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Results for “HYPERLIPEMIA”

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At least 127 records · Page 7Linked to original sources
PubMed1998

[Experimental study on reducing effect of shexiang baoxin pill from damage of arterial wall caused by hyperlipemia].

OBJECTIVE: To study the protecting effect of Shexiang Baoxin Pill (SXBXP) on arterial wall in hyperlipemia rabbit model. METHODS: Thirty-six male, New Zealand rabbits were randomized into three groups: control group, fed with common diet for 8 weeks: Hypercholesterolemia group (HC) and SXBXP group (SX), fed with 1% cholesterol and 3% lard diet for 8 weeks. In SX group, SXBXP was iven from 7th week for 2 weeks. The plasma levels of triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) were measured at the first, 6th and the 8th week of experiment. Serum superoxide dismutase (SOD) and electrocardiography (ECG) were also evaluated at the 8th week. Light microscopy and transmission electron microscopy were adopted to assess the degree of pathologic damage of arterial wall. RESULTS: SXBXP could reduce the levels of serum TC and LDL-C, as compared with the HC group, P < 0.05. It could also reduce the extent of atherosclerotic lesion and the severity of intimal proliferation. CONCLUSION: SXBXP has the effect of inhibiting development of experimental atherosclerosis.

Animals↗
PubMed1975

Genesis of fatty liver and hyperlipemia in the fetal guinea pig.

10 to 20% of [1-14C] palmitate injected into pregnant guinea pigs was recovered in lipids of their fetuses. From these data and the rate of transport of palmitate in maternal blood, it appears that placental transport of free fatty acids can account for the accumulation of lipids in late gestational fetuses. About 80% of the labeled palmitate in the fetus appeared initially in lipids of the liver. 14C appeared in plasma triglyceride fatty acids after a few minutes and subsequently accumulated in lipids of white and brown adipose tissue, suggesting that much of the palmitate deposited in adipose tissue were derived from hepatogenous triglyceride fatty acids. By contrast, 14C was usually maximal in heart and carcass lipids before it appeared in plasma triglyceride fatty acids. Lipoprotein lipase activity in fetal adipose tissue was low, and activity of cofactor protein of lipoprotein lipase in fetal blood plasma was much lower than that observed in other mammalian species. On the basis of these and earlier observations, it is concluded that the accumulation of triglycerides in liver and blood plasma of fetal guinea pigs during late gestation is at least partly the result of the large uptake of maternally derived free fatty acids by the fetal liver accompanied by rapid synthesis and secretion of triglyceride-rich very low density lipoproteins into the blood. However, limited uptake of triglyceride fatty acids in adipose tissue may contribute to the fatty liver and hyperlipemia.

Adipose Tissue↗
PubMedDate not supplied

[Hyperlipemia in birds induced by estrogens].

Long-term administration of diethyl stilboestrol propionate to 1-1.5 and 7-8 months old clocks induced hyperlipemia and hyperbetalipoproteidemia, a decrease in the lipolytic activity and lipoproteidlipase activity in blood. In the liver a decrease in the lipolytic activity was observed against the background of lipids accumulation. It is found that these changes do not depend on the avian age.

Aging↗
PubMed1992

[Interaction of foamy cells from experimental hyperlipemia rabbits with smooth muscle cells and the endothelial surface of intima preparation].

In the development of atherosclerosis (AS), circulating monocytes emigrate into and accumulate in the intima as foamy cells. Interaction of the lipid laden macrophage (M phi) with cells of the arterial wall may contribute to the formation of atheromatous plaque. Using subcutaneous and peritoneal foamy cells (FC) collected from diet-induced hyperlipemia rabbits, the authors observed the influence of lipid laden on macrophage's functions relevant to AS lesion formation. In comparison with normal M phi, peritoneal FC were 4.8 and 5.4 fold more adhesive to the endothelial surface of intima preparation and the smooth muscle cells (SMC), while the adhesion rate produced by subcutaneous FC were increased 0.79 and 0.16 fold. SMC migration stimulated by both FC-conditioned medium slowed 5.78 and 5.90 fold increased respectively as in comparing with the control's, whereas normal M phi-conditioned medium only gave a 2.3 fold increase of SMC migration stimulation. In addition, both FC-conditioned medium stimulated SMC growth making 1.96 and 2.59 fold increase, and normal M phi-conditioned medium produced a 1.3 fold increase as compared with the control's. The results suggest that lipid-laden macrophages, may accelerate AS development due to changes of their biological properties. Since more than 95% of peritoneal macrophages as well as macrophages in the pleura, pericardial and synovial cavities from experimental hyperlipidemia rabbits are fully filled with lipid assuming the morphologic characteristics of atheromatous intimal foamy cells, it is considered that these cells will be valuable as the model.

Animals↗
PubMed2005

[Effect of Laminaria japonica polysaccharides on lowing serum lipid and anti-atherosclerosis in hyperlipemia quails].

OBJECTIVE: To study the effect of Laminaria Japonica Polysaccharides on lowing serum lipid and anti-atherosclerosis in quails. METHODS: The hyperlipemia atherosclerosis (As) models of quails were induced by high lipids. After administration with Laminaria Japonica Polysccharides for two weeks, the content of total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL) and low density lipoprotein (LDL) in serum and the ratio of HDL/TC were determined, index of liver was calculated, the extent of aortic atherosclerosis and the atherosclerotic lesion were observed. RESULTS: The concentration of TC, TG, LDL in serum and index of liver decreased remarkedly, the ratio of HLD/TC increased remarkably, the the extent of aortic atherosclerosis and the atherosclerotic lesion lightened obviously. CONCLUSION: Laminaria Japonica Polysaccharides can effectively decrease the serum lipid and prevent the formation of atherosclerosis.

Animals↗
PubMed1991

Hyperlipemia and hyperlipoproteinemia [HLP] screening among the children from premature myocardial infarction risk families.

Serum lipids and lipoproteins were investigated in the premature myocardial infarction (PMI) risk families before 45 years of age with the aid of screening for hyperlipemia and hyperlipoproteinemia (HLP): in the case of 174 persons from Csongrád County from the Departments of Internal Medicine I and II and of 42 patients (fathers) suffering from PMI and their 79 "high risk" children from Heves County. In the investigated three groups of "high risk" children the genetically determined antiatherogenic HDL-Ch level diminished in 34.8, 52.3, 40.5 per cent. Significant negative correlation was detected between the serum HDL-Ch and beta-lipoprotein; significant positive correlations were found between the HDL-Ch and the serum lipase activity; between the beta-lipoprotein and the phospholipid level; significant negative correlation was proved between the HDL-Ch and the phospholipid level in the group of PMI patients and their offsprings. The Ch/Tg, and the HDL-Ch ratios were significantly diminished in the PMI patients' group against the risk children' group, while the Ch/HDL-Ch rate was significantly elevated.

Adolescent↗
PubMed1976

Lipid-laden aqueous humor associated with anterior uveitis and concurrent hyperlipemia in two dogs.

Two dogs with cloudy aqueous humor due to accumulation of lipid and lipoprotein had concurrent hyperlipemia and anterior uveitis. In 1 dog, serum and aqueous humor had similar lipoprotein electrophoretic patterns, and in the other dog, the patterns were different. The therapeutic approach included symptomatic treatment of the uveitis and reduction of dietary fat intake. Clearing of fat from aqueous humor followed control of the uveitis.

Animals↗
PubMed1976

[Hyperlipemia: practical attitudes].

Serum cholesterol and triglyceride levels may vary widely in a given patient, and therefore both of these lipid determinations should be repeated for initial evaluation. Later, the response of lipid values to diet and to drugs provides more information on the individual characteristics of a hyperlipoproteinemia than "typing" from one lipid evaluation. The type may actually change with lipid levels, whereas the basic tendencies to increased betalipoproteins (evaluated as cholesteremia) or prebetalipoproteins (evaluated as triglycerides) are more constant features in a patient. Alimentary conditions in most cases influence hyperlipemias, whether primary or secondary. Total caloric intake is a major factor in inducing augmented triglycerides in predisposed people. Hypertriglyceridemia is rare before 20 and not frequent in women. On the other hand, familial hypercholesteremia is present from the first weeks of life. Diet is of little help in these cases. When hypercholesteremia is related to food habits it usually appears after the third decade. The amount of fats rich in saturated fatty acids appears to be the chief causative factor in this regard. However, it is possible that genetic factors also affect the degree of alimentary influence on cholesterol level over many years. The use of hypolipemic drugs does not obviate the need for appropriate diet. If the prevention of early coronary disease is to be successful it should start in young people before the first clinical symptoms appear.

Cholesterol↗
PubMed1990

Postprandial hyperlipemia and platelet eicosanoid metabolism.

Platelet aggregations stimulated with different concentrations of collagen or ADP were reduced during postprandial hyperlipemia in normolipemic subjects. The concomitant formation of platelet AA metabolites (TXB2, 12-HHT, 12-HETE), however, was not significantly altered.

Adult↗
PubMedDate not supplied

[The induced hyperlipemia test. 10 years of experience].

The induced hyperlipemia test, which is easly to administer, yields very interesting information for the study of lipidic metabolism in arteriosclerosis patients. Its use, in both the pre- and post-operative phases, has brought out the valuable effect of ligature of the intestinal lymphatics in treating arteritis. It may also enable us to determine whether there is a hereditary factor or family predisposition to arteriosclerosis. Furthermore, the test makes it possible to confirm diagnosis of obstruction of the lymphatics of the gut in exsudative enteropathy and in various dysfunctious of the chyliferous vessels (sclerosis, rupture, tumoral invasion) without to resort to the use of radioactive substances.

Adult↗
PubMed1979

Effect of intravenous injection of CDP-choline, S-adenosyl-methionine and citiolone in subjects with hyperlipemia.

The effect of some drugs (CDP-choline, S-adenosyl-methionine and acetyl-homocysteinethiolactone) stimulating a number of liver enzymatic activities was studied in hyperlipemic patients to explore the role of liver function in hyperlipidemia. Recently a close connection between liver impairment and hyperlipemia has been observed. Twenty-eight, 13 and 10 hyperlipemic subjects received i.v. doses respectively, of CDP-choline (300 mg), S-adenosyl-methionine (SAMe) (45 mg) and citiolone (300 mg) in 100 ml saline solution during a 30 minute period. Plasma lipid fractions were evaluated basally and at the end of the injection. CDP-choline caused a significant decrease in plasma total lipids (p less than 0.001), cholesterol (p less than 0.01) and triglycerides (p less than 0.01) as well as a slight increase in beta - LP (p less than 0.05). SAMe injection was followed by a significant fall in plasma total lipids (p less than 0.05), cholesterol (p less than 0.001) and beta - LP+pre-beta LP/alpha - LP ratio (p less than 0.05), while alpha -LP increased significantly (p less than 0.05). Citiolone caused only a decrease in plasma cholesterol values (p less than 0.001). The data suggest that the hypolipidemic effect of the three compounds is due to a common mode of action, i.e., the stimulation of hepatic phospholipid biosynthesis, though in a different way.

Adult↗
PubMed1971

Mechanism of fatty liver development and hyperlipemia in rats treated with allylisopropylacetamide.

Treatment of rats with allylisopropylacetamide results in two related effects that occur sequentially. After one injection, serum FFA concentration increases and fatty liver develops without any decrease in lipoprotein synthesis. With repeated administration of the drug, fatty acid mobilization continues and acetate incorporation into lipids increases. However, fatty liver disappears with a concomitant increase in lipoprotein synthesis, resulting in hyperlipemia. It is postulated that accumulation of the liver lipid might be a regulating factor in the synthesis and transport of lipoproteins.

Acetates↗
PubMed1983

[Effect of trapidil on experimental hyperlipemia and atherosclerosis induced by cholesterol diet in SPF Japanese white rabbits].

The effect of trapidil on experimental hyperlipemia and atherosclerosis induced by 1% cholesterol diet in SPF male rabbits (JW/KBL) was investigated by the determination of the lipid contents of the plasma and thoracic aorta and examination of morphological changes in the aorta. Trapidil inhibited the increase of total lipid (TL), total cholesterol (TC), free cholesterol (FC) and phospholipid (PL) by the cholesterol diet in all groups. The level of cholesterol (HDL-C) and phospholipid (HDL-PL) in high density lipoprotein (HDL) remained unchanged after the cholesterol diet and trapidil administration. The atherogenic index (TC-HDL-C/HDL-C, PL-HDL-PL/HDL-PL) was improved by the inhibition of TC and PL by the administration of trapidil. A morphological study of the aorta showed that trapidil inhibited lipid deposition. A microscopic observation of the intima by Sudan III stain showed that inhibition of lipid deposition corresponded with the quantity of trapidil administration. An observation of aorta using transmission electron microscopy (TEM) showed that trapidil inhibited the presence of form cells due to HCD. This inhibition corresponded with the quantity of trapidil administration; and no form cells were seen in the 50 mg/kg-administered group. An observation of intima using scanning electron microscopy (SEM) showed that trapidil inhibited the irregularly elevated regions by HCD. The structure of intima in the 50 mg/kg-administered group was similar to that of the control groups. The observation of the head angiogram showed that trapidil improved the stenosis in the lingual and temporal arteries which was caused by HCD.

Animals↗
PubMed1984

Influence of diet composition on obesity, hyperlipemia and liver steatosis in Zucker fa/fa rats pair-fed with Zucker Fa/- rats.

The effect of a four-week experiment on ten fa/fa Zucker rats (aged seven weeks at the beginning) fed on a lipid-rich diet (HL: 31 per cent w/w lipids, 45.6 per cent starch) was compared to that of a control diet (C: 10 per cent lipids, 66 per cent starch) on control Fa/- rats using a special pair-feeding apparatus that made it possible to obtain an identical intake rhythm. Energy level of the intake was significantly higher for the HL diet than for the C diet. At the end of the experiment, fa/fa rats remained obese and hyperlipemic, and still showed liver steatosis. With equal energy levels ingested, the obesity of fa/fa rats was comparable for both diets; hypertriglyceridemia and hypercholesterolemia were identical for both diets. When compared to the C diet, the HL diet modified neither their obesity nor their hyperlipemia. Obese rat liver on the HL diet showed lower levels for triacylglycerols, cholesterol, GGT, ALT, LDH and aldolase activities, while hepatic glycerol kinase and AST activities were higher than and comparable to, respectively, the C diet. Thus the HL diet led to a decreased liver steatosis for fa/fa rats as compared to the C diet.

Animals↗
PubMed1983

Post-heparin plasma hepatic triglyceride lipase and monoglyceride hydrolase activities in hyperlipemia induced by a sucrose rich diet.

We have previously reported that normal Wistar rats fed an isocaloric, sucrose-rich (63%) diet (SRD) developed glucose intolerance and elevated triglyceride levels in plasma as well as in heart and liver tissue. This metabolic state was accompanied by hyperinsulinism both in vivo and in vitro, suggesting that a state of insulin resistance has developed. The aim of this study was to gather information on the various plasma post-heparin lipolytic activities in rats fed a SRD. Hepatic triglyceride lipase (H-TGL) was evaluated by both, protamine sulfate inhibition (PSI) of extrahepatic lipoprotein lipase (LPL) and heparin-Sepharose affinity chromatography (H-SAC). Both methods rendered comparable results. Total triglyceride lipase (T-TGL) was measured after Krauss et al. and monoglyceride hydrolase (MGH) after Vogel et al. Our results have shown a significant decline of plasma T-TGL (5.32 +/- 0.34 means +/- SEM vs. 7.48 +/- 0.64 mumol glycerol ml-1 h-1; p less than 0.01), H-TGL (3.71 +/- 0.28 vs. 5.05 +/- 0.69; p less than 0.05), LPL (1.61 +/- 0.26 vs. 2.42 +/- 0.41; p less than 0.05) and MGH (558 +/- 108 mumol glycerol l-1 min-1 vs. 1,165 +/- 45; p less than 0.001) activities. Thus, feeding a sucrose-rich diet induced a state of hyperlipemia and insulin resistance in which not only plasma T-TGL but also H-TGL and MGH activities were significantly decreased. This suggests that the latter two enzymes are also under nutritional and/or hormonal control.

Animals↗
PubMed1980

An experimental model of hyperlipemia.

Rats were given two kinds of diet: fat-rich (coconut oil, cholesterol, cholic acid) and fat-carbohydrate diet (coconut oil, margarine, cholesterol, wheat flour) for a period of 18 weeks. In the blood serum the triglyceride-cholesterol level and the electrophoretic pattern of lipoproteins were determined. Experimental models of experimental hyperlipemia adequate to type IIb and IV according to Fredrickson were obtained.

Animals↗
PubMed1980

Decreased oxygenation and hyperlipemia during intravenous fat infusions in premature infants.

Eighteen appropriate-for-gestational-age premature infants with birth weights ranging from 0.77 to 1.89 kg received 1 gm/kg of body weight of fat emulsion, intravenously, over a four-hour period. Infants less than 1 week of age developed a significant decrease in PO2 levels (P < 5.0) during the fat infusion period. There were no changes in other pulmonary function parameters. Infants less than 1 week of age also developed significantly higher peak levels of plasma triglycerides than infants 2 to 3 weeks old (P < .05). A correlation between increment in triglyceride levels and postnatal age was demonstrated (r = .75), with the younger infants presenting the higher triglyceride levels. This study demonstrates that: (1) small premature infants receiving intravenous fat are more susceptible to hyperlipemia and hypoxemia during the first week of life; (2) hypoxemia associated with intravenous fat infusion does not result from changes in lung dynamics; (3) the capacity to tolerate intravenous fats is enhanced after the first week of life.

Age Factors↗