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

Sodium dodecylsulphate precipitates very low density lipoproteins (VLDL and chylomicrons) rich in triglyceride and a narrow correlation (r = 0.9) was found between the turbidimetric index SDS and triglyceridemia. Heparin in calcium medium acts in the same way and precipitates also low density lipoproteins (LDL) rich in cholesterol. A correlation (r = 0.875) was drawn up between the cholesterol LDL and the difference between the turbidimetric indices (heparin Ca -- SDS). In the first case, we were thus measuring by turbidimetry a VLDL + chylomicron index and, in the second case, an LDL index which permits one to obtain simplified typing of the hyperlipoproteinemias. A nomogram linking the two indices of hyperlipoproteinemia type was drawn up experimentally. This orientation analysis may be completed by electrophoresis on polyacrylamide gel used in concentration gradient and pH. In the system proposed, the lipoproteins were previously stained with tetrazolium nitroblue and clearly shown up. The chylomicrons in particular, become separated from the VLDL, the sinking pre-beta-lipoprotein or Lp (a) was identifiable and the type III hyperlipemia was easily diagnosed.
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PMID:[Analysis of lipoproteins using polyacrylamide gel electrophoresis and fractionated precipitation with polyanions and detergents. Use in the classification of hyperlipoproteinemias]. 18 41

One unit (500 ml) of 10% Intralipid (an intravenous soy bean oil-egg yolk lecithin preparation) was infused into 20 normal subjects over 4 hr. Serum triglyceride concentration and plasma optic density (at 700 nm) increased to maximal levels of 339 +/- 102 mg/100 ml and 1.14 +/- 0.41, respectively, at the completion of the infusion, and returned to basal levels in most subjects within 4 hr. Pulmonary membrane diffusion was decreased in six subjects at rest and with exercise at 25 and 50% maximum oxygen uptake. Only one subject showed a minor change in PO2 and none showed clinical signs of ischemia. The changes in pulmonary diffusion reverted to basal levels when serum lipids were cleared. Heparin (60 IU/kg) prevented the marked increase in serum lipids and, as a consequence, the changes in pulmonary function. Changes in pulmonary function from Intralipid-induced lipemia are similar to those known to result from diet-induced lipemia. The findings suggest that in the presence of normal vasculature and pulmonary function, Intralipid-induced lipemia should cause no clinical consequences. However, patients with preexisting pulmonary or vascular disease may be at greater risk after Intralipid-induced lipemia.
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PMID:Relationship between Intralipid-induced hyperlipemia and pulmonary function. 81 3

We showed previously that net secretory output of apolipoprotein B (apo B) from cultured human hepatoma cells (HepG2) is regulated by rapid reuptake of nascent lipoproteins before they have diffused away from the vicinity of the cells. We now sought to determine if the nascent lipoproteins could be remodeled to enhance or impede reuptake. We found that lipoprotein lipase (LpL), an enzyme that hydrolyzes lipoprotein triglyceride, reduced HepG2 output of apo B to one-quarter to one-half of control. The reduction was apparent during co-incubations as short as 2 h and as long as 24 h. Heparin, which blocks receptor-mediated binding of lipoproteins, abolished the effect of LpL on apo B output, without causing enzyme inhibition. To assess uptake directly, we prepared labeled nascent lipoproteins. LpL tripled the cellular uptake of labeled nascent lipoproteins, from 15.2% +/- 0.7% to 48.7% +/- 0.3% of the total applied to the cells. Cellular uptake of 125I-labeled anti-LDL receptor IgG was unaffected by LpL; thus, LpL enhanced reuptake by altering lipoproteins, not receptors. Because LpL is present in the space of Disse in the liver, we conclude that LpL may act on newly secreted lipoproteins to enhance reuptake in vivo. LpL deficiency would reduce local reuptake of apo B, which would appear as overproduction, thereby providing a mechanistic link between partial LpL deficiency and familial combined hyperlipidemia.
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PMID:Lipoprotein lipase modulates net secretory output of apolipoprotein B in vitro. A possible pathophysiologic explanation for familial combined hyperlipidemia. 191 80

Approximately 70% of the W/WV mice lacking mast cells due to a genetic defect showed hypertriglyceridemia combined with hypercholesterolemia. Increases of various magnitudes in chylomicrons, very-low-density lipoprotein, and intermediate-density lipoprotein were observed in the plasma of W/WV mice compared to those in the plasma of congenic normal mice. The increase in these lipoproteins was seen even in normolipidemic W/WV mice. Activities of both lipoprotein lipase and hepatic triacylglycerol lipase in the plasma after heparin injection were markedly lower in the W/WV mice than in the congenic normal mice, although activities of both lipoprotein lipase in the heart and adipose tissue and hepatic triacylglycerol lipase in the liver were not decreased. These results suggest that the W/WV mice have genetic defects in one or more of the following: secretion of both lipases from their synthesising cells, transport to the endothelium, and anchoring to the endothelial surface. Heparin deficiency in these mice may be responsible for the impairment and, thereby, may partially contribute to the hyperlipidemia.
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PMID:Hyperlipidemia in mast cell-deficient W/WV mice. 375 4

Combined lipase deficiency (cld/cld) is a recessive mutation in mice which results in massive hyperlipemia and death within 3 days after birth. We studied the effect of this deficiency on lipolytic activities in liver and in pre- and postheparin plasma of mice less than 2 days old. Anti-hepatic lipase serum inhibited more than 85% of the lipolytic activity in liver and plasma of normal newborn mice when assayed in high-salt medium, validating the use of this medium for measuring hepatic lipase activity in mice. Anti-lipoprotein lipase serum, in contrast, inhibited only two-thirds of the lipolytic activity in liver and plasma when assayed in serum low-salt medium, and anti-hepatic lipase serum inhibited the rest. This indicates that assay with serum low-salt medium alone is not specific for lipoprotein lipase activity in mice. Therefore, immunoinhibition was used, as needed, for measuring lipoprotein lipase activity. The livers of unaffected newborn mice contained high levels of both hepatic and lipoprotein lipase activities, 228 and 187 mU/g, respectively. The plasma of unaffected mice contained a high level of hepatic lipase activity, 244 mU/ml, but practically no lipoprotein lipase activity. Heparin injected intraperitoneally increased plasma lipoprotein lipase activity to 152 mU/ml, but had no effect on plasma hepatic lipase activity, in unaffected mice. Hepatic lipase activity was virtually absent from both liver and plasma of cld/cld mice. Lipoprotein lipase activity was present in the liver at a surprisingly high level, 40% of that in normals, but was barely detectable in plasma. Heparin injection increased plasma lipoprotein lipase activity in cld/cld mice, but the increment was less than 10% of that in unaffected mice. Heparin had no significant effect on plasma hepatic lipase activity in defective mice. These findings confirm preliminary observations that hepatic lipase activity in liver and plasma and lipoprotein lipase activity in plasma are markedly reduced in combined lipase deficiency. The unexpected high level of lipoprotein lipase activity in liver of cld/cld mice suggests that regulation of lipoprotein lipase activity in liver of neonatal mice is different from that in other tissues.
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PMID:Effect of combined lipase deficiency (cld/cld) on hepatic and lipoprotein lipase activities in liver and plasma of newborn mice. 395 63

Rats treated chronically with the anticancer agent adriamycin (1.5 mg/kg/week X 14 weeks) exhibited cardiac and renal lesions typical of anthracycline toxicity, and had serum hyperlipidemia characterized by 4 to 10 fold elevations in all lipoprotein classes. Heparin-releasable lipoprotein lipase activity measured in perfused heart preparations was decreased 69% in adriamycin-treated rats compared to saline-treated controls. Residual (non-heparin-releasable) activity was not significantly different after adriamycin treatment. The decrease in functional cardiac lipoprotein lipase may account, at least in part, for the serum hyperlipidemia observed in adriamycin-treated rats, and might play a role in the development of heart muscle disease.
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PMID:Decreased cardiac lipoprotein lipase activity in rats treated chronically with adriamycin. 396 80

Severe toxemia of pregnancy is associated with hypercoagulability and hyperlipemia in general. Heparin, a substance having an anticoagulant action and a lipemia-clearing action, was used clinically, and the changes induced by the heparin administration were examined. The GI value was significantly improved. The body weight showed a tendency to decrease. Fibrinogen tended to be decreased. The urine volume was significantly increased. Histologic observations on the placenta gave the impression that fibrin deposition in the placental tissue had been decreased by heparin.
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PMID:Effect of heparin treatment in cases of severe toxemia. 665 69

This article reviews the experimental and clinical evidence regarding heparin therapy in the prophylaxis of coronary heart disease. The actions of heparin take place at the vascular endothelium where injected heparin concentrates, and within the bloodstream. At the endothelium heparin acts to prevent endothelial injury, prevent thrombin generation, prevent platelet adhesion to endothelium, and to decrease uptake of serum lipoproteins. Within the bloodstream heparin increases lipoprotein lipase activity and reduces the concentration of atherogenic very low-density lipoproteins. The reduction in lipemia enhances oxygen transfer from blood to the tissues, and decreases thrombin or ADP-induced platelet aggregation. Heparin increases the concentration of high-density lipoproteins. It decreases hypercoagulability and inhibits overactivation of serum complement. Heparin reduced atherosclerosis in most studies in cholesterol-fed animals. In human subjects who had a myocardial infarct at least one year before the onset of treatment, long-term intermittent heparin therapy significantly decreased cardiovascular deaths as compared to control groups.
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PMID:Heparin and atherosclerosis. A review of old and recent findings. 698 41

Patients with diabetic nephropathy frequently show increased levels of circulating low-density lipoprotein (LDL) and oxidized LDL, which have been reported to be related to the generation of oxygen-free radicals. In the present study, we evaluated the effects of insulin and heparin on the superoxide production of glomeruli, which were isolated from rats with streptozotocin-induced diabetes for one week, one month, and three months, respectively, and the glomeruli were stimulated with native and oxidized LDL. LDL was isolated from normal subjects with normolipidemia, and the superoxide was measured by using a spectrophotometer. The results demonstrated that the poorly controlled diabetic rat glomeruli showed a significantly higher production of superoxide than normal glomeruli under basal status and after stimulation, and this production increased further with the progression of diabetes. Insulin suppressed both the basal and stimulated production of superoxide in diabetic glomeruli, but not in normal glomeruli. Heparin suppressed superoxide production of diabetic glomeruli stimulated by either native or oxidized LDL, and it also partly suppressed superoxide production of normal glomeruli stimulated by oxidized LDL. Our results suggest that glomerular injury in diabetics with hyperlipidemia may be mediated through enhanced generation of oxygen-free radicals, which can be partially attenuated by insulin and heparin.
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PMID:Insulin and heparin suppress superoxide production in diabetic rat glomeruli stimulated with low-density lipoprotein. 1116 97

The effect of lipemia on peripheral blood flow was studied in patients with and without peripheral vascular disease. Blood flow was measured by venous occlusion plethysmography in the calf and/or finger four to six hours after a fatty meal and after intravenous heparin. The abolition of postprandial lipemia by heparin was determined by measuring the plasma lactescence.Heparin resulted in no change in finger flow of either group or in calf flow in the control group. In nine out of 10 patients with occlusive vascular disease of the legs, it resulted in a small but significant increase of calf blood flow. No such alteration was found when heparin was given following a non-fatty meal.In 12 patients with intermittent claudication the clearing of postprandial lipemia by heparin caused prolongation of claudication time, as measured by the appearance of pain on treadmill exercise.It is concluded that, in some cases, postprandial lipemia is associated with a decrease in blood flow in a limb which is already the site of occlusive vascular disease.
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PMID:THE EFFECT OF LIPEMIA ON PERIPHERAL BLOOD FLOW. 1414 62


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