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

Lipoprotein lipase (LPL) activity in postheparin plasma of 38 normolipidemic volunteers was related to the magnitude of postprandial lipemia after a fat meal, to triglyceride content of high density lipoprotein2 (HDL2), to hepatic lipase (HL) activity, and to HDL2 levels. LPL activity correlated indirectly with lipemia, triglyceride content of HDL2, HL activity, and levels of HDL2 but not of HDL3. HL activity correlated directly with lipemia and indirectly with HDL2 levels. Triglyceride content of HDL2 correlated directly with lipemia and indirectly with HDL2 levels. In HDL2, abundance of apolipoprotein (apo) A-II and the apoA-I/apoA-II ratio varied widely. The latter correlated positively with LPL activity and HDL2 levels, and, inversely, with HL activity, lipemia, and triglyceride content of HDL2. The study suggests that HDL-cholesterol is not an independent parameter of lipid transport, but is strongly affected by triglyceride metabolism through lipolytic enzymes, as exemplified by postprandial lipemia that affect both composition and plasma levels of HDL2.
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PMID:High density lipoprotein2. Relationship of the plasma levels of this lipoprotein species to its composition, to the magnitude of postprandial lipemia, and to the activities of lipoprotein lipase and hepatic lipase. 361 51

A 61-year-old woman was treated with tamoxifen for breast cancer and had marked hyperlipoproteinemia: high plasma triglyceride levels (2790 mg/dl); increased very low density lipoprotein (VLDL) cholesterol levels (241 mg/dl); and high VLDL apoprotein B levels (126 mg/dl). Low density lipoprotein (LDL) cholesterol was decreased (104 mg/dl) and LDL apoprotein B was at 107 mg/dl. A low activity of both postheparin plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (h-TGL) was also noted. All these observations were reversed following tamoxifen withdrawal. Plasma triglyceride levels fell to 361 mg/dl. VLDL cholesterol and VLDL apoprotein B decreased to 41 mg/dl (83%) and 21 mg/dl (83%), respectively. Meanwhile, LDL cholesterol rose to 194 mg/dl (86%) and LDL apoprotein B increased to 138 mg/dl (29%). LPL and h-TGL activities did increase following tamoxifen withdrawal. Our observations show that, in some patients, the previously described weak hypertriglyceridemic effect of tamoxifen is amplified. That observation supports the concept and helps to explain that, in such severe induced lipemia, reduction of the activities of LPL and h-TGL might impede the conversion of VLDL to LDL, thus causing an amplification of the effect.
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PMID:Severe lipemia induced by tamoxifen. 369 11

The main lipoprotein density classes, namely very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3 were investigated with respect to their influence on hepatic lipase (HTGL) activity in vitro. Lipoproteins from pooled normal plasma (NP) and from pooled hyperlipemic plasma (HP) were prepared by means of sequential ultracentrifugation. Hepatic lipase was determined radioenzymatically after preincubation with protamine sulfate. It could be demonstrated that IDL from HP were able to stimulate HTGL activity by approximately 100% above the baseline value. HDL3 from both NP and HP revealed an inhibiting effect on HTGL activity. VLDL, LDL, and HDL2 exhibited no significant effect on HTGL activity. It is speculated that HTGL could possibly represent a second pathophysiological pathway for the catabolism of IDL in hyperlipemia but this presumption is supported by only a few investigations in vivo.
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PMID:Stimulating effect of intermediate-density lipoproteins (IDL) from hyperlipemic plasma on hepatic lipase. 372

Several parameters of lipoprotein metabolism were examined in 38 men with primary hypertriglyceridemia (phenotype IV). Family investigation showed that 17 men had familial combined hyperlipidemia (FCH), seven had familial hypertriglyceridemia (FHT), and 14 had unclassified hypertriglyceridemia (UNC). In all three groups, plasma high density lipoprotein (HDL) cholesterol and the concentrations of apolipoprotein A-I and A-II were decreased, and apolipoprotein B was increased, each to the same extent. These results are compatible with an increased risk of cardiovascular disease in both FCH and FHT patients. The mean concentration of LDL cholesterol and the ratio of LDL to HDL cholesterol were significantly higher in FCH subjects, which could explain their increased risk. Postheparin lipoprotein lipase and hepatic lipase were the same in both groups. Determination of apolipoprotein C composition, which may modulate lipoprotein lipase activity, did not reveal any abnormalities in the different groups. In both FCH and FHT, the mean turnover rate of plasma triglycerides was almost twice normal, indicating that overproduction of plasma triglyceride plays an important role in both disorders. However, there was an overlap with normal controls, indicating impaired triglyceride removal in some subjects. The underlying mechanism of hypertriglyceridemia in FCH and FHT therefore seems to be heterogeneous.
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PMID:Plasma lipoproteins, apolipoproteins, and triglyceride metabolism in familial hypertriglyceridemia. 372 96

Lipoprotein lipase and hepatic lipase activities are very low in tissues of mice born with genetic combined lipase deficiency (cld/cld). Consequently, if allowed to suckle, the mice develop severe hyperlipemia and die within 3 days. The ultrastructure of capillaries and parenchymal cells in tissues that normally contain lipoprotein lipase and hepatic lipase was studied in tissues from cld/cld and unaffected mice 6 to 24 hours of age. Capillaries in tissues from suckled cld/cld mice were packed with numerous abnormally shaped chylomicrons. There was close contact between surfaces of chylomicrons and the luminal plasma membrane of endothelium. Chylomicrons were sometimes found between endothelial cells and in the subendothelial space in heart, lung, and liver, and in the lumen of lung alveoli. In contrast, capillaries of suckled unaffected mice contained very few chylomicrons, and the subendothelial spaces and lung alveoli were free of chylomicrons. Myocytes of diaphragm and heart from suckled cld/cld mice did not contain lipid droplets, whereas brown adipocytes contained a few small droplets. Parenchymal cells in diaphragm, heart, brown adipose tissue, and lung from suckled unaffected mice contained numerous large lipid droplets. Hepatocytes of suckled cld/cld mice contained small irregularly shaped lipoprotein particles (100 A) in endoplasmic reticulum and Golgi, numerous large lysosomes containing small lipoprotein particles, lipid spheres and lamellar structures, and no intracellular lipid droplets, whereas hepatocytes of suckled unaffected mice contained larger lipoprotein particles (400 A), large lipid droplets, and very few lysosomes. Triacylglycerol of chylomicrons from cld/cld mice was readily hydrolyzed by bovine lipoprotein lipase in vitro, and this effect was not augmented by heat-inactivated serum, indicating that the chylomicrons contained adequate amounts of apoprotein C-II. Thus, the large amount of chylomicrons in capillaries and small amount of lipid droplets in cells of suckled cld/cld mice reflect the very low level of lipoprotein lipase activity in these animals. The findings in hepatocytes indicate that lipoprotein metabolism in liver is markedly disturbed in cld/cld mice.
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PMID:Effect of the combined lipase deficiency mutation (cld/cld) on ultrastructure of tissues in mice. Diaphragm, heart, brown adipose tissue, lung, and liver. 374 49

With a view to elucidating the physiologic role of hepatic triglyceride lipase (H-TGL), we studied the relationship between the activity of H-TGL and the concentrations of the lipids of ultracentrifugally separated lipoprotein fractions in sera from 81 cases of primary hyperlipidemia, 5 of hypothyroidism, and 31 normal subjects. The activity of H-TGL in postheparin plasma was determined by the sensitive, nonradioisotopic method that was recently developed by us. In the entire group of subjects including the normals, the activity of H-TGL had a significant inverse correlation with the concentration of the cholesterol (r = -0.443, P less than 0.001) and phospholipid (r = -0.433, P less than 0.001) of intermediate density lipoprotein (IDL). When the patients were divided into subgroups according to the phenotype of hyperlipidemia, it was found that the correlation was more significant in type IIb (r = 0.695, P less than 0.001) or type IV + V (r = -0.664, P less than 0.0001). In the five cases of hypothyroidism, the mean IDL cholesterol level was high (28.3 +/- 12.3 mg/dL) and the H-TGL activity was very low (4.6 +/- 4.5 mumol/h/mL). The H-TGL activity was also significantly correlated with the ratio of high density lipoprotein-2 to high density lipoprotein-3 cholesterol (r = 0.351, P less than 0.001) in the entire group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of hepatic triglyceride lipase in the metabolism of intermediate-density lipoprotein--postheparin lipolytic activities determined by a sensitive, nonradioisotopic method in hyperlipidemic patients and normals. 394 9

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

Because of the high incidence for development of a secondary hyperlipemia during chronic alcohol intake, this study was performed to look for a possible reason, why some patients produce severe hyperlipemia and other ones not. 15 male patients with chronic alcoholism (group I) who produce under influence of alcohol a secondary type-V hyperlipoproteinemia (type-V HLP) were compared with 15 male controls. Additionally, 8 male patients with chronic alcoholism (group II) who were normolipemic under alcohol abuse, and 7 male patients (group II) who had also produced type-V HLP under chronic alcohol abuse, but were teetotal since at least 6 months, were investigated. In comparison with controls, patients of group I showed significantly (p less than 0.01) increased plasma concentrations of very low-density lipoproteins (VLDL) and significantly decreased plasma concentrations of low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3 (all p less than 0.01). Furthermore, the activities of postheparin lipoprotein lipase (LPL) and hepatic lipase (HTGL) were significantly decreased (both p less than 0.01). In patients of group III, the plasma concentrations of lipoproteins did not differ significantly from controls, but the activity of LPL was also significantly impaired (p less than 0.01), whereas the activity of HTGL was distinctly (p less than 0.01) increased. No significant difference between patients of group II and controls could be demonstrated. It is concluded that severe alcohol intake strongly impairs LPL in patients with chronic alcoholism. The pronounced increase of HTGL in patients of group III seems to protect these individuals from producing severe hyperlipemia under the influence of alcohol.
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PMID:[Lipoproteins, post-heparin lipoprotein lipase and hepatic triglyceride lipase in patients with and without severe hyperlipemia caused by alcoholism]. 401 22

Lipoprotein lipase and hepatic lipase were measured in rat plasma using specific antisera. Mean values for lipoprotein lipase in adult rats were 1.8-3.6 mU/ml, depending on sex and nutritional state. Values for hepatic lipase were about three times higher. Lipoprotein lipase activity in plasma of newborn rats was 2-4-times higher than in adults. In contrast, hepatic lipase activity was lower in newborn than in adult rats. Following functional hepatectomy there was a progressive increase in lipoprotein lipase activity in plasma, indicating that transport of the enzyme from peripheral tissues to the liver normally takes place. Lipoprotein lipase, but not hepatic lipase, increased in plasma after a fat meal. An even more marked increase, up to 30 mU/ml, was seen after intravenous injection of Intralipid. Plasma lipase activity decreased in parallel with clearing of the injected triacylglycerol. 125I-labeled lipoprotein lipase injected intravenously during the hyperlipemia disappeared somewhat slower from the circulation than in fasted rats, but the uptake was still primarily in the liver. Hyperlipemia, or injection of heparin, led to increased lipoprotein lipase activity in the liver. This was seen even when the animals had been pretreated with cycloheximide to inhibit synthesis of new enzyme protein. These results suggest that during hypertriglyceridemia lipoprotein lipase binds to circulating lipoproteins/lipid droplets which results in increased plasma levels of the enzyme and increased transport to the liver.
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PMID:Distribution of lipoprotein lipase and hepatic lipase between plasma and tissues: effect of hypertriglyceridemia. 406 80

Five patients with hypopituitarism due to Sheehan's syndrome showed hyperlipidaemia of various lipoprotein phenotypes. Postheparin plasma lipoprotein lipase activity was subnormal in 4 of the 5 patients and hepatic triglyceride lipase was markedly decreased in all patients studied. After supplementation of both corticosteroid and thyroid hormones, lipoprotein lipase activity was restored to normal within 2 months, while it took longer for hepatic triglyceride lipase to return to normal. Together with the normalization of the two lipase activities, hyperlipidaemia subsided. The findings suggest that reduced activities of the two lipases may, at least in part, account for the development of hyperlipidaemia in hypopituitarism. The study identifies a new group of patients with hyperlipidaemia secondary to a disorder in endocrine function.
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PMID:Hyperlipidaemia in patients with hypopituitarism. 409 Sep 8


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