Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of radioimmunoassays for measuring human apolipoprotein B (apo B), the A apolipoproteins of high density lipoprotein (apo A-I and apo A-II) and apolipoprotein C-II (apo C-II) in human plasma and in isolated lipoproteins is presented. The sensitivity, specificity and validity of each of these assays is discussed. In normolipidemic subjects the reported serum apo B concentrations ranged between 0.83 +/- 0.16 and 0.92 +/- 0.21 g per l (m +/- SD). Serum apo B concentrations were highest in Type II subjects (Type IIa homozygotes 3.83 +/- 0.43 g per l; Type IIa heterozygotes 2.37 +/- 0.47 g per l) and were less elevated in patients with Type IV and Type V disorders (1.32 +/- 0.21 g per l and 1.26 +/- 0.30 g per l, respectively). Preliminary data on the relationship between plasma apo B and cholesterol, the distribution of apo B amongst the lipoprotein classes and a comparison of the lipoprotein lipid-apo B ratios in the various hyperlipidemic disorders are summarized. In contrast to apo A-II, the immunoreactivity of apo A-I was not fully exposed in whole sera and in isolated lipoproteins. The different methods used to measure the apo A-I immunoreactivity are discussed. In normolipidemic subjects the serum apo A-I concentration in males and females was 1.13 +/- 0.061 and 1.24 +/- 0.068 g per l (m +/- SD), respectively, while the corresponding serum apo A-II values were 0.35 +/- 0.038 g per l and 0.41 +/- 0.046 g per l. In subjects with Tangier's disease, the serum apo A-I and apo A-II concentrations were less than 1 percent and 5 to 7 percent of that found in controls. The serum apo A-I level was also reduced in two subjects with abetalipoproteinemia (0.38 g per l and 0.30 g per l) and Tye II hyperlipoproteinemia (range 0.54 to 0.86 g per l). In normotriglyceridemic subjects and those with Type IIa hyperlipoproteinemia, the total plasma apo C-II concentrations were 0.0497 +/- 0.0040 g per l and 0.0562 +/- 0.0054 g per l (m +/- SE). Plasma apo C-II levels in Type IIb, Type IV and Type V lipoproteinemic subjects were 0.0899 +/- 0.0046, 0.0854 +/- 0.0069 and 0.1328 +/- 0.0021 g per l, respectively and were significantly higher than in the normotriglyceridemic subjects. An analysis of the relationship between the apo C-II content and the lipoprotein lipase activator properties of VLDL isolated from normo- and hypertriglyceridemic plasma samples is presented.
...
PMID:Recent progress in the development of radioimmunoassays for human serum lipoproteins. 20 63

Some properties of very low density lipoproteins were studied under conditions causing an increase of their concentration in blood plasma. Content of high molecular apolipoprotein B and low molecular lipoproteins were estimated after fractionation using column chromatography and selective precipitation with tetramethylurea. In 216 men (40-59 years old) with hypertriglyceridemia the increase in content of particles of very low density lipoproteins was accompanied by simultaneous alteration in their composition in blood plasma: content of low molecular polypeptides, triglycerides and cholesterol was increased per a weight unit of apoprotein B. At the same time, the absolute concent of apoprotein B and of low molecular apoproteins of very low density lipoproteins was increased in blood plasma. The most distinct alteration in the ratio of apolipoproteins to very low density lipoproteins was observed, if content of testosterone--activator of lipoprotein lipase--was decreased in blood plasma.
...
PMID:[Change in the apoproteins of very low density lipoproteins in the blood in hypertriglyceridemia]. 22 Aug 3

We sought to investigate effects of lipoprotein lipase (LpL) on cellular catabolism of lipoproteins rich in apolipoprotein B-100. LpL increased cellular degradation of lipoprotein(a) (Lp(a)) and low density lipoprotein (LDL) by 277% +/- 3.8% and 32.5% +/- 4.1%, respectively, and cell association by 509% +/- 8.7% and 83.9% +/- 4.0%. The enhanced degradation was entirely lysosomal. Enhanced degradation of Lp(a) had at least two components, one LDL receptor-dependent and unaffected by heparitinase digestion of the cells, and the other LDL receptor-independent and heparitinase-sensitive. The effect of LpL on LDL degradation was entirely LDL receptor-independent, heparitinase-sensitive, and essentially absent from mutant Chinese hamster ovary cells that lack cell surface heparan sulfate proteoglycans. Enhanced cell association of Lp(a) and LDL was largely LDL receptor-independent and heparitinase-sensitive. The ability of LpL to reduce net secretion of apolipoprotein B-100 by HepG2 cells by enhancing cellular reuptake of nascent lipoproteins was also LDL receptor-independent and heparitinase-sensitive. None of these effects on Lp(a), LDL, or nascent lipoproteins required LpL enzymatic activity. We conclude that LpL promotes binding of apolipoprotein B-100-rich lipoproteins to cell surface heparan sulfate proteoglycans. LpL also enhanced the otherwise weak binding of Lp(a) to LDL receptors. The heparan sulfate proteoglycan pathway represents a novel catabolic mechanism that may allow substantial cellular and interstitial accumulation of cholesteryl ester-rich lipoproteins, independent of feedback inhibition by cellular sterol content.
...
PMID:Mechanisms by which lipoprotein lipase alters cellular metabolism of lipoprotein(a), low density lipoprotein, and nascent lipoproteins. Roles for low density lipoprotein receptors and heparan sulfate proteoglycans. 132 15

To study the mechanisms of discrimination between various forms of vitamin E, four normal subjects, one patient with lipoprotein lipase deficiency, and three patients with abnormal apolipoprotein B-100 production were given an oral dose containing three tocopherols labeled with differing amounts of deuterium (2R,4'R,8'R-alpha-(5,7-(C2H3)2)tocopheryl acetate (d6-RRR-alpha-tocopheryl acetate), 2S,4'R,8'R-alpha-5-(C2H3)tocopheryl acetate (d3-SRR-alpha-tocopheryl acetate), and 2R,4'R,8'R-gamma-(3,4-2H)tocopherol (d2-RRR-gamma-tocopherol). The tocopherol contents of plasma, red cells, and lipoproteins were measured up to 76 h after the dose. In normal subjects all three tocopherols were absorbed and secreted in chylomicrons with equal efficiencies. Both d2-gamma- and d3-SRR-alpha-tocopherols peaked at similar concentrations in the other lipoprotein fractions, then decreased similarly, but 2-4 times more rapidly than did d6-RRR-alpha-tocopherol. A lipoprotein lipase-deficient patient and a patient with prolonged production of chylomicrons with absent apolipoprotein B-100 also demonstrated the lack of discrimination between tocopherols during absorption. Despite abnormal apolipoprotein B-100 production in two patients, the "VLDL" was preferentially enriched in d6-RRR-alpha-tocopherol. Our results show that there is no discrimination between the three tocopherols during absorption and secretion in chylomicrons, but subsequently there is a preferential enrichment of very low density lipoprotein (VLDL) with RRR-alpha-tocopherol. Catabolism of this VLDL results in the maintenance of plasma RRR-alpha-tocopherol concentrations.
...
PMID:Discrimination between forms of vitamin E by humans with and without genetic abnormalities of lipoprotein metabolism. 143 96

A comprehensive assessment of lipoprotein compositional/metabolic response to incremental caloric ethanol (EtOH) doses ranging from low to moderate to high was undertaken using male squirrel monkeys. Control monkeys were maintained on a chemically defined, isocaloric liquid diet, while experimental primates wee fed increasing doses of alcohol (6, 12, 18, 24, 30, and 36% of energy) substituted isocalorically for carbohydrate at 3-month intervals. Liver function tests and plasma triglyceride were normal for all animals. Plasma cholesterol showed a transient increase at the 12% caloric dose that was attributed solely to an increase in high density lipoprotein (HDL). A more pronounced increase in plasma sterol, beginning at 24% and continuing to 36% EtOH, was the result of increments in both HDL and low density lipoprotein (LDL) cholesterol, although the contribution by the latter was substantial primarily at the 36% dose. Plasma apolipoprotein elevations (HDL apolipoprotein A-I, LDL apolipoprotein B) generally accompanied the lipoprotein lipid increases, although the first atherogenic response for LDL became manifest as a significant increase in apolipoprotein B at 18% EtOH calories. Postheparin plasma lipoprotein lipase was not affected by dietary alcohol, whereas hepatic triglyceride lipase activity showed significant increases at higher (24 and 36%) EtOH doses. Plasma lecithin-cholesterol acyltransferase activity was normal at the 6 and 12% EtOH doses, but exhibited a significant reduction beginning at 18% and continuing to 36% EtOH. Alterations in these key lipoprotein regulatory enzymes may represent the underlying metabolic basis for the observed changes in lipoprotein levels and our earlier findings of HDL2/HDL3 subfraction modifications. Results from our study indicate that in squirrel monkeys, moderate (12%) EtOH caloric intake favors an antiatherogenic lipoprotein profile (increases HDL, normal LDL levels, and lecithin-cholesterol acyltransferase activity), whereas higher doses (24-36%) produce both coronary-protective (increases HDL) and atherogenic (increases LDL) responses. Moreover, the 18% EtOH level represents an important transition dose which signals early adverse alterations in lipoprotein composition (increases apolipoprotein B) and metabolism (decreases lecithin-cholesterol acyltransferase).
...
PMID:Alcohol produces dose-dependent antiatherogenic and atherogenic plasma lipoprotein responses. 157 Mar 59

The mechanism by which ethinyl estradiol (EE) decreases the concentration of lipids in the d less than 1.019 g/ml fraction (beta-very low density lipoprotein [beta-VLDL]) of homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits was studied. Treatment with EE increased the activity of hepatic lipase (HL) twofold to threefold in postheparin plasma and in liver biopsies. Postheparin plasma and adipose tissue lipoprotein lipase (LPL) activities were also increased twofold to fourfold after EE. The effects of EE on HL and LPL activities were associated with a threefold to sixfold elevation in liver HL mRNA and a fourfold elevation in adipose tissue LPL mRNA steady-state levels, pointing to an effect of EE on HL and LPL gene transcription. EE also increased liver low density lipoprotein (LDL) receptor mRNA levels threefold to fivefold. These results suggest a concerted action of LPL, HL, and the LDL receptor in the removal of beta-VLDL in homozygous WHHL rabbits with a defective LDL receptor. In addition, the content of apolipoprotein E in the d less than 1.019 g/ml fraction changed toward normal after EE. Because the remaining particles contained apolipoprotein B-100 almost exclusively, it is likely that apolipoprotein E-containing beta-VLDLs are preferentially removed. This may be the result of the increased activity of LPL and HL influencing the conformation of apolipoprotein E on the beta-VLDL particle in such a way that it is directly removed from the circulation, possibly by the induced LDL receptor.
...
PMID:Increased removal of beta-very low density lipoproteins after ethinyl estradiol is associated with increased mRNA levels for hepatic lipase, lipoprotein lipase, and the low density lipoprotein receptor in Watanabe heritable hyperlipidemic rabbits. 165 30

Oral administration of cholestyramine to adult male hamsters not only induced a marked decrease in plasma concentrations of cholesterol and LDL but had a similar lowering effect on plasma triacyglycerol and VLDL concentrations. The hypotriglyceridaemic effects of resin administration were not due to an increase in lipoprotein lipase, as post-heparin plasma lipoprotein lipase activities were unchanged, but rather to a 35% decrease in VLDL synthesis. Measurement of the disappearance rate of apolipoprotein B from VLDL after i.v. injection of 125I-labelled hamster or human VLDL into control and cholestyramine-fed recipient animals showed a 2-times lower T1/2 in the drug-treated animals. The fraction of VLDL apolipoprotein B, recovered at any time after injection in the LDL, was equal or higher in cholestyramine-fed animals as compared to controls. These data indicate that the lowering in plasma LDL by cholestyramine in male hamsters is due not only to LDL receptor up-regulation but also to a lower rate of VLDL synthesis. No indications were found for a decreased efficiency of VLDL to LDL conversion in cholestyramine-fed animals.
...
PMID:Effects of cholestyramine on lipoprotein levels and metabolism in Syrian hamsters. 173 48

Fourteen male patients with Type 2 diabetes were studied to identify relationships between insulin-mediated glucose disposal, basal and glucose-stimulated insulin secretion, fasting lipoproteins and apolipoproteins, and the activities of lipoprotein lipase and hepatic lipase. Sensitivity of glucose disposal to exogenous insulin correlated positively with HDL-cholesterol (r = 0.65, p less than 0.05), HDL2-cholesterol (r = 0.59, p less than 0.05), and apolipoprotein A1 (r = 0.57, p less than 0.05) and negatively with apolipoprotein B (r = -0.53, p less than 0.05) and total: HDL-cholesterol ratio (r = -0.68, p less than 0.01). Fasting C-peptide correlated negatively with HDL-cholesterol (r = -0.76, p less than 0.01), HDL2-cholesterol (r = -0.80, p less than 0.001) and apoprotein A1 (r = -0.56, p less than 0.05) and positively with total: HDL-cholesterol ratio (r = 0.64, p less than 0.05). Neither fasting plasma glucose nor the indices of stimulated insulin secretion (glucose-stimulated plasma insulin and C-peptide) were related to any of the lipoprotein measures. Insulin insensitivity and hyperinsulinaemia were both associated with higher levels of hepatic lipase activity but did not influence lipoprotein lipase activity. In multiple linear regression analysis, hepatic lipase activity was related to HDL-cholesterol independent of insulin insensitivity. In addition, fasting C-peptide alone accounted for 70% of the variance in hepatic lipase activity and this was independent of insulin sensitivity and body mass index. We propose that the abnormalities of HDL-cholesterol in Type 2 diabetes are closely related to enhanced hepatic lipase activity brought about by increased insulin secretion which, in turn, is secondary to the defect in insulin action.
...
PMID:The role of insulin insensitivity and hepatic lipase in the dyslipidaemia of type 2 diabetes. 183 57

Coffee consumption has been associated with elevated plasma cholesterol. One hundred eighty-one men consumed a standard caffeinated coffee for 2 mo followed by randomization to continue caffeinated coffee (control), change to decaffeinated coffee or no coffee for 2 mo. Plasma low-density-lipoprotein (LDL) cholesterol and apolipoprotein B concentrations increased significantly (0.12 +/- 0.65 mmol/L, P less than 0.025; 0.06 +/- 0.12 g/L, P less than 0.0004, respectively) in the group that changed to decaffeinated coffee. In a subgroup (n = 51), post-heparin lipoprotein lipase decreased significantly more (-270 mmol free fatty acids.L-1.h-1, P less than 0.003) in the decaffeinated-coffee group. Resting heart rate and blood pressure did not change significantly. Change from caffeinated to decaffeinated coffee increased plasma LDL cholesterol and apolipoprotein B whereas discontinuation of caffeinated coffee revealed no change. This finding suggests that a coffee component other than caffeine is responsible for the LDL cholesterol, apolipoprotein B, and lipase activity changes reported in this investigation.
...
PMID:Caffeinated and decaffeinated coffee effects on plasma lipoprotein cholesterol, apolipoproteins, and lipase activity: a controlled, randomized trial. 150 76

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.
...
PMID:Lipoprotein lipase modulates net secretory output of apolipoprotein B in vitro. A possible pathophysiologic explanation for familial combined hyperlipidemia. 191 80


1 2 3 4 5 6 7 8 9 10 Next >>

---