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

After enteral administration of 200 mg/kg alpha-hexachlorocyclohexane (alpha-HCH) female Wistar rats develop a hyperlipemia. 48 h after administration of alpha-HCH, serum triglycerides are increased by 300%, whereas both serum cholesterol and serum total phospholipids only increase by about 45%. Serum free fatty acids are not significantly altered. Fractionation of the serum lipoproteins by ultracentrifugation shows that the hyperlipemia is due to a fivefold increase in serum very low density lipoproteins. Hepatic triglyceride secretion, calculated after i.v. injection of Triton WR 1339, is increased in animals pretreated wtih alpha-HCH. Corresponding to this observation, drugs known to diminish the triglyceride secretion of the liver, such as actinomycin D, cycloheximide; glucagon, orotic acid, CFT 1201, and CFT 1042 reduce the alpha-HCH-induced hyperlipemia. We concluded from the results that hyperlipoproteinemia after alpha-HCH is due to an increased hepatic very low density lipoprotein secretion. At the same time, the blood sugar level was decreased in fasting animals after treatment with alpha-HCH. Earlier experiments suggest that this effect is due to a decreased gluconeogenesis in the liver.
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PMID:Increase of serum very low density lipoproteins in rats after administration of alpha-hexachlorocyclohexane. 6 95

We have studied the effects of diet-induced hypercholesterolemia on the rates of secretion of triglycerides into the plasma of fasted squirrel monkeys. Two groups of monkeys were studied: control animals which were fed a semipurified diet not associated with hyperlipemia (plasma cholesterol 127 +/- 8 mg/100 ml), and animals made hypercholesterolemic (plasma cholesterol 307 +/- 31 mg/100 ml) by being fed a diet containing 25% butter and 0.5% cholesterol. After intravenous infusion of Triton WR 1339 (300 mg/kg body wt), plasma triglycerides increased almost linearly for 9-12 hours. Analysis of individual lipoproteins separated by ultracentrifugation showed that newly secreted triglycerides were present almost exclusively in the very low density lipoprotein fraction. The rates of triglyceride secretion in the hypercholesterolemic group of monkeys (5.15 +/- 0.86 mg/kg/hr) were less than half those of the control animals (10.96 +/- 2.15 mg/kg/hr). We suggest that in monkeys with diet-induced hypercholesterolemia high concentrations of plasma low density lipoproteins may inhibit the synthesis and/or secretion of their parent very low density lipoprotein molecules into the circulation.
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PMID:Metabolism of lipoproteins in nonhuman primates. Reduced secretion of very low density lipoproteins in squirrel monkeys with diet-induced hypercholesterolemia. 17 53

In order to elucidate the mechanism(s) of hyperlipidemia following glucocorticoid administration, dexamethasone (0.125 mg/Kg) was administered daily intramuscularly for 2 wk to male Sprague-Dawley rats and the effects on plasma triglyceride (TG) and cholesterol (Chol), lipoprotein neutral lipids, hepatic triglyceride secretion rates (TGSR; Triton), and epididymal fat lipoprotein lipase (LPL) were determined. Special measures were taken to maintain positive caloric balance and keep the weights of control and dexamethasone-treated animals comparable. Significant increases (p less than 0.001) in TG and very-low density lipoprotein (VLDL) triglyceride associated with no change in Chol and actual reduction in both triglyceride and cholesterol in low density lipoprotein (ldl) were observed in the steroid-treated animals. Dexamethasone treatment was associated with increased basal insulin and glucose levels, an insignificant increment in TGSR, and a highly significant reduction (p less than 0.001) in LPL. These findings suggest that glucocorticoid treatment increases splanchnic triglyceride production rates, but the resulting hypertriglyceridemia is primarily a consequence of impaired VLDL removal due to low adipose tissue LPL activity.
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PMID:Glucocorticoids and triglyceride transport: effects on triglyceride secretion rates, lipoprotein lipase, and plasma lipoproteins in the rat. 17 40

In order to compare in vitro and in vivo aspects of lipid metabolism and lipoprotein secretion associated with the hyperlipemia of saturated fat feeding, gerbils were fed a diet containing 15% coconut oil or safflower oil for 6 weeks. In vitro incorporation of fatty acid was determined by measuring 14C-oleic acid incorporation into hepatic lipis in liver fasting gerbils following Triton WR1339 injection. The plasma lipoprotein profile was assessed by agarose electrophoresis. Coconut oil produced a hypertriglyceridemia and hypercholesterolemia associated with the appearance of very low density migrating lipoprotein, not seen with the safflower oil. Coconut oil also increased the hepatic triglyceride content, enhanced 14C-oleic acid incorporation into total lipid, and favored fatty acid incorporation into triglyceride; safflower oil facilitated esterification of oleic acid into phospholipid. Triton blockade of gerbils fed safflower oil resulted in twice the triglyceride secretion rate of those fed coconut oil. Our interpretation of the data is that dietary polyunsaturated fat favors incorporation of fatty acids into phospholipid, enhances both triglyceride secretion and the plasma transport and clearance of triglyceride and cholesterol and that the hyperlipemia of coconut oil feeding reflects a reduced metabolic clearnace of circulating lipid associated with that dietary fat.
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PMID:Effect of dietary fat on hepatic metabolism of 14C-oleic acid and very low density lipoprotein triglyceride in the gerbil. 18 36

BR-931 [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio-(N-beta-hydroxyethyl)-acetamide], a new hypolipidemic agent of low toxicity, was evaluated in several tests of lipolysis and hyperlipidemia in rats, and in the cholesterol-induced atherosclerosis in rabbits. Significant hypolipidemic activity was observed in rats with doses of the agent at 12.5--50 mg/kg. In the Triton-induced hyperlipidemia, 50 mg BR-931 per kg was equieffective as 200 mg of clofibrate (CPIB) per kg. In contrast with CPIB, BR-931 exerted a powerful antilipolytic activity against epinephrine, ACTH, nicotine and cold exposure. BR-931 was particularly effective in diet-induced hyperlipidemias. Ethanol lipemia was totally prevented by the agent at 100 mg/kg. With Nath's diet, doses as low as 25 mg/kg significantly reduced hypercholesterolemia and hypertriglyceridemia. In these last two tests, the distribution of lipoprotein cholesterol was also determined. CPIB did not affect HDL cholesterol levels that had been decreased by the diets; in contrast, BR-931, already at doses of 50 mg/kg, brought the HDL/total cholesterol ratio back toward normal. A significant HDL cholesterol increase, together with some reduction of atheromatosis, was also observed in cholesterol-fed rabbits. BR-931, a potent inducer of liver peroxisones and of mitochondrial carmitine acetyltransferase, appears to be a hypolipidemic agent of high efficacy and low toxicity for the clinical treatment of hyperlipidemias and atherosclerosis.
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PMID:Pharmacological profile of BR-931, a new hypolipidemic agent that increases high-density lipoproteins. 20 96

The isoflavone content of some commonly used legumes was determined. In Triton-WR1339-induced hyperlipidemia in male albino rats, biochanin A, formononetin and pratensein showed hypolipidemic activity, while diadzein did not, when these isoflavones were administered as individual compounds by gastric intubation.
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PMID:Effect of various isoflavones on lipid levels in triton-treated rats. 48 27

Chronic exercise training is recognized to reduce plasma lipid levels in man and animals, but the mechanism(s) mediating this phenomenon have not been defined. In the present study, we examined triglyceride (TG) production and disposal in vivo in a genetic model of human type IV hyperlipemia, the obese Zucker rat. Utilizing the normolipemic thin littermate as the control, we investigated endogenous production of TG utilizing the Triton methodology and peripheral disposal of an exogenous lipid emulsion utilizing Intralipid injection. In the sedentary state, the hyperlipemic obese Zucker rat demonstrated a threefold elevation in triglyceride secretion rate relative to the normolipemic thin littermate. After a 3-wk period of exercise training, a reduction of basal plasma TG concentration of 42% was associated with a 51% reduction in TG secretion rate, a change adequate to account for the hypolipemic response. Moreover, chronic exercise training also improved the ability to dispose of an Intralipid load. A similar reduction in TG production with reduced TG removal was observed in the thin normolipemic rats, a result that suggests that the lipid lowering response to exercise training may be predominantly mediated by reduced secretion of TG. The possible relationship between reduced TG secretion and alterations in the bihormonal axis of insulin and glucagon are discussed.
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PMID:Reduced triglyceride secretion: a metabolic consequence of chronic exercise. 62 36

The catabolism of chylomicrons was investigated in genetically obese rats and their nonobese littermates, and was compared with catabolism in older Sprague-Dawley rats with body weights similar to the obese rats and their younger controls. Labeled thoracic-duct lymph was collected from donor rats and the catabolism of the labeled chylomicrons was studied after a single intravenous injection or during steady intravenous infusion in unanesthetized, nonfasting, recipient rats. In the genetically obese rats clearances from the plasma of chylomicron triacylglycerol and cholesteryl ester were less than in their nonobese littermates. Fractional clearance rates were reduced for both triacylglycerol and cholesteryl ester but triacylglycerol turnover rate (mg min(-1)) was greater than controls. Chylomicron triacylglycerol clearance was more efficient than cholesteryl ester clearance so that radioactivity remaining in the plasma was relatively depleted in triacylglycerol. The large-bodied old Sprague-Dawley rats showed no reduction in clearance of chylomicron radioactivity in comparison with younger controls. These results suggest that hyperlipidemia in genetically obese rats may be due in part to an accumulation of chylomicron remnants in the plasma. Flotation characteristics of plasma lipoproteins in the obese rats were consistent with this interpretation. However, separate experiments showed that genetically obese, fasting rats also accumulated more triacylglycerol in the plasma after injection of Triton WR 1339. The enlarged plasma triacylglycerol pool appears to derive from a mixture of hepatic and intestinal triacylglycerol-rich lipoproteins which, together, overload their common removal mechanism. Addition of cholesterol to the diets of the obese rats exacerbated their hyperlipemia and hepatic steatosis whereas their nonobese littermates and the large-bodied Sprague-Dawley rats were unaffected.
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PMID:Catabolism of chylomicron triacylglycerol and cholesteryl ester in genetically obese rats. 90 8

Rats tube-fed a diet devoid of threonine accumulated triacylglycerols in their livers, starting on the third day of the diet. The fatty acid composition of the accumulated lipid and the contribution of novo synthesized fatty acids to the lipid accumulation, as determined with tritiated water as a radioactive precursor for fatty acid synthesis, suggested that an increased hepatic de novo synthesis of fatty acids is not a major factor for the development of this liver lipid accumulation. The metabolism of intravenous injected 3H-oleic acid, the Triton-induced hyperlipemia and the activity of lipoprotein lipase in adipose tissue was also studied. None of these studies revealed any significant difference between the threonine-deficient and control rats. It is concluded that the hepatic triacylglycerol accumulation in the threonine-deficient rats does not result from any gross abnormality in the rate of liver triacylglycerol formation or secretion to the plasma. It is suggested that a possible causative mechanism is a derangement in the metabolism of the storage pool of liver triacylglycerols.
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PMID:Metabolism of liver triacylglycerols in rats tube-fed a threonine-devoid diet. 95 47

To prove antilipemic and antiatherogenic effectiveness several animal species were given "essential" phospholipids (EPL) during different experimental procedures. The following actions were studied: 1. Effect of EPL-substance after prophylactic and therapeutic oral administration (dosage: 50, 150, 450 mg/kg bodyweight daily) in rats with acute and subacute hypelipemia induced by triton. 2. Effect of EPL-substance after prophylactic and therapeutic oral administration (dosage: 50, 150, 450, 1800 mg/kg bodyweight daily) in rats with dietetic hypercholesterolemia. 3. Effect of EPL-substance after daily oral administration (dosage: 50, 150, 450 mg/kg bodyweight) on the development of coronary and aortic atherosclerosis and various biochemical parameters in cholesterol-fed cockerels. 4. Effect of EPL-substance after dialy oral administration (dosage: 50, 150, 450 mg/kg bodyweight) on subacute triton-hyperlipemia in mini pigs. Triton-administration causes a greater or smaller increase in all parameters of the lipid metabolism measured. EPL treatment decreases these parameters during therapeutic and prophylactic administration in some cases even reaching normal values. The effect was clearly dose-dependent. EPL inhibit the increase in total lipids in dietetic hypercholesterolemia during therapeutic as well as during prophylactic administration. The effect was clearly dose-dependent in all doses, being statistically significant at the highest dosage level. In cockerels EPL were effective at all dose levels in counteracting the development of coronary atherosclerosis while the effect in atherosclerosis of aorta was less distinct. Except for non-esterified fatty acids, EPL reduced all biochemical parameters measured.
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PMID:[The anti-hyperlipemic and anti-atherogenic effect of "essential" phospholipids: a pharmacologic trial]. 103 12


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