• Journal of the Korean Applied Science and Technology
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• v.2 no.1
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• pp.77-81
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• 1985

In order to investigate the effect of ginseng saponins on the activity of lipoprotein lipase, it was attempted to conform the enzymatic hydrolysis of chylomicron with post-heparin induced plasma lipoprotein lipase of normal rabbit in vitro. And the activity of lipoprotein llipase was determined by the quantitative determination of liberated free fatty acids on the hydrolysis of chylomicron. As the result, it was observed that the ginseng saponins accelerated the hydrolysis of chylomicron by post-heparin plasma in vitro. And the optimum concentration of ginseng saponins for the activity of the lipoprotein lipase in the 2% bovine serum albumin was $10^{-4}%$. But ginseng saponins on the hydrolysis of chylomicron was influenced by the presence and the absence of albumin. And the optimum concentration of albumin and Na-cholate on the activity of lipoprotein lipase was each of the $10^{-6}%$ albumin and 5mM Na-cholate. From these results, it seems that ginseng saponins might stimulate the intravascular hydrolysis of chylomicron.

• BMB Reports
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• v.34 no.4
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• pp.329-333
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• 2001

Active lipoprotein lipase (LPL) is known as a noncovalent homodimer of identical subunits, and dissociation of the dimer to a monomeric form renders the lipase inactive. In this study, the oligomerization status of LPL in human and rat plasma was investigated. The LPL activity was barely detectable in the control rat and human plasma. After the injection of heparin, the total lipolytic activity of plasma was rapidly increased, and reached its maximum in 30 min. Changes of the LPL protein correlated well with those of lipolytic activity. The LPL protein that is released by heparin into both human and rat plasma was active and dimeric in the sucrose density gradient ultracentrifugation. In control rat plasma, LPL was inactive, and a great fraction was present as an aggregate. However, the inactive LPL protein in the control human plasma retained the dimeric state, indicating that dimerization can be an entity independent of the catalytic activity of LPL. The released LPL is transported as a complex with lipoproteins in plasma. Lipoprotein profiles, determined by NaBr ultracentrifugation, exhibited typical LDL- and HDL-mammal patterns in humans and rats, respectively, with a smaller amount of the LDL fraction observed in rats. The difference in the lipoprotein profiles might influence the fate of the released LPL in plasma.

• Asian-Australasian Journal of Animal Sciences
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• v.14 no.11
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• pp.1592-1597
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• 2001

Sixteen pigs from 2 distinct genetic lines (LGAH and VFIL) obtained after eight generations of divergent selection for high (H) and low (L) lean tissue growth rate with ad-libitum feeding (LGA) and voluntary feed intake (VF1), respectively, were used in this study. The objectives of this investigation were to establish appropriate working conditions for the postheparin plasma lipoprotein lipase (LPL) assay and to study relationships between fat deposition and plasma lipids, very low density lipoprotein (VLDL) lipids, VLDL-subfractions and postheparin plasma LPL activity in growing pigs. Four preliminary experiments were performed to determine the appropriate working conditions for the postheparin plasma LPL assays. Postheparin plasma preincubated with SDS (20-50 mM) at $26^{\circ}C$ for 45 minutes inhibited hepatic lipase activity. A total of $2{\mu}l$ VLDL/assay produced maximum stimulation of LPL activity. Postheparin plasma protein and increasing incubation time contributed an optimum response. LGAH pigs had a significantly higher proportion subtraction 2 than VFIL pigs. No differences were observed in postheparin plasma LPL activity and backfat thickness for two lines of pigs. There were positive correlations between backfat thickness and proportion of subtractions 2 and postheparin plasma LPL activity but the results were not statistically significant. Backfat thickness was not statistically correlated with proportion of subtraction 2 and postheparin plasma LPL activity in a multiple regression analysis. It is believed that the apolipoprotein E, which is present in higher quantities in VLDL-subfraction 2 plays an important role for clearing VLDL triacylglycerol into adipose tissue. LPL activity of pigs can be measured by using postheparin plasma technique. If the relationships of backfat thickness and VLDL-subfraction 2 and postheparin plasma LPL activity can be established, it suggests that these parameters could be used as indicators in selection programmes. Further experiments need to be conducted by using larger sample size and different breed of pigs with greater differences in backfat thicknesses to confirm these trends.

• Preventive Nutrition and Food Science
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• v.4 no.2
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• pp.139-144
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• 1999

Lipoprotein lipase (LPL) I san enzyme that catalyzed the hydrolysis of triacylglycerols of chylomicrons and VLDL to produce 20acylglycerols and fatty acids. The enzyme, LPL, is localized on the surface of the capillary endothelium and is widely distributed in extrahepatic tissues including heart, skeletal muscle and adipose tissue. LPL has been isolated from boving milk by affinity chromatography on heparin-separose in 2 M NaCL, 5mM barbital buffer, pH 7.4. To elucidate the lipid-binding regin, LPL was digested with trypsin and then separated by gel filtration. Lipid binding region of LPL has been investigated by recombining LPL peptides with DMPC vesicles. Proteolytic LPL fragments with DMPC were reassembled and stabilized by cholate. Lipid-binding region of LPL was identified by a PTH-automated protein sequencer, as AQQHYPVSAGYTK. The analysis of the secondary structure of the lipid-binding peptides revealed a higher probability of $\alpha$-helix structure compared to the whole LPL protein. The prediction of hydrophobicity of lipid -binding region was highly hydrophobic (-1.1) compared to LPL polypetide(-0.4).

• Childhood Kidney Diseases
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• v.26 no.1
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• pp.25-30
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• 2022

Dyslipidemia in nephrotic syndrome (NS) is often characterized by marked increases in the levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol, and other lipoproteins, such as very low-density lipoprotein, intermediate-density lipoprotein, and lipoprotein(a). It has been suggested that impaired catabolism of lipoproteins and cholesterol is mainly due to decreased lipoprotein lipase and hepatic lipase activity, and increased biosynthesis of lipoproteins in the liver. The management strategies for dyslipidemia in patients with NS consist of lifestyle modification, lipid-lowering agents represented by statins, second-line agents such as fibrates and bile acid sequestrants, and lipid apheresis. Compared with dyslipidemia in adult NS patients, whose risks of atherosclerotic disease and progressive renal injury are considered high, clinical data on dyslipidemia in pediatric NS patients are limited. Therefore, it is necessary to pay more attention to the evaluation and management of dyslipidemia in pediatric patients with NS in clinical practice.

• Asian-Australasian Journal of Animal Sciences
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• v.16 no.3
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• pp.403-408
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• 2003

The study investigated the lipid metabolism of Tsaiya ducks under fasting and ad libitum feeding conditions. Sixty Tsaiya ducks in their growing period (8-12 wk-old) and sixty Tsaiya ducks in their laying period (26-30 wk-old, 10-14 weeks after the onset of laying) were randomly divided into ad libitum feeding and 3-day fasting groups. The activities of lipid metabolism related enzymes were determined. Experimental results indicated that fasting depressed the activities of lipogenesis related enzymes such as fatty acid synthetase and NADP-malic dehydrogenase in both periods (p<0.05). Fasting also increased the activities of liver fatty acid $\beta$-oxidation enzymes (p<0.05). However, the activities of lipoprotein lipase in adipose tissue, heart and ovarian follicle in both periods and the hormone-sensitive lipase of adipose tissue in the growing period were decreased by fasting (p<0.01).

• Nutrition Research and Practice
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• v.12 no.5
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• pp.371-377
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• 2018

BACKGROUND/OBJECTIVES: Elevation of postprandial lipemia characterized by a rise in triglyceride (TG)-rich lipoproteins can increase the risk of atherogenesis. The objective of this study was to investigate postprandial lipemia response to a single dietary fat/sugar load test and monitor beneficial changes induced by the consumption of Platycodi radix (AP) beverage in healthy subjects. SUBJECTS/METHODS: A total of 52 subjects were randomly assigned to either placebo or AP beverage group with a high-fat shake in a randomized controlled crossover trial. Postprandial blood was collected at 0, 1, 2, 4, and 6 h and analyzed for TG and lipoprotein lipase mass. Inhibition of pancreatic lipase was determined in vitro. RESULTS: AP inhibited pancreatic lipase activity in vitro ($IC_{50}=5mg/mL$). Compared to placebo beverage, AP beverage consumption with a high-fat shake induced significant increase of plasma lipoprotein lipase mass (P = 0.0111, ${\beta}$ estimate = 4.2948) with significant reduction in very low-density lipoprotein (VLDL) TG concentration (P = 0.038, ${\beta}$ estimate = -52.69) at 6 h. Based on significant correlation between high-fat dietary scores MEDFICTS and postprandial TG responses in VLDL (P = 0.0395, r = 0.2127), subgroup analysis revealed that 6 h-postprandial VLDL TG response was significantly decreased by AP consumption in subjects with MEDFICTS ${\geq}40$ (P = 0.0291, ${\beta}$ estimate = -7214). CONCLUSIONS: AP beverage might have potential to alleviate postprandial lipemia through inhibiting pancreatic lipase activity and elevating lipoprotein lipase mass. Subgroup analysis revealed that subjects with high-fat dietary pattern could be classified as responders to AP beverage among all subjects.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.392.3-393
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• 2002

The increase of triglyceride in blood can be a signal of an increasing danger of arterial diseases when insulin resistance. diabetes. HDL -cholesterol decrease is accompanied. It is adjusted to triglyceride level in blood by a balance. which seems to be absorbed from VLDL metabolism in liver and by lipoprotein lipase activity. The hyper-triglyceride disease treatment proposal role should match with suppression does into liver or elimination of a triglyceride. (omitted)

• Korean Journal of Plant Resources
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• v.24 no.2
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• pp.181-188
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• 2011

This study was carried out to estimate beneficial effects of Foeniculi fructus water extract on activities of key enzymes such as lipoprotein lipase (LPL), acyl-CoA synthetase (ACS), and hormone sensitive lipase (HSL) on lipid metabolism related with obesity. LPL and ACS were extracted from the epididymal adipose tissue and liver of C57BL/6J normal and obese mouse. Foeniculi fructus water extract treatment significantly reduced the activity of normal and obese LPL. When 100 ppm of Foeniculi fructus water extracts were tested, they decreased obese LPL activity by 12.0%. Foeniculi fructus water extract activated obese ACS activity by 7-fold compared with control at 1,000 ppm concentration. Expression of HSL mRNA was increased in Foeniculi fructus water extracts treated cells compared with non treated cells. All things considered, Foeniculi fructus water extract efficiently inhibits the influx of fatty acid into the cell, and activates metabolic process that uses fatty acids flowing as an energy source. Thus, it suggest that Foeniculi fructus water extract may have great potential as a novel anti-obesity agent.

• BMB Reports
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• v.33 no.2
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• pp.148-154
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• 2000

The glycation process plays an important role in accelerated atherosclerosis in diabetes, and the uptake of atherogenic lipoproteins by macrophage in the intima of the vessel wall leads to foam cell formation, an early sign of atherosclerosis. Besides the lipolytic action on the plasma triglyceride component, lipoprotein lipase (LPL) has been reported to enhance the cholesterol uptake by arterial wall cells. In this study, some properties of LPL-mediated low-density lipoprotein (LDL) uptake and the effect of LDL glycation were investigated in RAW 264.7 cell, a murine macrophage cell line. In the presence of LPL, $^{125}I$-LDL binding to RAW 264.7 cells was increased in a dose-dependent manner. At concentrations greater than $20\;{\mu}g/ml$ of LPL, LPL-mediated LDL binding was increased about 17-fold, achieving saturation. Without LPL, both very low-density lipoprotein (VLDL) and high-density lipoprotein (HDL) were ineffective in blocking the binding of $^{125}I$-LDL to Cells. However, LPL-enhanced LDL binding was inhibited about 50% by the presence of VLDL, while no significant effect was observed with HDL. Heat inactivation of LPL caused a 30% decrease of LDL binding. In the presence of LPL, the cells took up 40% of cell-bound native LDL. No significant difference was observed in cell binding between native and glycated LDL. However, the uptake of glycated LDL was significantly greater than that of native LDL, reaching to 70% of the total cell bound glycated LDL. These results indicate that LPL can cause the significant enhancement of LDL uptake by RAW 264.7 cells and the enhanced uptake of glycated LDL in the presence of LPL might play an important role in the accelerated atherogenesis in diabetic patients.