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

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

In rats maintained on a fat-free diet, hepatic production of very low density lipoprotein (VLDL) fell by only 18% after 20 hours of fasting (as judged by rates of triglyceride accumulation in plasma following administration of Triton WR1339). Infusion of heparin into fed rats caused a rapid accumulation in plasma of two distinct lipase activities in approximately equal amounts: heparin releasable lipoprotein lipase (HR-LPL) and heparin releasable triglyceride lipase (HR-TGL). Fasting reduced the former by 67%, but the latter by only 20 to 25%. To gain insight into the effects of nutritional status on the interorgan distribution of these enzymes, experiments were designed for the perfusion of liver and heart by standard procedures, and of epididymis, gastrocnemius muscle (red fiber), and psoas muscle (white fiber) by micro techniques. After addition of heparin, perfusates were analyzed for each species of lipase. The objective was to selectively monitor the capillary-bound, physiologically functional lipase without significant contamination by intracellular enzyme. HR-TGL was found only in liver, where it represented the major lipase activity; it was only minimally affected by fasting. In epididymis HR-LPL fell by 85% in fasted animals and, remarkably, rebounded almost to ad libitum fed values after only two hours of refeeding. In both heart and gastrocnemius muscle, directional changes in HR-LPL were exactly reciprocal to those seen in epididymis. By contrast, HR-LPL of psoas muscle was unresponsive to fasting. Qualitatively, the data were in keeping with documented nutritionally-induced shifts in tissue disposal of VLDL-triglycerides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of lipoprotein lipase in different rat tissues. 337 26

In order to determine the metabolic consequences of lipoprotein glucosylation, the glucosylated 125I-VLDL turnover was analyzed in comparison to the native one. Autologous in vitro glucosylated VLDL, separated by affinity chromatography, was injected into a nondiabetic rabbit and the amount of the radioactivity distributed in all lipoprotein fractions measured. Glucosylated--125I-VLDL metabolism versus control--125I-VLDL after six hours were: glc-VLDL = 35 +/- 4.5%, control- VLDL = 35 +/- 4.9%, glc-IDL = 51 +/- 3.8% control-IDL = 31 +/- 4.3% p less than 0.01; glc-LDL = 9 +/- 2.2%, control-LDL = 12 +/- 2.6%; glc-HDL = 5 +/- 1.4%, control-HDL = 22 +/- 2.9% p less than 0.001. A retained turnover of glc-VLDL and prolonged retaining of the triglyceride-rich lipoproteins (VLDL, IDL) in the circulation were found. The results suggest that the incorporation of glucose into lipoproteins may influence the steric configuration of molecules by blocking the sites of the lipolytic action of lipoprotein lipase. The data presented provide strong support for the idea that there are factors other than reduced LPL activity which contribute to defective VLDL removal in diabetes mellitus.
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PMID:Nonenzymatic glucosylation of very-low density lipoprotein alters its metabolism in the rabbit. 344 10

The enzyme lipoprotein lipase plays a central role in the processing of energy in the form of calorically dense triglyceride. Classical LPL deficiency usually presents in childhood with the multiple manifestations related to chylomicronemia. Many patients with genetic variations have been noted who differ in one of many ways from the classical patients. With the development of techniques to measure enzyme mass and to study gene expression, the molecular defects in each of these families should become evident.
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PMID:Primary lipoprotein lipase deficiency. 354 17

Men with regular physical training habits voluntarily increased their dietary fat intake from 43 to 54% of energy (E%) for four weeks. This was followed by a low-fat (29 E%), high-carbohydrate diet for another four weeks. During the high-fat diet period, the muscle lipoprotein lipase activity (LPLA) increased from 59 +/- 8 to 106 +/- 12 mU/g (mean +/- SE) (P less than 0.05). After the high-carbohydrate diet, LPLA was 57 +/- 16 mU/g, and unchanged relative to the pre-trial value. The triglyceride content in m. vastus lateralis increased from 30 +/- 4 to 47 +/- 9 mmol/kg d.w. (P less than 0.05; mean +/- SE) following the high-fat diet and to 41 +/- 8 following the high-carbohydrate diet. Neither of the diets affected the serum triglyceride and insulin concentrations, nor glucose, glycerol, beta-hydroxybutyrate, citrate and lactate levels in the blood. Nor did they alter enzyme activities in muscle used as markers for the oxidative (citrate synthase, beta-hydroxy-acyl CoA dehydrogenase) and glycolytic (glyceraldehyde phosphate dehydrogenase, lactate dehydrogenase) capacity. It is concluded that one month's adaptation to a high-fat diet results in increased muscle-LPL activity indicating a higher capacity for uptake of fatty acids from circulating serum triglycerides into the muscle cell in association with a greater capacity for triglyceride storage in the muscle. Under these conditions serum triglycerides were not decreased despite the increased muscle LPLA, and serum insulin variations could not explain the change in muscle LPLA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein lipase activity and intramuscular triglyceride stores after long-term high-fat and high-carbohydrate diets in physically trained men. 354 51

Adipose tissue distribution is an important predictor of obesity-associated morbidity and mortality. A central ('male') fat distribution is associated with increases in intra-abdominal adipose tissue which might be of metabolic importance. Although many recent studies have pointed out significant regional differences in the size and metabolism of subcutaneous fat cells intra-abdominal depots have not been systematically examined. We compared fat cell sizes (FCS) and lipoprotein lipase activity (LPLA) of two internal (omental, mesenteric) and four subcutaneous (SQ) sites (femoral, gluteal, abdominal, epigastric) in morbidly obese patients (26 premenopausal women and 14 men). Men had larger internal FCS than women while women had larger SQ FCS in the gluteal and femoral depots. Mesenteric FCS were largest of all sites in men. In women, omental fat cells were the smallest of all sites sampled but omental fat cells were as large as SQ sites in men. A more central distribution of fat in women (high waist/hip ratio) was associated with large mesenteric fat cells. Calculation of total fat cell number based on SQ FCS only, revealed sex differences that were eliminated by also using intra-abdominal FCS in the calculation. Averaged across all six sites, women had higher LPLA than men. Higher LPL activities were found in the lower-body subcutaneous sites with enlarged fat cells in women. However, the relative enlargement of intra-abdominal FCS in men was not associated with increased LPLA. In conclusion, sex- and site-specific variations in the distribution of FCS and LPLA in internal and SQ fat depots emphasize the importance of analyzing these depots in studies of fat cell number and adipose tissue metabolism.
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PMID:Sex differences in regional distribution of fat cell size and lipoprotein lipase activity in morbidly obese patients. 361 Apr 66

Post-heparin plasma lipoprotein lipase activity was measured in 28 cancer patients with varying degrees of weight loss, and in 16 normal volunteers. Total lipoprotein lipase activity was decreased by 35.4% (P less than 0.001) in the cancer group. The component lipase activities, hepatic (HLPL), and peripheral (PLPL), were decreased by 40% (P less than 0.001) and 38% (P less than 0.005) respectively. In addition, the level of total peripheral lipoprotein lipase correlated well with the percent body weight lost by these patients (r = 0.6, P less than 0.01). Regardless of extent of disease, patients with lung cancer showed the lowest enzyme activity (mean 191 mU/ml +/- 30 SEM, P less than 0.001) and the greatest percent of weight loss (mean 16%), while patients with breast cancer had nearly normal lipase activity (mean 315 mU/ml +/- 50 SEM, normal 340 mU/ml +/- 22 SEM, P less than 0.10) and minimal weight loss (mean 8.4%). Fasting serum triglycerides were significantly elevated in the patient group (mean 120 mg/dl +/- 9.7 SEM) as compared to normal (mean 71 mg/dl +/- 7 SEM, P less than 0.001). The mean fasting insulin level was elevated in the patient group (13 mU/ml +/- 3.0 SEM), although in the majority of the patients it was found within the normal range (4-24 mU/ml). We conclude that the significant decrease in the total LPL activity may be responsible in part for the characteristic hypertriglyceridemia present in cancer patients.
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PMID:Reduced plasma lipoprotein lipase activity in patients with malignancy-associated weight loss. 378 75

The kinetics of human and bovine milk lipoprotein lipase (HM-LPL and BM-LPL, respectively) were compared by varying apolipoprotein C-II (C-II) or triacylglycerol (TG) concentrations. The apparent Km (TG) and Km (C-II) for HM-LPL were 2.2 and 6.7-fold higher than for BM-LPL. Plots of 1/v vs 1/[TG] or 1/[C-II] intercepted the respective abscissas at the same points: C-II had no effect on Km (TG) and TG had no effect on Km (C-II). Replots of slope 1/s vs 1/[C-II] gave straight lines which yielded KA values identical to Km (C-II). It is concluded that the HM-LPL system follows a random, bireactant, rapid equilibrium mechanism as shown previously for BM-LPL.
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PMID:Kinetics of human and bovine milk lipoprotein lipase and the mechanism of enzyme activation by apolipoprotein C-II. 396 87

Changes in the activity of blood plasma lipoprotein lipase (EC 3.1.1.34, LPL and hepatic triacylglycerol lipase EC 3.1.1.3, H-TGL) were studied in rabbits injected intravenously by homologous and heterologous albumins (bovine, fraction Y, Sigma, BSA) alone and in combination with heparin. Rabbit albumin enhanced the effect of heparin on the LPL activity, while heterologous protein, to the contrary, diminished it. The in vitro experiments showed that BSA caused a more distinct effect on the LPL activity as compared with that of rabbit albumin. The activity of H-TGL was not significantly altered under the influence of both proteins.
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PMID:[Comparison of the effect of homologous and heterologous albumin on the activity of lipoprotein lipase and liver triglyceride lipase in rabbit plasma]. 402 38

A model for peripheral modulation of feeding behavior is discussed. This model proposes that under certain genetic, hormonal or dietary conditions adipose tissue lipoprotein lipase (AT-LPL) acts as a gatekeeper directing triglyceride derived fuels to adipose tissue and away from other tissues. It is proposed that shifts in the activity of the gatekeeper enzyme LPL result in changed feeding behaviors in rodents and possibly in man. In the fafa rat, the alterations in LPL activity may play the role of a developmental trigger or initiator. In other cases, the changes in AT-LPL may be adaptive rather than initiatory and may be permissive of behaviors rather than necessary antecedents.
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PMID:The relationship of enzyme activity to feeding behavior in rats: lipoprotein lipase as the metabolic gatekeeper. 406 24

In short-term experiments, healthy fasting persons were given a basic dose of 0.5 g of ethanol/kg body weight, followed by hourly maintenance doses of 0.15 g of ethanol/kg body weight. After 10 h there was a significant increase of triglycerides in the VLDL, LDL, and HDL, the main rise (from 42 to 92 mg/dl) being found in the VLDL triglycerides. Other subjects, who received nourishment isocaloric with ethanol, likewise showed a significant rise of triglycerides in all lipoprotein fractions. Chylomicron triglycerides increased from 9.3 to 35.5 mg/dl. There was no significant change in postheparin HTGL, but postheparin LPL activity decreased after 10 h from 17.9 to 12.2 mmol FFA/ml/h in the fasting subjects, and from 28.5 to 10.2 mmol/FFA/ml/h in the persons receiving food. In long-term experiments after 4 weeks of 70 - 80 g of ethanol and isocaloric food daily, triglycerides increased, especially in the VLDL (from 50 to 82 mg/dl). The increase in the HDL, however, was also significant. After 4 weeks of ethanol, the chylomicron triglycerides in the plasma of the fasting subjects reached a value of 29.3 mg/100 ml, LDL cholesterol decreased, and HDL cholesterol increased. After 4 weeks of ethanol there was an increase in the lipoprotein lipase of the adipose tissue.
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PMID:Lipoprotein fractions, lipoprotein lipase and hepatic triglyceride lipase during short-term and long-term uptake of ethanol in healthy subjects. 408 59


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