Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our aim was to determine whether the increase in serum pancreatic lipase values, reported in patients with chronic renal failure maintained on haemodialysis, is the result of haemoconcentration by fluid removal during dialysis, or whether it is due to lipase stimulation by endothelial lipoprotein lipase, induced by the heparin used as an anticoagulant. We therefore compared the increases in serum lipase, when heparin was used, with those observed when this was replaced by the antithrombotic agent, defibrotide, which has no effect on lipoprotein lipase. In addition, in order to determine the effects of haemoconcentration, variations in total protein concentration and haematocrit values were determined on the same samples, both before and after dialysis. The results showed a statistically significant post-dialysis increase in lipase only when heparin was used (p < 0.03). There was also a mean percentage post-dialysis increase of 16.2% in total protein (p < 0.0001) and 15.5% in haematocrit (p < 0.0001), due to fluid removal. No significant correlation in percentage increases was found between lipase vs total protein or haematocrit values. These findings suggest that heparin-induced lipoprotein lipase stimulation is the principal cause of the post-dialysis increase in pancreatic lipase, and that fluid removal during dialysis makes only a minor contribution to this increase.
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PMID:Influence of haemodialysis on lipase activity. 912 46

In a recent study, we found marked downregulation of lipoprotein lipase (LPL) gene expression in fat, myocardium, and skeletal muscle of rats with chronic renal failure (CRF). Recently, hepatic lipase expression was shown to be depressed in CRF rats, and parathyroidectomy (PTX) was shown to reverse this abnormality. This study was undertaken to determine whether down-regulation of LPL expression in CRF is due to secondary hyperparathyroidism. Accordingly, LPL mRNA (Northern analysis), protein mass (Western analysis using mouse antibovine LPL monoclonal antibody, 5D2), and catalytic activity of the fat pad and soleus muscle were compared in five-sixths-nephrectomized male rats (CRF), parathyroidectomized CRF rats, and sham-operated control animals. The CRF animals exhibited marked hypertriglyceridemia and significant reductions of fat and skeletal muscle LPL mRNA abundance, protein mass, and catalytic activity (P < 0.05 vs. controls, for all parameters). PTX completely normalized the LPL mRNA, protein mass, and enzymatic activity and partially ameliorated the CRF hypertriglyceridemia (P < 0.05 vs. CRF group, for all parameters). Thus secondary hyperparathyroidism is responsible for impaired LPL expression in experimental CRF. This abnormality is completely corrected by PTX.
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PMID:Secondary hyperparathyroidism downregulates lipoprotein lipase expression in chronic renal failure. 943 81

Recent studies have revealed marked down-regulation of hepatic lipase (HL), lipoprotein lipase (LPL) and very low density lipoprotein-receptor (VLDL-R) expressions in animals with chronic renal failure (CRF). Acquired deficiency of these proteins, which together play an important role in catabolism of triglyceride-rich lipoproteins, is involved in the pathogenesis of CRF hypertriglyceridemia. Down-regulation of HL and LPL expressions in CRF can be completely reversed by parathyroidectomy (PTx), suggesting the role of excess parathormone (PTH). However, the role of hyperparathyroidism in the pathogenesis of CRF-induced VLDL-R deficiency has not been investigated before, and was studied here. To this end, VLDL-R mRNA (Northern analysis) and VLDL-R protein (Western analysis) of the fat pad and soleus muscle were compared in CRF (5/6 nephrectomized) rats, CRF animals with PTx (CRF-PTx) and sham-operated control animals. The CRF animals exhibited marked hypertriglyceridemia coupled with significant reductions in skeletal muscle and adipose tissue VLDL-R mRNA abundance and protein mass. Parathyroidectomy resulted in a significant, but partial, amelioration of CRF hypertriglyceridemia. However, in contrast to its effect on HL and LPL expressions, PTx did not improve VLDL-R expression, suggesting a PTH-independent mechanism for the latter abnormality. The differential effect of PTx on HL and LPL on the one hand and VLDL-R on the other can, in part, account for partial as opposed to complete correction of the associated hypertriglyceridemia with PTx in the CRF animals.
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PMID:Role of secondary hyperparathyroidism in the genesis of hypertriglyceridemia and VLDL receptor deficiency in chronic renal failure. 950 7

The high incidence of arteriosclerotic disease in patients with chronic renal failure seems to be due to certain peculiarities in their lipid metabolism. These are principally a disorder in the transportation of lipoproteins and a concomitant defect in triglyceride metabolism causing an accumulation of triglyceride-rich-lipoproteins which predispose to atherosclerosis. We studied the disturbances in concentration of apolipoproteins, notably Apo C-II and C-III, which modulate the activity of lipoprotein lipase (LPL), in patients with chronic renal failure (CRF) without replacement therapy and in hemodialysis patients with and without hyperlipidemia. LPL hydrolyses triglycerides in the lipoprotein-triglyceride (LPRTG) core. The main lipid parameters were measured in 4 groups of normolipidemic and hyperlipidemic patients with and without CRF in comparison with healthy controls. We found that the lipolytic activity index (A-I/C-III) was decreased, and Apo C-III levels were increased, in patients with CRF and patients on HD, including normolipidemic patients. We conclude that high Apo C-III levels are found in uremic patients before starting dialysis and do not change during dialysis treatment. This increase could be one of the initial causes of impaired triglyceride catabolism and LPRTG accumulation even in normolipidemic patients with CRF and may be one explanation of the high mortality from cardiovascular disease in these patients.
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PMID:[Apolipoprotein C-II and C-III anomalies in normolipemic and hyperlipemic patients with chronic kidney failure]. 1082 22

Hypertriglyceridemia associated with chronic renal failure (CRF) and elevated plasma concentration of very-low-density lipoprotein (VLDL) are thought to be a consequence of the depressed lipoprotein lipase and hepatic lipase activities and impaired clearance of lipoproteins. However, there is some evidence that the lipoproteins overproduction might also contribute to hypertriglyceridemia in CRF. This study was performed to test the hypothesis that the increased rate of lipogenesis consequent to upregulation of fatty acid synthase (FAS), a key lipogenic enzyme, gene expression could contribute to overproduction of triacylglycerols and to hypertriglyceridemia in CRF. FAS activity, FAS protein mass (Western blot analysis), and FAS mRNA level (Northern blot analysis) in liver and epididymal white adipose tissue (WAT) were measured in male Wistar rats 6 weeks after subtotal (5 of 6) nephrectomy or sham operation. Moreover, the rate of lipogenesis in WAT was determined. The CRF group showed significant increase in FAS gene expression (measured as activity, mRNA, and protein abundance) in both liver and WAT. This was associated with the increase in the lipogenesis rate and with the increase in plasma triacylglycerol and VLDL concentrations. Our results suggest that not only decreased removal, but also an increase of triacylglycerol production could contribute, in part, to the CRF-associated hyperlipidemia. Upregulation of FAS gene expression, shown in this report for the first time, reveals another factor involved in disturbed lipid metabolism in CRF. It seems that elevated plasma insulin and cytokine concentration could play an important role in the mechanism responsible for the increased FAS gene expression in CRF.
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PMID:Upregulation of fatty acid synthase gene expression in experimental chronic renal failure. 1248 75

The effects of hemodialysis duration (HD) on lipoprotein lipase (LPL) and hepatic lipase (HL) activities and very low density lipoprotein (VLDL), low density lipoproteins (LDL) amounts and compositions were investigated in 58 patients, divided according to HD: GI: under 1 year, GII: 1-5 years, GIII: 5-13 years. HL and LPL activities were reduced in GIII versus GI (P<0.01) and 47% of GIII patients had negligible HL activity. LPL and HL activities were correlated with HD (r=-0.80, P<0.001). Apo C-III concentrations were correlated with HD (r=0.58, P<0.05). Compared with controls, triacylglycerols (TG) were increased in GI, GII (P<0.01) and GIII (P<0.001), and were correlated with HD (r=0.75, P<0.05). VLDL amounts and VLDL-cholesteryl esters (CE) were enhanced in GIII versus GI and GII (P<0.05). VLDL-TG and VLDL-phospholipids (PL) were correlated with HD (r=0.60, P<0.05). LDL-apolipoproteins and unesterified cholesterol (UC) were increased in GII versus GI (P<0.05) and in GIII versus GII and GI (P<0.01). LDL-PLs were decreased in GIII versus GI (P<0.05). Compared with controls, LDL-TGs were higher in GI and GII (P<0.01) and in GIII (P<0.05). Long-term treatment with acetate hemodialysis using cuprophane membrane does not improve lipolytic activity decrease and lipoprotein alterations generated by chronic renal failure (CRF).
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PMID:Plasma lipoprotein lipase, hepatic lipase activities, VLDL, LDL compositions at different times of hemodialysis. 1292 78

Apolipoprotein Cs (apoC-1, apoC-II, and apoC-III) are lipoprotein components that have regulatory effects on enzymes involved in lipoprotein metabolism. Owing to their low molecular weights, apoCs can adsorb onto and/or pass through dialysis membranes. Our study determines the consequence of hemodialysis (HD) on plasma concentrations of apoCs and on the activities of enzymes modulated by apoCs. Plasma samples were collected from 28 patients with chronic renal failure before and after HD. Plasma apoC-II levels were unchanged, whereas apoC-III levels were slightly decreased in post-dialysis plasmas. The apoC-I content was markedly reduced during HD. This was due to a significant decrease in the apoC-I content of very low-density lipoprotein (VLDL), whereas the apoC-I content of high-density lipoprotein (HDL) was unchanged. Although HDL bound apoC-I is thought to inhibit cholesterol ester transfer protein, no change in the ability of pre- and post-dialysis VLDL to interact with the transfer protein were observed. Complementary experiments confirmed that VLDL-bound apoC-I has no transfer protein inhibitory potential. In contrast, an increase in the ability of post-dialysis apoC-I-poor VLDL to act as substrate for lipoprotein lipase (LPL) was found compared to pre-dialysis VLDL. Our study shows that apoC-I losses during HD might be beneficial by improving the ability of VLDL to be a substrate for LPL thus improving plasma triglyceride metabolism.
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PMID:Hemodialysis reduces plasma apolipoprotein C-I concentration making VLDL a better substrate for lipoprotein lipase. 1788 38

Secondary hyperlipidemia is common and occurs frequently in patients with endocrine disease such as hy- pothyroidism, Cushing's syndrome, and acromegaly, metabolic disease such as diabetes mellitus, renal dis- ease such as nephrotic syndrome and chronic renal failure, liver disease such as obstructive liver disease, and as a side-effect of glucocorticoids and estrogens. The underlying cause of high serum lipid levels will often be missed if it is not actively sought. We describe. the causes and abnormal lipid laboratory values of sec- ondary hyperlipidemia in endocrine disease patients such as those with hypothyroidism, Cushing's syndrome, and acromegaly. Hypothyroidism is associated with elevated serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), and normal or elevated high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG), respectively. The lipid abnormalities are due to the reductions in hepatic LDL receptor function and hepatic TG lipase (HTGL) activity. Cushing's syndrome is associated with elevated serum TC, LDL-C, and TG and elevated or normal HDL-C. The lipid abnormalities are due to the glucocorticoid- induced increase in very low-density lipoprotein (VLDL) and elevation in lipoprotein lipase (LPL) activity. Acromegaly is associated with normal serum TC, reduced LDL-C and HDL-C, and elevated TG. The lipid abnormalities are due to the growth hormone-induced reductions in LPL and HTGL activity and increase in hepatic LDL receptors. When we examine hyperlipidemic patients, it is important to diagnose the true name of the disease, usually in consideration of the possibility of the cause of secondary hyperlipidemia. [Review].
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PMID:[Causes and Abnormal Lipid Laboratory Values of Secondary Hyperlipidemia: Endocrine Disease]. 3069 60


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