevation in ApoA-I. A parallel placebo group of 44 patients experienced reduction in diastolic blood pressure and an elevation in ApoA-I. These changes indicate that pinacidil will be a useful antihypertensive agent having properties on lipoprotein metabolism which would favor decreased risks of atherosclerosis.
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PMID:Lipid and apolipoprotein levels during therapy with pinacidil combined with hydrochlorothiazide. 154 18

We describe the first Finnish LCAT-deficient family with two affected, one questionably affected and one healthy family member. The affected family members presented stomatocytes in the peripheral blood, exhibited low serum levels of total, LDL and HDL cholesterol, triglycerides, phospholipids and apolipoprotein A-I and especially A-II. Apolipoprotein A-I catabolism was accelerated to moderately high and very high levels in the two affected subjects. Cholesterol esterification percentage was low in all lipoprotein fractions. The intestinal cholesterol absorption efficiency and cholesterol and bile acid synthesis were within normal limits. The esterification percentage of demethylated cholesterol precursor sterols, cholestanol and plant sterols resembled mostly that of cholesterol, while those of VLDL and LDL methostenols, precursor sterols esterified by acyl-CoA:cholesterol acyltransferase (ACAT), suggested normal ACAT activity. In HDL all sterols were poorly esterified. The observations on stomatocytes, normal absorption and synthesis of cholesterol and bile acids, abnormal kinetics of apolipoprotein A-I, evidence of normal ACAT activity and abnormal esterification of non-cholesterol sterols are findings presented for the first time in LCAT deficiency.
Atherosclerosis 1992 Jul
PMID:Non-cholesterol sterols, absorption and synthesis of cholesterol and apolipoprotein A-I kinetics in a Finnish lecithin-cholesterol acyltransferase deficient family. 164 89

We tested the hypothesis that testosterone and estrogen modulate apoA-I gene expression and metabolism by different mechanisms that may be influenced by genetic factors. Male and female C3H/HeJ (atherosclerosis-resistant) and C57BL/6J (atherosclerosis-susceptible) mice (n = 5/group) were castrated (Placebo). Castrates were given 17 beta-estradiol (E2) at 0.16 microgram/g (E2L) or 5 micrograms/g (E2H) body weight per day, or testosterone (Testo) 1 microgram/g per day, 14 days after surgery, for 14 days. Plasma total cholesterol concentrations (TC) were higher in male Placebo mice than in females. Testosterone altered TC and high density lipoprotein (HDL) cholesterol by gender and strain; however (HDL-C)/TC ratios and apoA-I concentrations were unaltered. Testosterone did reduce HDL particle diameters in both genders of C3H mice only. Low density lipoprotein-cholesterol (LDL-C)/TC ratios remained constant and apoB increased in males only. E2L and E2H decreased TC, HDL-C/TC ratios, and apoA-I. Decrements varied by strain. HDL diameters decreased in both genders in C3H mice only; however, HDL size distributions were altered in both strains. LDL-C/TC ratios increased in all groups. E2L mice showed variable responses of apoB, but apoB rose uniformly in all E2H groups. Testosterone increased and E2H decreased hepatic apoA-I synthesis. ApoA-I mRNA concentrations remained stable in both Testo and E2 groups. ApoA-I gene transcription varied by strain and gender, but all changes were less than twofold. Testosterone did not affect hepatic apoB or LDL receptor mRNA, however, E2H increased both mRNAs in males but not in females. On Western blotting of liver membranes, E2H had little effect on mouse LDL receptor protein mass; by contrast, E2H increased LDL receptor approximately threefold in rats. In summary, responsiveness of mouse lipids to testosterone and E2 vary by strain and gender. Testosterone and E2 differ in their regulation of apoA-I production mainly at the level of translation. Hormones operate at several levels of gene regulation, suggesting that complex mechanisms are involved. Mice differ from rats and rabbits in their LDL receptor responsiveness to estradiol treatment.
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PMID:In vivo regulation of apolipoprotein A-I gene expression by estradiol and testosterone occurs by different mechanisms in inbred strains of mice. 179 39

Apolipoprotein A-I, the major protein of high-density lipoproteins, and apolipoprotein B, the major protein of low-density lipoproteins can serve as important predictor of the risk of cardiovascular diseases. The lack of an internationally valid standardization is a serious impediment to a broad application of the apolipoprotein measurements in the laboratory diagnosis of atherosclerosis. A common effort is at the present made by the IFCC Committee on Apolipoproteins together with several commercial organizations to achieve a consensus on a practical standardization procedure for the measurement of apolipoprotein A-I and B. The aim is a) to calibrate all commercially available Apo A-I and Apo B test kits using frozen serum pools previously standardized against primary reference materials and b) to select the secondary serum reference preparations which will substitute the frozen serum pools and will be used for the control of the validity of the own calibration. The available results from a preliminary exercise prove with a variation less than 5% for Apo A-I and less than 8% for Apo B with patients' samples that the use of common reference materials leads to the harmonization of the results obtained with different test systems for measurement of apolipoprotein A-I and B.
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PMID:[Standardization of the immunochemical detection of apolipoprotein A-I and B]. 212 24

Dramatic advances have been made over the last decade in understanding the role of low-density lipoprotein (LDL) in atherosclerotic cardiovascular diseases and how to manage elevated levels of LDL cholesterol. Understanding the role of high-density lipoprotein (HDL) and how to intervene therapeutically in HDL action offers the possibility of even greater benefits. Epidemiologic studies have shown a strong inverse relation between HDL cholesterol and the risk of coronary artery disease (CAD). Whereas several subfractions of HDL can be identified, none convincingly offers better predictive value than total HDL cholesterol. Apolipoprotein A-I, the major apolipoprotein of HDL, also is inversely related to atherosclerotic risk. Unfortunately, measurements of HDL cholesterol or apolipoprotein A-I are considerably less precise and less accurate than measurements of total or LDL cholesterol. The biologic phenomena responsible for these epidemiologic relations are not yet clear. Moreover, several apparently contradictory observations and puzzling exceptions to the simplistic inverse relation of HDL cholesterol to CAD suggested by epidemiologic studies have created considerable confusion. The current confusion is not likely to be resolved until HDL metabolism and the cellular and molecular events responsible for the apparent protective effects of HDL are better understood. One current hypothesis that could explain the protective effects of HDL is that it mediates reverse cholesterol transport, the process by which cholesterol is removed from sites of deposition and delivered to the liver for excretion. From the standpoint of current therapy, each intervention that changes HDL cholesterol levels must be evaluated individually, on its own merit, in light of its effect on atherosclerosis and coronary events rather than on alterations in HDL cholesterol levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High-density lipoprotein cholesterol levels as a marker of reverse cholesterol transport. 267 25

Reports of increased susceptibility of persons from the Indian subcontinent to coronary heart disease led us to examine serum lipids and apolipoproteins in a group of physicians born in India now living in the U.S. A matched sample of U.S.-born physicians working at the same institution was recruited as controls. Fasting triglyceride (TG) levels were twice as high among the Indians (174 vs 86 mg/dl, P = 0.002), total cholesterol modestly increased (193 vs 177 mg/dl, P less than or equal to 0.01) and high density lipoprotein-cholesterol (HDL-C) fraction depressed 36 vs 40 mg/dl, P = 0.006). Both TG and HDL-C were strongly determined by relative obesity in the Americans, but not among the immigrants. Calculated values of low density lipoprotein-cholesterol (LDL-C) were similar in the two groups. Apolipoprotein A-I was significantly lower in a subsample of the Indians, while Apo B was higher. Minor differences between the groups in body mass index, food frequency intake, smoking patterns, alcohol intake and exercise did not significantly influence the results. Hereditary differences in lipid metabolism may have a role in these findings, however, the delayed effects of adaptation to U.S. lifestyle cannot be ruled out.
Atherosclerosis 1986 Aug
PMID:Serum lipids of Indian physicians living in the U.S. compared to U.S.-born physicians. 309 38

Earlier studies have shown that African green monkeys develop a more modest hypercholesterolemia, higher high density lipoprotein (HDL) concentrations, and less atherosclerosis than cynomolgus monkeys fed diets with the same cholesterol content. In the present study, cynomolgus monkeys were fed less cholesterol than was fed to African green monkeys to induce equivalent hypercholesterolemia in both species. African green monkeys still had 2-fold higher plasma HDL cholesterol concentrations and 2.7-fold higher plasma apolipoprotein (apo) A-I concentrations. Therefore, the higher HDL concentration in African green monkeys appears to result from factors that act independently of dietary cholesterol intake or total plasma cholesterol concentration. Two aspects of HDL production were examined to determine the metabolic basis of the species difference in HDL concentration. The rate of hepatic apoA-I secretion, as estimated by the accumulation of apoA-I in the medium during recirculating liver perfusion, was 5-fold higher in livers of African green monkeys. In addition, the concentration of apoA-I mRNA was 2-fold higher in the liver and 3.7-fold higher in the intestine of African green monkeys. Taken together, these findings indicate that differences in apoA-I production in the liver and small intestine are large enough to be responsible for the differences in the plasma concentrations of HDL and apoA-I between these species. Factors which regulate apoA-I secretion, including modulation of tissue apoA-I mRNA concentrations, are important determinants of plasma HDL concentrations and may contribute to the relative resistance of African green monkeys to dietary cholesterol-induced hypercholesterolemia and atherosclerosis. ApoA-I mRNA was also detected at low levels in the kidney and testis of African green and cynomolgus monkeys but not in the adrenal or brain. The tissue distribution and abundance of apoA-I mRNA in peripheral tissues was very different than that seen for apoE mRNA. Kidney and testis apoA-I mRNAs were the same size as liver apoA-I mRNA when examined by Northern blot analysis. Testis apoA-I mRNA appeared to be functionally active as judged by its presence in cytoplasmic polyribosomes. The low levels of apoA-I expression in kidney and testis are unlikely to contribute significantly to the plasma apoA-I pool but might function in some aspect of local lipid metabolism within these tissues.
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PMID:Apolipoprotein (apo) A-I production and mRNA abundance explain plasma apoA-I and high density lipoprotein differences between two nonhuman primate species with high and low susceptibilities to diet-induced hypercholesterolemia. 312 37


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