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

Rats fed a diet containing a high percentage of butter, cholesterol, cholic acid and proply thiouracil (HFD) showed weight loss and developed hyperlipidemia, marked fatty infiltration of the liver, moderate elevation of SGPT, degenerative changes of the heart muscle, bradycardia, alterations of the QRS complex in the electrocardiogram, and initial hemoconcentration followed by moderate anemia. Treatment with adriamycin (18 X 1 mg/kg i.p.) resulted in significant augmentation of the cardiotoxic effects of this drug demonstrated by electrocardiographic measurements and myocardial histopathology. Adriamycin-induced atrophy of the lymphatic tissue was seen only in rats fed HFD and not in animals receiving ground chow. Adriamycin levels in the heart after single i.p. injection were higher in rats receiving HFD. This effect was present already after 10 days on HFD. At this time histopathological liver changes were present and SGPT was elevated. It is concluded that the increase in adriamycin toxicity is, at least in part, due to diminished excretion by the liver. These experimental findings are in accordance with clinical observations which have identified liver disease as one of the important risk factors for the development of adriamycin cardiomyopathy.
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PMID:Modification of adriamycin toxicity in rats fed a high fat diet. 86 Jun 72

Adriamycin, an anticancer drug, caused dramatic increases in the serum lipid levels of rats fed a high-cholesterol diet. Male Lewis inbred rats were fed a basal or 1.5% cholesterol diet containing 0.5% cholic acid for 8 weeks. The rats were injected with adriamycin in doses of 1.5 mg/kg body weight, twice a week, and 6.0 mg/kg body weight, every other week. The serum lipid peroxide level gradually rose in adriamycin-treated rats, reaching a four-fold level at the end of the experiment. Cholesterol feeding, however, had a lowering effect on the lipid peroxide level. Adriamycin treatment or cholesterol feeding moderately elevated serum lipid levels, but their combination exerted a synergistic effect. In rats injected with a large dose of adriamycin and fed a high-cholesterol diet, the serum cholesterol, triglyceride and phospholipid levels strikingly increased by approx. 2000, 1500 and 1300 mg/100 ml, respectively. However, the ester ratio of cholesterol remained almost constant. Furthermore, serum GOT, GPT and ALP activities were only slightly different from the control values. Adriamycin treatment produced severe hypoalbuminemia. Ascites was also observed in rats given a large dose of adriamycin. The present findings indicate that the hyperlipidemia we observed may basically result from adriamycin-induced nephrosis and can be markedly enhanced when rats are fed a high-cholesterol diet. In spite of remarkably high levels of serum lipids and lipid peroxides, the aortic cholesterol level increased only slightly.
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PMID:Hyperlipidemic effects of adriamycin in rats. 409 81

Adriamycin induced hyperlipemia: its features and mechanism(s) in rats were investigated. Massive hyperlipemia occurred 14-21 days after a single dose of adriamycin (7.5 mg/kg i.v.). All lipoprotein fractions were affected. Mild but significant changes in tissues were observed (liver and intestine triglycerides and kidney phospholipids were reduced). Lipid synthesis and secretion was decreased, as shown by the Triton WR1339 test 7 days after treatment, but subsequently returned to normal. Mitochondrial oxidation of long-chain fatty acids was markedly reduced in kidney, and a slight reduction was also observed in heart. Lipoprotein lipase activity was reduced in adipose tissue. These results suggest that adriamycin hyperlipemia is due to reduced lipid storage and utilization. Carnitine did not counteract hyperlipemia and proteinuria after adriamycin. Analogies to hyperlipemia following puromycin aminonucleoside-induced nephrotoxicity are discussed.
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PMID:Adriamycin causes hyperlipemia as a consequence of nephrotoxicity. 666 4

The effect of melatonin (MEL) on the nephropathy and the oxidative stress induced by a single and high dose of Adriamycin (AD) has been studied in Wistar male rats. MEL (50 microg/kg/day) was injected intraperitoneally 3 and 7 days, respectively, before and after AD injection (20 mg/kg i.p.). Trunk blood was drawn and triglycerides, total cholesterol, phospholipids, high-density lipoprotein cholesterol, urea, creatinine, total protein, lipoperoxides, and reduced glutathione (GSH) levels and catalase activity (CAT) were determined in serum. In kidney homogenates, lipoperoxides, GSH, and CAT were measured as well as total protein in urine. AD administration resulted in hyperlipidemia and high-grade proteinuria and a marked increase in serum lipoperoxides, urea, and creatinine. In the kidney, the increase in lipoperoxides was accompanied by a significant decrease of GSH and CAT. The efficiency of MEL was specially remarkable in restoring GSH, CAT, and proteinuria to the levels of controls. These results confirm the involvement of free radicals in the pathogenesis of nephrotoxicity induced by AD. Likewise, they show the high antioxidative power of MEL and its marked effect on the prevention and suppression of this nephropathy.
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PMID:Hyperlipidemic nephropathy induced by adriamycin: effect of melatonin administration. 922 37

Estrogen replacement therapy is considered antiatherosclerotic because it reduces LDL cholesterol and fibrinogen and increases HDL cholesterol concentrations. However, exogenous estrogen is also known to increase hepatic triglyceride production. Hyperlipidemia in the nephrotic syndrome is probably due to increased lipoprotein secretion into plasma and decreased clearance of lipoprotein cholesterol and triglycerides. Previously, lipid-lowering effects of ovariectomy in analbuminemic rats were observed, suggesting that in the presence of hypoalbuminemia, estrogen replacement may have adverse effects on the lipid profile. To test this hypothesis, ovariectomized control rats and rats with Adriamycin-induced nephrotic syndrome were treated with estradiol. In ovariectomized controls, estradiol reduced plasma LDL cholesterol, apolipoprotein B, and fibrinogen and increased apolipoprotein A-I and triglycerides. Nephrotic rats were characterized by a marked decrease in plasma colloid osmotic pressure, hyperfibrinogenemia, hyperlipidemia, and stimulated hepatic fatty acid synthesis. The beneficial effects of estradiol on LDL cholesterol, apolipoprotein B, and fibrinogen found in ovariectomized controls were not present in estradiol-treated nephrotic rats. This suggests that in hypoalbuminemia, downregulation of the LDL receptor overrides putative estradiol-induced increases in LDL receptor activity. Moreover, estrogen replacement in the nephrotic syndrome doubled fatty acid synthesis and triglyceride secretion, and markedly exacerbated hypertriglyceridemia, suggesting saturation of triglyceride clearance. Thus, severe hypoalbuminemia in rats induces an atherosclerotic metabolic response that is aggravated by estrogen replacement. These findings suggest that estrogen replacement in hypoalbuminemic subjects could be contra-indicated.
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PMID:Estrogen replacement during hypoalbuminemia may enhance atherosclerotic risk. 940 89

Hyperlipidemia associated with nephrotic syndrome may play a role in the deterioration of renal function. Tsutsumi et al have previously reported that the novel compound NO-1886 increases lipoprotein lipase (LPL) activity, resulting in a reduction of plasma triglycerides and an elevation of high-density lipoprotein (HDL) cholesterol in normal rats. The aim of this study was to ascertain whether NO-1886 suppresses the renal injury by treatment of the hyperlipidemia in an Adriamycin (Kyowa Hakko Kogyo, Tokyo, Japan) induced nephrosis rat model fed a high-protein diet that induced renal dysfunction and tubulointerstitial injury. Administration of Adriamycin caused hyperlipidemia, proteinuria, and edema with ascites in rats in 4 weeks. Furthermore, a combination of Adriamycin and a high-protein diet increased plasma creatinine and blood urea nitrogen (BUN) and decreased plasma albumin. Histologically, in Adriamycin-treated rats, marked interstitial cellular infiltration, tubular lumen dilation, and tubular cast formation in the kidney were observed. NO-1886 decreased plasma triglyceride and increased HDL cholesterol in Adriamycin-induced nephrotic rats. NO-1886 treatment reduced plasma creatinine and BUN levels and increased plasma albumin in Adriamycin-treated rats; it also ameliorated the ascites and proteinuria. Histologically, NO-1886-treated rats showed a quantitatively significant preservation of tubulointerstitial lesions. These data suggest that NO-1886 may have a protective effect against Adriamycin-induced nephrosis with tubulointerstitial nephritis in rats by a modification of the plasma lipid disorder.
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PMID:Effect of the lipoprotein lipase activator NO-1886 on adriamycin-induced nephrotic syndrome in rats. 1083 Nov 67

Adriamycin (doxorubicin) is one of the most effective chemotherapeutic agents against a variety of cancers, but its usefulness is seriously curtailed by the risk of developing heart failure. Available laboratory evidence suggests that an increase in oxidative stress, brought about by increased free radical production and decreased myocardial endogenous antioxidants, plays an important role in the pathogenesis of heart failure. Adriamycin-induced apoptosis and hyperlipidemia may also be involved in the process. Probucol, a lipid-lowering drug and an antioxidant, completely prevents the occurrence of heart failure by reducing oxidative stress as well as by the modulation of apoptosis and high lipid concentrations. Thus, combined therapy with adriamycin and probucol has a high potential for optimizing the treatment of cancer patients.
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PMID:Adriamycin-induced heart failure: mechanism and modulation. 1088 30

The present study was performed to determine quantitatively the effect of hypercholesterolemia induced by a lipid-rich diet on glomerulosclerosis in an animal model of nephrotic syndrome (NS) induced by Adriamycin (ADR). Twenty NS Wistar rats administered ADR with a single intravenous dose of 5 mg/kg body weight were divided into standard and lipid-rich chow groups. Another 20 weight-matched non-NS rats that received a vehicle alone were grouped as controls. Quantitative analyses of renal histological changes were performed with determination of blood and urine biochemical parameters. It was found that serum cholesterol was markedly higher in rats with lipid-rich chow in both NS and non-NS rats. Urinary protein was significantly higher in rats on the lipid-rich diet in the NS group. The mesangial matrix and cell indices were significantly increased in rats with the lipid-rich diet and the most obvious changes were found in the NS group. Lipid deposits and foam cells were observed in mesangial areas, and some glomeruli had progressed to form focal and segmental glomerulosclerosis in the NS group. Findings indicated that diet-induced hyperlipidemia can lead to proliferation of mesangial cells and accumulation of mesangial matrices, and further aggravate glomerulosclerosis in Adriamycin-induced nephrosis.
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PMID:Glomerulosclerosis in adriamycin-induced nephrosis is accelerated by a lipid-rich diet. 1114 10

This article provides a comprehensive review of 30 years of research on the use of coenzyme Q10 in prevention and treatment of cardiovascular disease. This endogenous antioxidant has potential for use in prevention and treatment of cardiovascular disease, particularly hypertension, hyperlipidemia, coronary artery disease, and heart failure. It appears that levels of coenzyme Q10 are decreased during therapy with HMG-CoA reductase inhibitors, gemfibrozil, Adriamycin, and certain beta blockers. Further clinical trials are warranted, but because of its low toxicity it may be appropriate to recommend coenzyme Q10 to select patients as an adjunct to conventional treatment.
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PMID:Coenzyme Q10 and cardiovascular disease: a review. 1259 59

Adriamycin widely used in the treatment of neoplastic conditions is nephrotoxic. In the present study the protective effect of lipoic acid was investigated in adriamycin-induced nephrotoxicity in adult male albino Wistar rats. Adriamycin-induced nephrotoxicity was characterized by hyperlipidemia, proteinuria, and hypoproteinemia, by decreased activities of the enzymes N-acetyl-beta-D-glucosaminidase and cathepsin D, by increased lipid peroxidation and decreases in serum catalase and glutathione activities, and by increased urinary and serum urea, creatinine and urinary glycosaminoglycans. Pretreatment with lipoic acid restored the changes, indicating that lipoic acid is renoprotective in adriamycin nephrotoxicity.
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PMID:The influence of lipoic acid on adriamycin-induced hyperlipidemic nephrotoxicity in rats. 1284 41


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