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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus is a significant risk factor for cardiovascular complications. Experimental evidence suggests that oxidative stress plays a dominant role in the pathogenesis of diabetes mellitus. This study was undertaken to investigate the effect of vanadyl sulfate on blood glucose, serum and tissue lipid profiles and on stomach and spleen tissues in STZ-induced diabetic rats. In this study, male 6-6.5-month-old Swiss albino rats were used. Rats were randomly divided into four groups. Group I: control animals (normal, nondiabetic animals) (n = 13); Group II: vanadyl sulfate controls (n = 5); Group III: streptozotocin (STZ)-diabetic, untreated animals (n = 11); and Group IV: STZ diabetic animals given vanadyl sulfate (n = 11). Experimental diabetes was induced by intraperitoneal (i.p.) injection of STZ in a single dose of 65 mg kg(-1) body weight. Vanadyl sulfate was administered by gavage at a dose of 100 mg kg(-1). The levels of cholesterol, phospholipid, high density lipoprotein-cholesterol (HDL-), low density lipoprotein-cholesterol (LDL-), very low density lipoprotein-cholesterol (VLDL-), triglycerides and lipid peroxidation (LPO) in serum and cholesterol in liver were assayed according to standard procedures. The levels of lipid peroxidation, glutathione (GSH) and nonenzymatic glycosylation (NEG) in stomach and lipid peroxidation and glutathione (GSH) in spleen tissues were analyzed. After 60 days of treatment, serum cholesterol, LDL-cholesterol, triglyceride, phospholipid, VLDL-cholesterol, LPO, blood glucose levels, stomach LPO and NEG, spleen LPO significantly increased, but serum HDL-cholesterol, stomach GSH and spleen GSH levels significantly decreased in the diabetic group. On the other hand, treatment with vanadyl sulfate reversed these effects. These results reveal that diabetes mellitus increased oxidative damage in stomach and spleen tissues and vanadyl sulfate has an ameliorating effect on the oxidative stress via its antioxidant property. The administration of vanadyl sulfate may be able to reduce hyperglycemia and hyperlipidemia related to the risk of diabetes mellitus.
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PMID:Effect of vanadyl sulfate on the status of lipid parameters and on stomach and spleen tissues of streptozotocin-induced diabetic rats. 1643 Nov 26

Treatment with vanadium, a representative of a class of antidiabetic compounds, alleviates diabetic hyperglycemia and hyperlipidemia. Oral administration of vanadium compounds in animal models and humans does not cause clinical symptoms of hypoglycemia, a common problem for diabetic patients with insulin treatment. Gene expression, using Affymetrix arrays, was examined in muscle from streptozotocin-induced diabetic and normal rats in the presence or absence of oral vanadyl sulfate treatment. This treatment affected normal rats differently from diabetic rats, as demonstrated by two-way ANOVA of the full array data. Diabetes altered the expression of 133 genes, and the expression of 30% of these genes dysregulated in diabetes was normalized by vanadyl sulfate treatment. For those genes, the ratio of expression in normal animals to the expression in diabetic animals showed a strong negative correlation with the ratio of expression in diabetic animals to the expression in diabetic animals treated with vanadyl sulfate (P = -0.85). The genes identified belong to six major metabolic functional groups: lipid metabolism, oxidative stress, muscle structure, protein breakdown and biosynthesis, the complement system, and signal transduction. The identification of oxidative stress genes, coupled with the known oxidative chemistry of vanadium, implicates reactive oxygen species in the action of this class of compounds. These results imply that early transition metals or compounds formed from their chemical interactions with other metabolites may act as general transcription modulators, a role not usually associated with this class of compounds.
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PMID:Diabetes-altered gene expression in rat skeletal muscle corrected by oral administration of vanadyl sulfate. 1668 4

Treatment of HIV infection has typically been carried out using two nucleoside analogs and a protease inhibitor. Such regimens can be complex and have high pill burdens. Use of alternative regimens, such as triple nucleoside-based regimens, can improve adherence and decrease toxicities associated with protease inhibitor therapy. A formulation of abacavir sulfate/lamivudine/zidovudine allows a dosing schedule of one pill twice daily. The components have performed favorably compared with protease inhibitor-based regimens, such as indinavir. Compared with efavirenz-based regimens, abacavir sulfate/lamivudine/zidovudine has not performed as well. The combination is being studied as a cornerstone for induction maintenance strategies, in which switching a patient to abacavir sulfate/lamivudine/zidovudine has been associated with similar virologic outcomes as continuing with either protease inhibitor- or efavirenz-based regimens. Administration of abacavir sulfate/lamivudine/zidovudine also avoids side effects of antiretroviral therapy, such as hyperlipidemia, but its use is associated with a hypersensitivity reaction in a small number of patients. The combination of abacavir sulfate/lamivudine/zidovudine is an important part of the HIV armamentarium. Its potency and ease of administration make it worth consideration in the treatment of HIV, either by itself or in combination with other agents.
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PMID:Abacavir sulfate/lamivudine/zidovudine fixed combination in the treatment of HIV infection. 1730 42

We developed a simple separative method for measuring serum amyloid A (SAA) in both high-density-lipoprotein (HDL) and low-density-lipoprotein (LDL) fractions. It was devised using the SAA agglutination method and phosphotungstic acid-Mg2+ precipitation procedure for evaluating HDL-cholesterol (HDL-C). The new method is also able to detect amyloid A (AA) in each fraction with precision. The results of both the present method and the method using SAA agglutination and the dextran sulfate-Mg2+ precipitation procedure showed a strong correlation when used to measure the level of SAA in the LDL fraction of patients (r = 0.997; p < 0.0001). Reference intervals in normal healthy subjects (n=75) ranged from 0.5 to 4.7 microg/ml in the HDL fraction and from 0.1 to 1.9 microg/ml in the LDL fraction. SAA in the LDL fraction of subjects with hyperlipidemia was significantly higher than in normal subjects and subjects with normal lipidemia. SAA in the HDL fraction and total sera of subjects with hyperlipidemia was significantly higher than in normal subjects; however, it was not higher than in patients with normal lipidemia. The present methods for detecting SAA, especially in the LDL fraction, might benefit from analyzing patho-physiological events in various lipid disorders.
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PMID:[A simple separative method for measuring serum amyloid A in high-density-lipoprotein and low-density-lipoprotein fractions using the phosphotungstic acid-Mg2+ precipitation procedure]. 1751 Dec 61

Many low density lipoprotein (LDL) apheresis systems have been applied to patients with hyperlipidemia, but these systems usually work on the basis of complicated equipment and the cost of treatment is expensive. In order to achieve effective treatment of hyperlipidemia at a lower cost, we developed a new LDL apheresis system with dextran sulfate (LAS-DS). In this study, 50 patients with hyperlipidemia were treated 120 times with the new LAS-DS. In each treatment, 600 +/- 100 mL of plasma (equal to approximately 25% of the total plasma of patients) was collected by apheresis, and DS solution and calcium chloride solution were added into the collected plasma as LDL absorber and catalyzer, respectively. DS selectively binds LDL cholesterol (LDL-C) under the catalysis of calcium ion and the LDL-C-DS complex is removed by centrifugation. The treated plasma was transfused back into the patients and the excessive calcium in the plasma was removed by the cation exchange column integrated in the transfusion set. After treatment with our new system, the acute mean LDL-C reduction was 97% in the apheresis plasma of hyperlipidemia patients. The corresponding reduction was 55.2% and 69.4% for total cholesterol and total triglyceride. There were insignificant reductions of high density lipoprotein cholesterol (HDL-C) and albumin. The new LDL apheresis system with DS that we developed is very simple to operate without relying on complicated equipment, and it can achieve significant clinical results at a much lower cost compared with existing systems. Based on this study we think the new system can provide a safe, effective and much cheaper means for the treatment of hyperlipidemia patients.
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PMID:Treatment of hyperlipidemia with a modified low density lipoprotein apheresis system with dextran sulfate. 1825 22

New evidence about diabetic microangiopathy has enabled us to identify an integrated pathogenesis of diabetic complications, including classic metabolic pathways induced by hyperglycaemia, insulin-resistance, hyperinsulinaemia, hormonal alterations and growth factors. Oxidative stress is the most important cause of endothelial damage inducing leukocyte adhesion, altered coagulation and inflammation. Adhesion molecules are a marker of endothelial damage and a potential therapeutic target. Changes in the extracellular matrix induced by TGFbeta1 and lower levels of eparan-sulfate, increased thickness of basement membranes and loss of pericytes are early events of diabetic retinopathy and diabetic nephropathy. Capillary rarefaction produced by genetic factors or by fetal undernourishment contributes to the beginning of insulin-resistance and hypertension. Psychophysical tests, electroretinogram and evoked potentials show retinal functional alterations; fundoscopy and retinal fluorescein angiography show retinal anatomic alterations. The diagnosis of diabetic neuropathy is based not only on traditional neurological examination and electroneurograms, but also on neurothesiometry for sensory testing. Medical treatment of diabetic microangiopathy is based on control of glycaemia, lipemia and blood pressure using glytazones, ACE-inhibitors, angiotensin II receptor antagonists and statins. New knowledgeabout microangiopathy pathogenesis suggests potential drugs for its therapy (ruboxistaurin, AGE-inhibitors, angiopoietin-1 and anti-VEGF, etc.), not yet on sale.
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PMID:Diabetic microangiopathy: physiopathological, clinical and therapeutic aspects. 1791 58

Age-related decline in serum testosterone and dehydroepiandrosterone sulfate concentrations occur in men. Low concentrations of these endogenous androgens have been linked with insulin resistance, which is an important upstream driver for metabolic abnormalities such as hyperglycemia, hypertension, or hyperlipidemia, and increased cardiovascular risk. Moreover, men with diabetes have significantly less circulating androgen than nondiabetic men. Here, we summarize how androgen affects insulin resistance and atherosclerosis in men with type 2 diabetes. Low serum concentrations of endogenous androgens are associated with visceral fat accumulation. Androgen deprivation by castration to treat prostate cancer increases insulin resistance, while testosterone administration in type 2 diabetic men with androgen deficiency improves glucose homeostasis and decreases visceral fat, in addition to alleviating symptoms of androgen deficiency including erectile dysfunction. Androgen correlates inversely with severity of atherosclerosis and has beneficial effects upon vascular reactivity, inflammatory cytokine, adhesion molecules, insulin resistance, serum lipids, and hemostatic factors. Because men with type 2 diabetes have relative hypogonadism, testosterone supplementation could decrease both insulin resistance and atherosclerosis.
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PMID:Role of endogenous androgen against insulin resistance and athero- sclerosis in men with type 2 diabetes. 1822 Jun 53

We investigated whether a low plasma testosterone level is related to endothelial dysfunction in men with coronary risk factors. One hundred and eighty-seven consecutive male outpatients (mean age+/-SD: 47+/-15 years) who underwent measurement of flow-mediated vasodilation (FMD) of the brachial artery using ultrasonography were enrolled. The relationship between plasma hormones and FMD was analyzed. Total and free testosterone and dehydroepiandrosterone-sulfate (DHEA-S) were significantly correlated with %FMD (r=0.261, 0.354 and 0.295, respectively; p<0.001), while estradiol and cortisol were not. %FMD in the highest quartile of free testosterone was 1.7-fold higher than that in the lowest quartile. Multiple regression analysis revealed that total and free testosterone were related to %FMD independent of age, body mass index, hypertension, hyperlipidemia, diabetes mellitus and smoking (beta=0.198 and 0.247, respectively; p<0.01), and were independent of age, body mass index, systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, fasting plasma glucose, smoking and nitroglycerin-induced dilation (beta=0.196 and 0.227, respectively; p<0.01). DHEA-S was not significantly related to %FMD in multivariate analysis. In conclusion, a low plasma testosterone level was associated with endothelial dysfunction in men independent of other risk factors, suggesting a protective effect of endogenous testosterone on the endothelium.
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PMID:Low testosterone level is an independent determinant of endothelial dysfunction in men. 1825 May 51

Age-related decline of plasma dehydroepiandrosterone-sulfate (DHEA-S) levels may be associated with the risk of cardiovascular disease in women. We investigated whether plasma DHEA-S levels are related to endothelial function in postmenopausal women with coronary risk factors. One hundred and fifteen postmenopausal women (mean age+/-SD: 57+/-5 years; range: 48-65 years) who underwent measurement of flow-mediated vasodilation (FMD) of the brachial artery using ultrasonography were enrolled. Plasma hormone levels were determined in the morning after a 14-h fast, and the relationship between hormone levels and FMD was analyzed. DHEA-S was significantly correlated with %FMD (r=0.392, p<0.001), while estradiol, total testosterone and cortisol were not. %FMD in the highest quartile of DHEA-S was 1.8-fold higher than that in the lowest quartile (5.3+/-1.3 vs. 2.9+/-2.0 [means+/-SD], p<0.01). Multiple regression analysis revealed that DHEA-S was related to %FMD independent of age, body mass index, hypertension, hyperlipidemia, diabetes mellitus and smoking (beta=0.344, p<0.01), and was itself independent of age, body mass index, systolic blood pressure, total cholesterol, high-density lipoprotein (HDL) cholesterol, fasting plasma glucose and smoking (beta=0.291, p<0.05). In conclusion, plasma DHEA-S levels were weakly but significantly related to endothelial function in postmenopausal women independent of other coronary risk factors, suggesting a protective effect of DHEA on the endothelium.
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PMID:Association of plasma dehydroepiandrosterone-sulfate levels with endothelial function in postmenopausal women with coronary risk factors. 1836 20

This study ascertains the effects of zinc, a major component of particulate matter, on pulmonary and systemic endpoints using hyperlipidemic rabbits to model diet-induced human atherosclerosis. New Zealand White rabbits were fed a normal or cholesterol-enriched diet and then were intratracheally instilled 1x/week for 4 weeks with saline or 16 microg/kg of zinc, equal parts sulfate and oxide. Physiologic responses, blood after each exposure, and terminal bronchoalveolar lavage (BAL) were assessed. Rabbits fed a cholesterol-rich diet developed hyperlipidemia and had consistently higher circulating leukocyte counts than rabbits fed normal chow. Within minutes after zinc instillation, saturation of peripheral oxygen was decreased in hyperlipidemic rabbits and heart rate was increased in hyperlipidemic rabbits with total serum cholesterol levels greater than 200 mg/dl. Total circulating leukocytes levels were increased 24 h after the first zinc instillation, but upon repeated exposures this effect was attenuated. After repeated zinc exposures, BAL fluid (BALF) N-acetylglucosaminidase activity was increased regardless of hyperlipidemic state. Hyperlipidemic rabbits had an increase in BALF-oxidized glutathione and a decrease in serum nitrite. The study elucidates mechanisms by which the zinc metal component of PM drives cardiovascular health effects, as well as the possible susceptibility induced by hyperlipidemia. Furthermore, the study exemplifies the benefits of monitoring circulatory physiology during exposure as well as after exposure.
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PMID:A hyperlipidemic rabbit model provides new insights into pulmonary zinc exposure effects on cardiovascular health. 1895 71


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