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

Oral administration of the benzodiazepines (diazepam, lorazepam, chlordiazepoxide, bipotassium chlorazepate) in Triton WR-1339-induced (200 mg/kg, blood collection 18 h later) hyperlipidaemia in rats elicited marked decrease of serum total lipids, total cholesterol and triglyceride levels, and alterations in free fatty acid and free glycerol content. The optimal doses for diazepam, lorazepam, chlordiazepoxide and bipotassium chlorazepate were estimated to be 5 mg/kg. Other benzodiazepines, namely oxazepam, medazepam and nitrazepam, elicited only minor changes in serum lipids levels, while with grandaxin no change was observed. The optimal doses of diazepam and lorazepam brought about the same changes in serum lipid content as did clofibrate (90 mg/kg, p. o.). If diazepam, lorazepam, chlordiazepoxide and bipotassium chlorazepate were administered in doses of 5 mg/kg in Triton WR-1339-treated rats (blood collection taken 3 h later), a significant decrease of total lipids and triglyceride levels was observed. The free glycerol level only altered after the administration of chlordiazepoxide, which brought about a significant reduction.
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PMID:Effects of some benzodiazepine derivatives on Triton WR-1339-Induced hyperlipidaemia in rats. 0 63

Two isoflavones, biochanin-A and formononetin isolated from gram Cicer arietinum, have been shown to possess hypolipidemic properties for Triton WR-1339 induced hyperlipidemia in male albino rats, when administered as a crude extract or as individual compounds.
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PMID:Hypolipidemic principles of Cicer arietinum: biochanin-A and formononetin. 17 35

Total flavonoids from clover red and nut, containing isoflavones, decreased the content of cholesterol and triglycerides in intact rats, inhibited the development of hyperlipidemia, caused by Triton WR-1339, prevented accumulation of triglycerides in rat liver and blood caused by ethanol administration. The flavonoids from these plants inhibited lipolysis, stimulated by adrenaline.
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PMID:[Effect of the total flavonoids from red clover and chick-pea on the lipid content in the blood and liver of rats]. 47 86

Growth of Ehrlich ascites carcinoma induces hyperlipemia in mice. In the present study using male Swiss-Webster mice, we examined whether the usual elevations of plasma triglyceride levels in cancerous mice would occur in the absence of dietary fat. Hypertiglyceridemia developed at a similar rate and to a comparable degree in tumerous mice eating a fat-free (58% glucose) diet and in those fed Purina chow. Maximal hyperlipidemia was observed on day 6 or day 8 in tumorous mice fed either diet. To determine whether the endogenous cancer-induced hyperlipidemia was due to hypersecretion of triglycerides by the liver, triglyceride secretion rates were studied 0, 2, 4, 6, 8, 10, and 12 days after tumor inoculation using Triton WR-1339. The secretory rates did not increase prior to or during the development of hypertriglyceridemia in tumorous mice and were not significantly different from those of control mice. On days 10 and 12, triglyceride secretion actually decreased in tumorous mice. Other possible causes for hypertriglyceridemia are discussed in light of the present findings of undetectable differences in triglyceride secretion rates accompanying growth of Ehrlich ascites carcinoma in mice.
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PMID:The role of dietary fat and hepatic triglyceride secretion in cancer-induced hypertriglyceridemia. 75 Aug 29

The antilipidemic properties of certain benzofuran-, 2,3-dihydrobenzofuran-, and 3(2H)-benzofuranone-2-carboxylate analogs of clofibrate in a hyperlipidemic rat model are described. The hyperlipidemia was induced by intraperitoneal injection of Triton WR-1339. The results were analyzed in light of structural modifications as well as the lipid solubility of substituted compounds as assessed by a consideration of calculated log P values. Comparisons are made between the activity of these compounds and the activity of related cyclic analogs previously reported. Among the various compounds tested, only the 5-C1 and phenylsybstituted dihydrobenzofurans were selective against elevated serum cholesterol levels in this animal model. The data presented support the hypothesis that the cholesterol and triglyceride lowering activity of clofibrate related analogs in this animal model may be separated through a consideration of log P, conformational, and electronic changes. The proposal is advanced that relatively minor structural modification of clofibrate related analogs may lead to compounds which are not only selective in the Triton model but also to compounds which are likely to exert their effects by differing modes of action.
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PMID:Comparative antilipidemic effects of various ethyl 5-substituted benzofuran-, 2,3-dihydrobenzofuran-, and 3(2H)-benzofuranone-2-carboxylate analogs of clofibrate in a triton hyperlipidemic rat model. 127 76

We examined the effect of ethyl all-cis-5,8,11,14,17-eicosapentaenoate (EPA-E) with high purity on circulating lipids in rats under several experimental conditions. In normolipidemic rats, EPA-E decreased the lipids in a dose-dependent manner. Clofibrate (100 mg/kg/day) was more potent in lowering the lipids than EPA-E (1000 mg/kg/day). In high cholesterol diet-fed rats, EPA-E (300 mg/kg/day) decreased the total cholesterol. However, clofibrate (300 mg/kg/day) had little effect on the total cholesterol. In hypertriglycemic rats induced by corn oil, EPA-E (300 mg/kg/day) or clofibrate (100 mg/kg/day) reduced the rise of triglycerides. EPA-E (300 mg/kg/day), clinofibrate (100 mg/kg/day) or clofibrate (300 mg/kg/day) caused a significant reduction in the lipids induced by the injection of Triton WR-1339. Furthermore, EPA-E (300 mg/kg/day) or clinofibrate (100 mg/kg/day) decreased the elevation of lipids produced by feeding the rats a casein-rich diet. These results show that EPA-E possesses potent inhibitory activity on experimental hyperlipidemia induced either exogenously or endogenously.
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PMID:Hypolipidemic effect of ethyl all-cis-5,8,11,14,17-eicosapentaenoate (EPA-E) in rats. 143 27

1. Vitamin E content in the adipose tissue was examined in rats with and without vitamin E deficiency. With the progression of vitamin E depletion, the more rapid decrease in tocopherol concentration was observed in brown adipose tissue (BAT) than in white adipose tissue (WAT), and the rate of decrease of tocopherol was approximately three times faster in BAT than in WAT. After the intramuscular administration of 10 mg/kg of all-rac-tocopheryl acetate twice a week for two weeks to vitamin E-deficient rats, a similar pattern of increase was observed in the tocopherol concentrations of BAT and WAT, although the rate of increase was slower in WAT than in BAT. 2. Changes of tocopherol concentration in BAT and WAT were investigated in normo-nourished rats with hyperlipemia produced by the intramuscular injection of Triton WR-1339 for 7 days. A marked increase in tocopherol concentration was observed in both BAT and WAT in the late period of hyperlipemia, with the increase being greater in WAT. 3. The fatty acid composition of adipose tissue was compared between rats with and without vitamin E deficiency. No significant differences were observed in BAT and WAT between the two groups. 4. The glucose uptake of WAT was not altered in vitamin E-deficient rats when compared with control rats.
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PMID:Adipose tissues and vitamin E. 208 75

Changes in coagulative and fibrinolytic activities were studied in rats with hyperlipidemia induced by Triton WR-1339 (T-WR). After intravenous injection of T-WR (150, 200 or 300 mg/kg) into S.D. rats, dose-related increases in plasma lipids (total cholesterol, triglyceride, free cholesterol and phospholipid) were observed. In hyperlipidemic rats that received 300 mg/kg of T-WR, decreases in red blood cell count and Hb value were found. Significant increases in the ma value of the thromboelastogram and the fibrinogen level were observed in these T-WR treated rats. The alpha 2-plasmin inhibitor activity was found to decrease dose-relatedly. These results indicate that T-WR induced hyperlipidemia in rats is accompanied with an increase in coagulative activity and an indirect enhancement of fibrinolytic activity.
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PMID:Changes in coagulative and fibrinolytic activities in Triton WR-1339-induced hyperlipidemia in rats. 231 41

Previous studies have shown that tumor necrosis factor (TNF) administration acutely increases serum triglyceride levels and stimulates hepatic de novo fatty acid synthesis. We now demonstrate that 60-90 min after TNF administration the incorporation of glycerol into triglycerides in the liver is increased 57% in chow-fed rats. Additionally, the quantity of labeled lipid in serum is increased 96% in the TNF-treated animals. TNF also acutely increases hepatic lipid synthesis and the quantity of labeled lipids in serum in rats fed a high sucrose diet. Moreover, using the Triton WR-1339 method, from 1-2 h after TNF administration there is a 52% increase in total hepatic triglyceride secretion. In contrast, in animals fasted before TNF administration, the characteristic increase in serum triglyceride levels is not observed, and neither the incorporation of glycerol into hepatic lipids nor the quantity of labeled lipids in the circulation are increased. By 17 h after TNF administration the incorporation of glycerol into hepatic lipid and the quantity of labeled lipid in the serum are no longer increased. These results indicate that in addition to TNF acutely stimulating de novo fatty acid synthesis, TNF also acutely stimulates hepatic triglyceride synthesis. The increase in hepatic triglyceride synthesis leads to increased secretion of lipids into the circulation. These observations provide strong support for our hypothesis that a TNF-induced stimulation of hepatic lipid synthesis and secretion contributes to the TNF-induced hyperlipidemia.
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PMID:Tumor necrosis factor stimulates hepatic lipid synthesis and secretion. 270 58

The hypolipidemic effects of bezafibrate were examined in normal rats and an experimentally induced hyperlipidemic model of rats. Oral administration of bezafibrate at 1 mg/kg/day or more to normal rats for 7 days significantly decreased serum triglyceride (TG) and at 3 mg/kg/day or more for 7 days caused significant reduction of serum total cholesterol (TC). A single oral dose of 100 mg/kg of bezafibrate significantly inhibited the increase of serum TC and TG in hyperlipidemic rats induced by Triton WR-1339. When normal rats were given 75% fructose solution for 7 days, serum TG increased in concentration about four times. Oral administration of bezafibrate for 7 days at 1 mg/kg/day or more inhibited the increase of serum TG in this model. Serum TC increased in concentration about twice in 1% cholesterol diet-fed rats for 8 weeks. Oral administration of bezafibrate at 30 mg/kg/day or more inhibited the increase of serum TC. These results suggest that bezafibrate is effective in the treatment of hyperlipidemia.
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PMID:[Pharmacological investigation of bezafibrate, a hypolipidemic agent (1). Effects of bezafibrate on normal and experimental hyperlipidemia in rats]. 324 7


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