Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

VLDL from hypercholesteremic (HC) rabbits display features which are suggestive of inherent atherogenicity. The lipid composition, compared to that of control VLDL, shows an enrichment of cholesterol esters, which have a very high 18:1/18:2 ratio in their fatty acids, and an increased sphingomyelin content, with decreased PC/Sph ratio. This lipid composition is very similar to that of the atherosclerotic plaqua. Apoprotein peptides of HC VLDL show a predominance of arg-rich proteins, similar to human conditions (Type III hyperlipoproteinemia and hypothyroidism) characterized by early and severe atherosclerosis. Turnover of 125I-labelled HC VLDL is significantly slower than that of control VLDL, both when the lipoprotein is injected into the donor animals and into controls. Conversion of HC VLDL into lipoproteins of higher density is also very small, as compared to control VLDL. Uptake of radioactivity into the aortic wall after injection is about doubled, as compared to control VLDL, when HC rabbits receive HC VLDL. This experimental model suggests that structural modifications of the HC VLDL make them poorly metabolizable, and possible more akin to the recently described arterial lipoprotein complexing factor (ALCF). Metformin was selected as the test compound, because it has been shown to decrease aortic and liver lipid accumulation in cholesterol fed rabbits, while only slightly affecting plasma cholesterol levels. VLDL from rabbits fed cholesterol and metformin (HC+Met), while still enriched in cholesterol esters, have a higher protein content, less sphingomyelin and more phosphatidylethanolamine and phosphatidylinositol than HC VLDL, while fatty acid composition of cholesterol esters does not differ. Turnover of HC+Met VLDL is extremely rapid, with a t1/2 even shorter than that of control VLDL.
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PMID:Turnover and aortic uptake of very low density lipoproteins (VLDL) from hypercholesteremic rabbits as a model for testing antiatherosclerotic compounds. 17 94

The lipid and apoprotein composition of very low density lipoproteins (VLDL) (d less than 1.019 g/ml) from normal and hypercholesteremic (h.c.) rabbits are compared. Significant changes are observed in the apoproteins, as well as in the fatty acid composition of cholesterol esters, and in the relative distribution of phospholipids. Apoproteins show a marked increase of peptides with slow mobility (R2 and R3), corresponding to arginine-rich proteins, both in the rabbit and in some types of human hyperlipoproteinemias (hypothyroidism and Fredrickson Type III). VLDL were separated into the two fractions, VLDL-1 and VLDL-2. Peptides of slow mobility were shown to be present in a higher concentration in VLDL-1. Cholesterol esters of h.c. VLDL have a very high content of oleic acid, the 18:1/18:2 ratio being about three times higher than in normal VLDL. Phospholipid distribution in h.c. VLDL is characterized by an increase of sphingomyelin and decrease of phosphatidylethanolamine. The PC/Sph ratio is about one fifth that of normal. These changes in VLDL lipids are very similar to those occurring in the lipid composition of the atherosclerotic plaques in mammals.
Atherosclerosis
PMID:Very low density lipoproteins in normal and cholesterol-fed rabbits: lipid and protein composition and metabolism. Part 1. Chemical composition of very low density lipoproteins in rabbits. 23 65

A strain of genetically selected White Carneau pigeons (WC-2) with increased atherosclerosis at similar plasma cholesterol concentrations as randomly bred (RBWC) pigeons was studied to evaluate the commonly known risk factors for atherosclerosis. Indicators for the presence of hypertension, diabetes mellitus, "stress", hyperuricemia and hypothyroidism were determined. In pigeons fed the atherogenic diet, major differences in atherosclerosis were seen between WC-2 and RBWC. WC-2 pigeons had more aortic surface covered with plaque and greater concentrations of aortic nonesterified cholesterol, esterified cholesterol, uronic acid, and hydroxyproline, as well as a greater prevalence and severity of coronary artery atherosclerosis. For WC-2 and RBWC pigeons we found similar levels of hypercholesterolemia, mean blood pressure, plasma triglyceride and glucose concentrations. In addition, several other physiological variables such as plasma uric acid, calcium and phosphorus concentrations, adrenal and thyroid weights which have been implicated in the pathogenesis of atherosclerosis were similar. The findings indicate that the differences in extent and severity of atherosclerosis between WC-2 and RBWC cannot be explained by differences in the risk factors studied. Possible genetic regulation of atherosclerosis by mechanisms operable in the arterial wall of WC-2 pigeons is suggested.
Atherosclerosis 1978 Dec
PMID:Risk factors in pigeons genetically selected for increased atherosclerosis susceptibility. 72 42

The prevention of induced hypercholesterolemia and atherosclerosis was studied by means of intestinal lymphatic blockade and of bile diversion in the dog. Hypercholesterolemia and atherosclerosis were produced by high cholesterol feeding after induction of hypothyroidism with radio-iodine plus thiouracil. Complete diversion of bile, by shunting all bile into the urinary bladder, effectively prevented hypercholesterolemia and atherosclerosis; in contrast, blockade of the intestinal lymphatics failed to prevent the consequences of the atherogenic regimen, because of the development of collateral lymphatic channels.
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PMID:Prevention of induced atherosclerosis by diversion of bile or blockade of intestinal lymphatics in dogs. 81 79

Hypothyroidism is associated with severe coronary atherosclerosis. In spite of this the reported incidence of angina pectoris and myocardial infarction in untreated hypothyroidism is small. Since many authors consider the formation of a thrombus in coronary arteries to be the final event of the process which leads to myocardial infarction, changes in the platelet function may explain the paradoxical rarity of myocardial infarction in untreated hypothyroidism. To evaluate this hypothesis, platelet adhesiveness has been estimated before and after treatment in 9 hypothyroid and 16 thyrotoxic patients. In thyrotoxicosis the platelet adhesiveness was significantly increased, but decreased to normal after treatment. In hypothyroidism platelet adhesiveness was abnormally low but increased to normal value after thyroid hormone replacement. This may be an important factor in precipitating myocardial infarction in patients with hypothyroidism and coronary artery atherosclerosis.
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PMID:The adhesiveness of human blood platelets and thyroid function. 112 57

Dietary lipid, following incorporation into chylomicrons, is rapidly removed from the blood by a two-stage process. Most of the triglyceride is taken up by extrahepatic tissue, particularly muscle and adipose tissue. The residual triglyceride and virtually all of the cholesterol ester is removed by the liver through the clearance of a particle called a chylomicron remnant. The remarkable rapidity and specificity of uptake of this particle seems to be due to its acquisition of apoE in the plasma. Uptake is mediated in part by the LDL receptor, the LRP (alpha a-macroglobulin receptor), and perhaps by a sieving mechanism that leads to trapping, but not endocytosis. Uptake is modulated by the type of apoE inherited, the amount of apoC present on the particle, and, perhaps, the phospholipid and fatty acyl chain composition of the particle. The process may be slowed in diabetes and hypothyroidism. The metabolic effects of the particle can be variable, depending on the composition of the diet, and this can affect whole body cholesterol metabolism significantly. Furthermore, even moderately prolonged residence of these particles in the circulation could contribute in a significant way to atherogenesis. Thus, the remnant particle and its uptake by the liver may be important links in determining the dietary contribution to the rate of atherosclerosis.
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PMID:Hepatic clearance of plasma chylomicron remnants. 133 75

Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. Excessive vasoconstriction resulting from noradrenaline (norepinephrine) in neurogenic hypertension, phaeochromocytoma, orthostatic hypertension and alpha-adrenergic drug administration; angiotensin excess due to renal ischaemia brought about by aortic coarctation, renal arterial and arteriolar stenosis, intraluminal obstruction, external renal compression, renin-producing tumours, intrinsic kidney diseases and excessive renin substrate; and vascular structural disorders such as atherosclerosis, arteriolitides and fibrosis with or without calcification of major arteries may also induce hypertension. Secondary hypertension of uncertain mechanism may occur in hyperparathyroidism, hyper-or hypothyroidism, or acromegaly. All are best treated by appropriate correction of the endocrine excess or deficiency. It may also occur in pregnancy, where the mechanism may involve prostaglandin-thromboxane imbalance or calcium deficiency; calcium deficiency with some evidence of benefit from calcium supplements; and the recumbent hypertension paradoxically associated with autonomic failure. Excellent responses to specific correction of the underlying cause or pathogenetic mechanism is usual in young individuals but less frequent in older patients.
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PMID:Secondary hypertension. An overview of its causes and management. 137 54

We reported a 53-year-old woman with hypothyroidism due to ectopic thyroid gland. She showed intellectual impairment, bilateral pyramidal tract sings, slight cerebellar signs, and degenerative changes of brain white matter on CT and MRI, which were similar to symptoms and signs in cerebrotendinous xanthomatosis (CTX). We found increases of serum cholestanol in the patient and additional 3 patients with hypothyroidism. Total bile alcohol was also increased in the serum of the patients. We speculate that hypothyroidism and CTX might have a similar pathophysiological background on the development of neurological complications and atherosclerosis.
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PMID:[Hypothyroidism with increased serum levels of cholestanol and bile alcohol--analogous symptoms to cerebrotendinous xanthomatosis]. 191 25

Xanthomas are important clinical manifestations of a variety of disorders, including lipoprotein abnormalities, hypothyroidism, diabetes and certain forms of cancer. Many patients with these lesions are also at risk for premature atherosclerosis. Family physicians are often the first to recognize xanthomas. Early detection and identification of the lesions leads to appropriate diagnosis and treatment of the related diseases.
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PMID:Clinical significance and treatment of xanthomas. 192 35

Acquired hyperlipidemia (secondary dyslipoproteinemias) results from underlying disorders that lead to alterations in plasma lipid and lipoprotein metabolism. Secondary dyslipoproteinemias may mimic primary forms of hyperlipidemia and can have similar consequences. They may result in increased predisposition to premature atherosclerosis or, when associated with marked hypertriglyceridemia, may lead to the development of pancreatitis and other features of the chylomicronemia syndrome. Diabetes mellitus and use of drugs such as diuretics, beta blockers, and estrogens are commonly encountered causes of secondary dyslipoproteinemia. Other conditions leading to acquired hyperlipidemia include hypothyroidism, renal failure, nephrotic syndrome, alcohol usage, and some rare endocrine and metabolic disorders. When secondary and familial forms of hypertriglyceridemia coexist, triglyceride removal mechanisms may be saturated and marked hypertriglyceridemia with fasting chylomicronemia might ensue. Treatment of the underlying condition, when possible, or discontinuation of the offending drugs usually leads to an improvement in the hyperlipidemia. Specific lipid-lowering therapy may be required in certain circumstances.
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PMID:Acquired hyperlipidemia (secondary dyslipoproteinemias). 219 73


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