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

The effects of estrogens on LDL modification by copper ions, U 937 monocyte-like cells or endothelial cells was studied by determination of the lipid peroxidation product content and measurement of the relative electrophoretic mobility. The presence of estradiol, estriol and estrone inhibited LDL oxidation in a dose-dependent manner in the range of concentrations from 5 to 50 microM. In the case of oxidation by Cu2+, the decreasing order of efficiency was: estradiol, estriol, estrone. In monocyte-induced oxidation, the protective effect of estrogens was more marked, and the order of efficiency was the same, except that estrone was as active as estriol. Pretreatment of monocyte cells with estrogens also inhibited the subsequent modification of LDL by these cells, tested in the absence of the hormones. Testosterone had no effect in all the studied systems. Furthermore, the degradation by J774 macrophage like cells of LDL modified either by Cu2+ or monocytes was markedly reduced when modification has been performed in the presence of estrogens. Since oxidative modification of LDL is believed to be involved in the appearance of atherosclerotic plaques, this effect of estrogens might be related to their protective action against atherosclerosis.
Atherosclerosis 1991 Aug
PMID:Estrogens inhibit copper and cell-mediated modification of low density lipoprotein. 179 45

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

Associations of plasma testosterone and estradiol with some haemostatic factors (factor VII activity, fibrinogen, antithrombin III and alpha 2-antiplasmin) were cross-sectionally examined in 251 healthy, middle-aged men participating in the Paris Prospective Study II on risk factors for ischaemic heart disease. Testosterone levels were negatively correlated to factor VII activity and alpha 2-antiplasmin, the main inhibitor of fibrinolysis. No association was found either between testosterone levels and both fibrinogen and antithrombin III, or between estradiol levels and the set of haemostatic variables. The associations between testosterone and both factor VIIc and alpha 2-antiplasmin were independent of HDL-cholesterol, LDL-cholesterol, triglycerides, smoking, alcohol, body mass index and blood pressure. These results suggest that low circulating testosterone levels might be associated with a hypercoagulability state and therefore could contribute to an increased risk of IHD.
Atherosclerosis 1988 May
PMID:Relationship between sex hormones and haemostatic factors in healthy middle-aged men. 337 81

Serum high-density lipoprotein (HDL) cholesterol, testosterone and sex-hormone-binding globulin (SHBG) were measured in 300 men, aged 35-64 years, of African and Indian descent who represented a 40% sample of participants in a community survey of coronary heart disease in Trinidad. Free testosterone was calculated from total testosterone and SHBG. In 113 men, HDL2 and HDL3 cholesterol were measured by a precipitation technique. Indian men had a significantly lower HDL-cholesterol concentration than African men (P = 0.003), which is known to be due to a reduction in the HDL3 fraction (demonstrable only in younger men in the subsample drawn for this study). Testosterone did not differ with ethnic group, but SHBG was reduced in Indians (P = 0.03). After allowance for age, ethnic group, alcohol consumption and smoking habit, HDL cholesterol was associated positively with SHBG (P = 0.025) but was not related significantly to either total testosterone or its free and bound components. Serum HDL2 cholesterol was associated positively and independently with SHBG (P = 0.001) and total and bound testosterone (P = 0.002), whereas HDL3 cholesterol showed no significant associations with these factors. Neither SHBG or testosterone afforded an explanation for the relatively low HDL and HDL3 cholesterol concentrations in Indian men.
Atherosclerosis 1985 Jun
PMID:Serum high density lipoprotein subclasses, testosterone and sex-hormone-binding globulin in Trinidadian men of African and Indian descent. 404 Mar 71

The effects of testosterone on cell proliferation and prostacyclin production were investigated using rat aortic smooth muscle cells in culture. Testosterone at 10(-10)-10(-6) M did not have any significant effect on cell proliferation, but it significantly inhibited prostacyclin production by the cells. Maximal inhibition of prostacyclin production (70%) was observed when cells were treated with a physiological concentration of 19(-8) M testosterone for 5 consecutive days. These results suggest that testosterone may stimulate thrombus formation and accelerate atherosclerosis by suppressing prostacyclin production in arterial smooth muscle cells.
Atherosclerosis 1981 May
PMID:Testosterone inhibits prostacyclin production by rat aortic smooth muscle cells in culture. 701 4

The HDL-raising effect of estrogen replacement is mediated by an increase in HDL-apolipoprotein A-I production and not by a decrease in the clearance rate. Large-scale clinical trials have shown that medroxyprogesterone acetate removes most of the HDL-raising effects of concomitant estrogen treatment. Testosterone decreases HDL levels in both men and women. Lipoprotein (a) levels are reduced by estrogen replacement, but are not affected by medroxyprogesterone. The acute systemic administration of estrogen to postmenopausal women improves the endothelium-dependent vasodilation of coronary arteries and forearm resistance vessels. Usual doses of oral estrogen replacement therapy improve the endothelium-dependent and endothelium-independent vasodilator responses in the forearm in women who have risk factors for atherosclerosis. These effects may be mediated by an antioxidant action of estrogen.
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PMID:Sex hormones, lipoproteins, and vascular reactivity. 764 5

Hyperestrogenemia and hypotestosteronemia have been observed in association with myocardial infarction (MI) and its risk factors. To determine whether these abnormalities may be prospective for MI, estradiol and testosterone, as well as risk factors for MI, were measured in 55 men undergoing angiography who had not previously had an MI. Testosterone (r = -.36, P = .008) and free testosterone (r = -.49, P < .001) correlated negatively with the degree of coronary artery disease after controlling for age and body mass index. When the patient group was successively reduced to a final study group of 34 men by excluding the patients with other major disorders, the testosterone and free testosterone correlations persisted (r = -.43, P < .02 and r = -.62, P < .001, respectively). Neither estradiol nor the risk factors, except for high-density lipoprotein cholesterol, correlated with the degree of coronary artery disease in the final group. Testosterone correlated negatively with the risk factors fibrinogen, plasminogen activator inhibitor-1, and insulin and positively with high-density lipoprotein cholesterol. The correlations found in this study between testosterone and the degree of coronary artery disease and between testosterone and other risk factors for MI raise the possibility that in men hypotestosteronemia may be a risk factor for coronary atherosclerosis.
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PMID:The association of hypotestosteronemia with coronary artery disease in men. 817 48

We investigated the effects of long-term testosterone replacement in hypogonadal and elderly men on lipids and lipoproteins. Twenty-two men with initial serum testosterone concentrations below 3.5 ng/ml took part in the study: 11 with hypopituitarism (1st group) and 11 otherwise healthy elderly men with low testosterone levels (2nd group). Testosterone deficiency was replaced by intramuscular injections of testosterone enanthate 200 mg every second week. Plasma levels of sex hormones, gonadotropins, SHBG, lipids and lipoproteins were determined before the treatment and after 3, 6 and 12 months of treatment. During the treatment serum testosterone and estradiol increased significantly, reaching normal levels. This was associated with a decrease in total cholesterol (from 225 +/- 16.9 mg/dl to 202 +/- 13.6 mg/dl after 6 months and 198 +/- 12.8 mg/dl after 1 year of testosterone administration, P < 0.0001 in men with hypoandrogenism associated with aging and from 255 +/- 12.1 mg/dl to 214 +/- 10.6 mg/dl after 6 months and 206 +/- 9 mg/dl after 1 year of treatment, P < 0.0001 in men with hypopituitarism) and LDL-cholesterol concentrations (from 139 +/- 12.5 mg/dl to 126 +/- 10.7 mg/dl after 6 months and 118 +/- 9.8 mg/dl after 1 year of testosterone administration, P < 0.0001 in men with hypoandrogenism associated with aging and from 178 +/- 10.3 mg/dl to 149 +/- 10.2 mg/dl after 6 months and 140 +/- 7.3 mg/dl after 1 year of treatment, P < 0.001 in men with hypopituitarism). However, no significant decrease in HDL-cholesterol levels or HDL2- and HDL3-cholesterol subfractions was observed. The effects of testosterone replacement therapy on lipids and lipoproteins were similar in both groups with different aetiology of hypogonadism. No side effects on the prostate were observed. The results of this study indicate that testosterone replacement therapy in hypogonadal and elderly men may have a beneficial effect on lipid metabolism through decreasing total cholesterol and atherogenic fraction of LDL-cholesterol without significant alterations in HDL-cholesterol levels or its subfractions HDL2-C and HDL3-C.
Atherosclerosis 1996 Mar
PMID:Effect of testosterone replacement therapy on lipids and lipoproteins in hypogonadal and elderly men. 867 22

Male gender is an independent risk factor for coronary artery disease, and androgen administration has been associated with increased atherosclerosis in experimental animals. Since endothelial dysfunction is an important event in the atherogenic process, we hypothesized that androgen deprivation in adult men might be associated with enhanced arterial endothelial function. Using external vascular ultrasound, brachial artery diameter was measured at rest, after flow increase (causing endothelium-dependent dilatation) and after nitroglycerin (an endothelium-independent dilator). We studied 30 adult males aged 40 to 70 years: 10 had had bilateral orchidectomy and/or maximal androgen blockade for > or = 6 months for treatment of prostate cancer, and all were in complete remission (group 1). Ten healthy controls (group 2) and 10 controls who had remission from nonprostate cancers (group 3) were matched for age and smoking history. Testosterone levels were lower in men in group 1 versus groups 2 or 3 (0.8 +/- 0.1 versus 19.2 +/- 8.4 or 16.1 +/- 4.9 nmol/L, P < .001). By contrast, endothelium-dependent dilatation was markedly higher in group 1 than in groups 2 or 3 (6.2 +/- 3 versus 2.7 +/- 2 or 2.0 +/- 1.9%, P < .001). The nitroglycerin response was similar in all three groups (P = .92). On multivariate analysis, increased endothelium-dependent dilatation was significantly associated with low serum testosterone levels (P = .001) but not with cholesterol levels or with a past history of malignancy (P > .25). The withdrawal of male sex hormones may be associated with enhanced endothelial function in adult men. This is consistent with a deleterious effect of physiologic levels of male sex steroids on the arterial wall.
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PMID:Androgen deprivation is associated with enhanced endothelium-dependent dilatation in adult men. 935 65

Lower androgen levels have been suggested to be associated with type 2 diabetes and central obesity and are probably involved into the development of atherosclerosis. The present study investigates the effect of acute and chronic exercise on Dehydroepiandrosterone (DHEA) levels in relation to abdominal fat distribution and metabolic status in type 2 diabetes. Twenty weight-stable, middle-aged males with type 2 diabetes were enrolled in the study and participated in a submaximal (VO(2) peak) and moderate (50% VO(2) peak) exercise bout. The subjects were randomly assigned either to a trained or a control group, respectively. Physical training consisted of an 8 week program of aerobic exercise (75% VO(2) peak, 45 min), twice a week and intermittent exercise, once a week, on a bicycle ergometer. Acute exercise significantly increased DHEA and Testosterone (T) levels. Physical training increased VO(2) peak (42%, p <0.001), insulin sensitivity index (K(ITT) ) (57.5%, p <0.02), and basal DHEA levels (36%, p <0.05), and decreased HbA1c (29%, p <0.001), visceral adipose tissue (VAT) (44%, p <0.01) and subcutaneous adipose tissue (SAT) levels (18%, p <0.01). Body weight, BMI and insulin, T levels were not modified. Changes in DHEA levels were not correlated with changes in insulin sensitivity and abdominal fat distribution. In conclusion, exercise training favourably affects DHEA levels independently of improvements of metabolic status and abdominal fat distribution in patients with type 2 diabetes.
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PMID:Effects of a single bout of exercise and exercise training on steroid levels in middle-aged type 2 diabetic men: relationship to abdominal adipose tissue distribution and metabolic status. 1117 15


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