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

The effect of short-term (6 months) administration of conjugated equine estrogen (Premarin) on content and composition of the aortic sterols in male shite Carneau pigeons while they were on a cholesterol-free grain diet was investigated. Estrogen treatment resulted in a 38% increase (P less than 0.05) in free sterol concentration, with a 28.8% concomitant decrease (P less than 0.05) in the percent of cholesteryl esters. The total sterol concentration remained unchanged. This finding suggests that estrogens might influence the synthetic or hydrolytic (or both) processes that control the concentration of cholesteryl esters in the aorta. Fatty acid composition of steryl esters did not change significantly. The cholesterol content of plasma showed a mild reduction (14%) whereas the triglycerides increased significantly (30%).
Atherosclerosis 1977 May
PMID:Effect of estrogens on the concentration and composition of arterial sterols and steryl esters in male white carneau pigeons. 19 27

The influence of daily oral cyclical estrogen therapy on the plasma lipid and lipoprotein levels in postmenopausal women was determined. Included were 39 women with distressing postmenopausal vasomotor symptoms. Ethinyl estradiol (EE2) .05 mg was given to 20 women and estradiol valerinate (EV) to 19 others. The drugs were given as tablets once daily for 3-week cycles with 1-week intervals. After overnight fasts, blood samples were taken before and during treatment at 1, 3, and 6 months. During EV therapy, the HDL-TC and the HDL-phosphlipid concentrations increased 10-15% after 6 cycles. The net effect on the risk of development of ischemic cardiovascular disease due to the change in plasma lipids induced by EE2 is uncertain. The plasma lipid changes during EV therapy might possibly retard the development of atherosclerosis. However, the lipid metabolism of postmenopausal women may be different from that of fertile women.
 ...
PMID:Metabolic and hormonal effects of post-menopausal oestrogen replacement treatment. II. Plasma lipids. 20 45

Fourteen patients with prostatic carcinoma were treated with 1.0-0.5 mg ethinyl estradiol orally daily and 160-80 mg polyestradiol phosphate im monthly. Lipid concentrations were determined in plasma and the high density lipoprotein fraction, and the plasma lecithin-cholesterol acyl transfer rate was measured before and 1 and 6 months after the start of therapy. During treatment, the concentration of total cholesterol was unchanged while there was a 60% increase of high density lipoprotein-total cholesterol. Triglyceride (TG) concentration increased 40%, indicating an augmented level of very low density lipoprotein concentration. The plasma lecithin-cholesterol acyl transfer rate increase 20-35%, indicating that an increased rate of production and turnover of TG, cholesteryl esters, and very low density lipoproteins probably was a main cause of the elevated TG concentration. The potential effects on the development of atherosclerosis by the plasma lipid changes during estrogen treatment are discussed.
 ...
PMID:Changes of plasma lipid metabolism in males during estrogen treatment for prostatic carcinoma. 23 77

The aim of this study was to examine in detail the lipid and apoprotein concentrations in the serum of rats treated with pharmacologic doses (5 mg/kg/d for 5 d) of the synthetic estrogen derivative ethinyl estradiol. The results show that in rats, estrogen-induced hypolipidemia is associated with a nearly complete absence of the lipid and protein moieties normally found in d less than 1.21 fraction of serum. Quantitation of specific apolipoproteins by immunoelectrophoresis show that most apolipoproteins are decreased by more than 90% in the serum of estrogen-treated rats. In contrast to the changes in d less than 1.21 lipoproteins, estrogen treatment only slightly reduced serum phospholipid concentrations (by only 10%) and caused no change in the concentration of serum albumin. The results show that the ethinyl estradiol-treated rat is an excellent model of drug-induced hypolipidemia.
Atherosclerosis 1978 Aug
PMID:Pharmacologically induced hypolipidemia. The ethinyl estradiol-treated rat. 70 87

The effect of cholesterol feeding and estrogen administration on synthesis of fatty acids in liver mitochondria, microsomes and cytoplasm of male rabbits has been investigated. The synthesis was measured by the incorporation of [1(-14)C] acetyl CoA or [2(-14)C]malonyl CoA into long chain fatty acids under optimal conditions. It was found that atherogenesis markedly decreased the fatty acid synthesis in cytoplasm. The mitochondrial fatty acid synthesis was not affected by the disease. There was a small but measurable decrease in the synthesis of fatty acids in microsomes. Estrogen had no effect on the synthesis of fatty acids in mitochondria or microsomes. But if effectively counteracted, after a short lag period, the decreased synthesis of cytoplasmic fatty acids observed in atherosclerosis. It is possible that liver fatty acid synthetase is one of the enzyme systems through which estrogens exert their atherosclerosis-retarding effect. The decreased cytoplasmic fatty acid synthesis observed in atherosclerosis might account for the low levels of saturated fatty acids reported in liver and plasma lipids of atherosclerotic animals.
Atherosclerosis 1977 Aug
PMID:Effect of cholesterol feeding and estrogen treatment on synthesis of fatty acids in liver. 88 99

Lipoprotein lipase (LPL) activity was measured in adipose tissue, heart and diaphragm in Sprague--Dawley rats after estrogen therapy or orchiectomy. Enzyme activity was measured by incubation of tissue fragments with a triolein emulsion in the presence of serum and heparin. In confirmation of other work, depression of adipose tissue LPL followed estradiol treatment in pharmacologic or near-physiologic doses. Cardiac and diaphragmatic muscle LPL were increased. Estrogen-treated male animals showed growth retardation. However, they gained weight steadily and did not show significant differences in serum insulin, glucose of D-beta-hydroxybutyrate. The effects of estradiol in male animals were reversed by sequential fasting and re-feeding. At times during growth and aging in normal female rats, adipose tissue activity was decreased while cardiac and skeletal muscle activities were increased relative to males of the same age or body weight. Castration of male rats failed to reproduce the effect of estrogens on tissue lipoprotein lipase. These in vitro data suggest that exogenous estrogens may shift the flux of triglyceride fatty acids from storage in the adipose organ toward incorporation by muscle. These, and other data, raise the possibility that physiological estrogen secretion exerts a tonic influence over the synthesis and ultimate destination of triglyceride fatty acids.
Atherosclerosis 1976 Sep
PMID:Estrogen treatment and gonadal function in the regulation of lipoprotein lipase. 97 48

Epidemiological data have revealed that the progestogen in oral contraceptives (OCs) is involved in hypertension, ischemic heart diseases, and stroke. Atherosclerotic lesions were implicated owing to the androgenic properties of progestogens. However, atherosclerosis did not develop despite reduced high density lipoprotein (HDL) and elevated low density lipoprotein (LDL), presumably because of the strong effect of ethinyl estradiol (EE) upon induction of hepatic LDL- and remnant-receptors. A series of findings indicate that vasospasms caused by the effect of progestogens are involved in arterial thromboses. In postmenopausal women, the addition of progestogens to the estrogen treatment may trigger ischemic diseases. Estrogens exert a vasodilatory effect and stabilize the vascular tonus through the responsiveness of the endothelium, neurotransmitter release, and direct blocking of calcium channels. Progestogens increase the sensitivity of arteries to vasoconstrictory compounds and reduce blood flow. In women treated with ovulation inhibitors, and EE-induced activation of the renin-angiotensin-aldosterone system was observed. Aldosterone acts vasodilatorily, while progestogens with high affinity to the aldosterone receptor may exert a strong vasoconstrictory effect. If vascular lesions are present, the vasoconstrictory action of progestogens may cause acute ischemic attacks. Therefore, the lowest effective dose of the progestogen has to be used for replacement therapy. In hysterectomized women, the extra administration of progestogens should be avoided and in women with arterial diseases they should be prescribed with discretion. Additional progestogens given for 14 days 3 months apart may suffice for the prevention of endometrial hyperplasia. Both the EE and progestogen doses in OCs should be reduced. Progestogen-dominant ovulation inhibitors should be restricted to cases with an additional indication.
 ...
PMID:[Hormonal contraception and substitution therapy: the importance of progestogen for cardiovascular diseases]. 145

Two artificial estrogens, ethinyl estradiol and mestranol, were found to cause cirrhosis in the rabbit liver during a study of atherosclerosis. These drugs showed protective effects against atherosclerosis in cholesterol-fed rabbits when administered orally (1 ppm in diet). These drugs and two naturally occurring estrogens, estrone and estradiol, were similarly effective when administered intramuscularly (1.5 mg per rabbit per week) to rabbits fed a diet lower in cholesterol. Reduction by estrogens of plasma cholesterol did not fully account for the reduction of extent of aortic atherosclerosis. Also, no differences in aortic or platelet eicosanoid production from exogenous arachidonic acid were found to explain the effect on atherogenesis. The 2 artificially modified estrogens, ethinyl estradiol and mestranol, caused portal fibrosis with biliary proliferation (even in rabbits not fed cholesterol). Estrone, estradiol, and testosterone were not injurious in this regard at the dosages used. Only the unmodified estrogens reduced atherosclerosis without damaging the rabbit liver.
 ...
PMID:Estrogen protection against atherosclerosis and synthetic estrogen production of cirrhosis in the rabbit. 157 Apr 4

To verify whether the LDL receptors from different animal species recognize the binding domain of human apo B-100 we studied the interaction of LDL from control and familial binding defective apo B-100 (FDB) with cultured cells. Human, monkey, bovine, guinea pig and rabbit LDL receptors distinguish between normal and binding defective LDL with a displacement ratio (defective/normal) of 3.3, 2.6, 3.4, 3.1 and 2.0, respectively. Guinea pig and rabbit receptors, however, showed affinities 2-3-fold lower than the human receptor. Hamster, rat and mouse cells failed to differentiate between normal and FDB LDL with a ratio of 1.2, 0.8, and 1.4; the apparent affinities were 4-8 times lower than that of the human receptor. The data from the latter species suggest that the LDL receptor recognizes an area of human apo B different from the human receptor binding domain. The ability of antibody Mb47 to inhibit the binding of human LDL to human, rabbit and guinea pig but not to mouse cells further stresses this concept. Moreover, in 17 alpha-ethinyl estradiol-treated rats the rate of disappearance from plasma of FDB and control 125I-labelled LDL was identical, thus confirming the in vitro observations. These data suggest that the binding domain of the LDL receptor is functionally conserved in man, monkey, cow, rabbit and guinea pig, but is quite distinct in rat, mouse and hamster.
Atherosclerosis 1992 Mar
PMID:Ability of the LDL receptor from several animal species to recognize the human apo B binding domain: studies with LDL from familial defective apo B-100. 159 8

Researchers have found that oral contraceptives (OCs) change carbohydrate and lipoprotein metabolism and these changes are like those linked with increased risk of cardiovascular (CV) disease, especially myocardial infarction and stroke. Since CV disease is the major cause of death in US women, it is important that OCs not induce changes in carbohydrate and lipoprotein metabolism. A new progestin, norgestimate, has an advantage over other progestins in that it tends not to induce male traits. This is beneficial because androgenicity is related to atherosclerosis which increases the risk of myocardial infarction. Further studies show that the new combined OC (250 mcg norgestimate/35 mcg ethinyl estradiol) does not influence serum glucose tolerance levels. It also does not affect the physiologic regulating system of prostacyclin, the inhibitor of platelet aggregation, by high density lipoprotein (HDL). In addition, it increases prostacyclin metabolites and HDL which may indeed decrease the risk of occlusive thrombotic vascular diseases. Moreover a study in Germany demonstrates that it causes no changes in fibrinopeptide A,m the anticoagulation factors antithrombin III and protein C, or coagulation promoting factors fibrinogen, factor VII, and the components of VIII. In women, it is absorbed well and metabolized extensively before the body eliminates it. Moreover this new combined OC has an overall Pearl index of 0.25. Studies to data indicate that norgestimate/ethinyl estradiol may be more advantageous than other OC formulations. Yet only long term epidemiologic studies can determine if it can indeed decrease the risk of CV diseases linked with older OCs.
 ...
PMID:Norgestimate: a clinical overview of a new progestin. 160 87


1 2 3 4 5 6 7 8 9 10 Next >>