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 the present work the effect of the precursor of Co a D-bis (N- pantothenyl-beta-aminoethyl) disulfide--pantethine on post heparin lipolytic activity and the intensity of lipid peroxidation has been investigated. Pantethine in doses of 5 mg/kg enhanced post heparin lipolytic activity (60.6%) and lipoprotein lipase activity (39.9%) in plasma and reduced the amount of NEFA (35.1%) and content of MDA (57.4%) in the mitochondria.
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PMID:[Effect of pantethine on post-heparin lipolytic activity and lipid peroxidation in the myocardium]. 205 71

A mixed metabolic alkalosis and metabolic acidosis, resulting in an alkalemic state, occurred in a hyperlipemic patient with previously diagnosed non insulin dependent diabetes. The metabolic alkalosis, due to large loss of gastric HCl, was more severe than the diabetic acidosis and resulted in an alkaline blood pH. Initially the metabolic acidosis was due to ketoacidosis and coexistent lactic acidosis. During the improvement of the alkalemic and hyperglycemic state, lactic acidosis disappeared but a paradoxical rise of plasma NEFA and ketone body concentrations supervened so that the high anion gap metabolic acidosis was virtually unchanged. The rise of plasma NEFA was probably related to the marked removal of plasma triglycerides, by insulin activation of lipoprotein lipase, and consequent saturation of the pathways of fatty acid incorporation into adipose tissue.
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PMID:Metabolic alkalosis in diabetic ketosis: a case report. 643 80

In this method for measuring lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) in post-heparin plasma, we determine the released free fatty acids enzymically. After release, they are extracted by Dole 's method (J. Biol. Chem. 235: 2595-2599, 1960), solubilized with Triton X-100, then measured with an enzymic kit (NEFA Kit-K; Nippon Shoji Kaisha Ltd.) after residual turbidity is removed by centrifugation with chloroform. A 5-microL sample of post-heparin plasma suffices to measure the activity of LPL and H-TGL; thus the method is as sensitive as the radioisotopic method. Selective assay of LPL and H-TGL, by adding sodium dodecyl sulfate to inactivate H-TGL or NaCl to inactivate LPL, is also feasible. The mean activities +/- SD of LPL and H-TGL in plasma of normal healthy men were respectively 9.4 +/- 2.3 mumol/h per milliliter (157 +/- 38 U/L) and 20.1 +/- 10.4 (335 +/- 173 U) mumol/h per milliliter (U/L).
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PMID:Sensitive non-radioisotopic method for measuring lipoprotein lipase and hepatic triglyceride lipase in post-heparin plasma. 671 36

The Authors investigated on the main lipidemic parameters in vascular diseases after acute administration of glucuronyl-glucosamine-glycan sulfate (3GS). The study was carried out in 48 subjects, aged 33 to 78, of whom 38 males and 10 females so divided: 6 metabolically healthy controls (N), 10 with vascular cerebral disease (VCD), 15 with coronary heart disease, 17 with peripheral vascular disease (PVD). Each subject, fasting and without drug treatment at least since 14 hours, after venous blood withdrawal, was given endovenous rapid bolus of 570 lipasemic units of glucuronyl-glucosamine-glycan sulfate (3GS); after 10', 20' and 30' other blood samples were taken; plasma NEFA (colorimetric method) triglycerides (TG), total cholesterol (TC) and HDL-cholesterol (C-HDL) (enzyme method) were assayed; C-HDL/TC ratio was calculated and LDL-cholesterol value (C-LDL) according to the Friedwald-Fredrickson's formula was obtained. In controls NEFA increase after 20' (+ 57%) and triglycerides drop (-49%) were detected; TC significant fall (-13%, P less than 0,05) after 20' was found, preceded by both C-HDL marked increase and C-HDL/TC ratio, and followed (30') by C-LDL slight rise. In the 3 groups of vascular patients a striking NEFA increase (respectively + 50%, + 43%, + 26%) was found; in subjects with PVD/TG blunted drop was observed, whereas in VCD and in CHD TG percentage fall -41 and -44%) did not differ from that one of controls. Evident remarked in control, drop of total cholesterolemia, lacked in the 3 groups of vascular diseases; in patients with VCD and PVD C-HDL and C-HDL/TC ratio increasing profile was like normal, while in CHD both progressive reduction of C-HDL (-19% after 30') and C-HDL/TC ratio with C-LDL increase were appreciated. On the basis of their results the Authors believed that in PVD a striking deficit of total plasma lipoprotein lipase (LPL), already in vitro documented, may occur, whereas LPL resulted normal in VCD and in CHD; on the contrary, in CHD an abnormally cholesterol-apo-VLDL affinity, like metabolic atherogenic derangement, was found; in the 3 groups of vascular diseases slow peripheral cholesterol removal was detectable.
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PMID:[Rapid effect of glucuronyl glucosamine glycan sulfate on the blood levels of HDL-cholesterol in vascular diseases]. 713 83

The activities of hepatic and lipoprotein lipase and the levels of lipo- and apoproteins were compared in two groups of normoglycaemic men representing the highest (n = 18) and lowest (n = 15) fasting insulin quintiles of first degree male relatives of non-insulin-dependent diabetic patients. The high insulin group representing insulin-resistant individuals had significantly lower post-heparin plasma lipoprotein lipase activity than the low insulin group (14.2 +/- 4.0 vs 20 +/- 5.8 mumol NEFA.ml-1.h-1, p < 0.001); hepatic lipase activity did not differ between the two groups (24.2 +/- 11 vs 18.0 +/- 5.3 mumol NEFA.ml-1.h-1, NS). The lipoprotein lipase/hepatic lipase ratio in the high insulin group was decreased by 66% as compared to the low insulin group (0.75 +/- 0.57 vs 1.25 +/- 0.65, p < 0.01). In the high insulin group both total and VLDL triglycerides were higher than in the low insulin group (1.61 +/- 0.57 vs 0.86 +/- 0.26 mmol/l, p < 0.001 and 1.00 +/- 0.47 vs 0.36 +/- 0.16 mmol/l, p < 0.001, respectively) whereas HDL cholesterol and HDL2 cholesterol were lower (1.20 +/- 0.30 vs 1.43 +/- 0.22 mmol/l, p < 0.05 and 0.49 +/- 0.21 vs 0.71 +/- 0.17 mmol/l, p < 0.05, respectively). Total cholesterol, LDL cholesterol or HDL3 cholesterol did not differ between the two groups. The mean particle size of LDL was smaller in the high insulin group than in the low insulin group (258 +/- 7 vs 265 +/- 6 A, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes of lipolytic enzymes cluster with insulin resistance syndrome. Botnia Study Group. 775 82

Six patients with type 2 diabetes underwent detailed metabolic studies before and after a minimum of 3 months' glibenclamide therapy. Treatment was associated with a small but significant increase in body weight. Despite improvements in almost all the measured parameters of glucose homeostasis (plasma glucose, glycosylated haemoglobin (HbA1), hepatic glucose production and insulin-mediated glucose disposal) neither fasting serum triglycerides nor HDL cholesterol changed and apoprotein A1 concentrations actually decreased significantly. NEFA and glycerol in fasting plasma and during the clamp studies did not change significantly with treatment. Post-heparin lipoprotein lipase and hepatic lipase activity did not change significantly. Thus, despite substantial improvements in glycaemic control and insulin sensitivity with sulphonylurea therapy, several aspects of lipid and lipoprotein metabolism remain largely unaffected. This small study suggests either that lipoprotein concentrations in type 2 diabetes are not influenced by insulin sensitivity or that the improvement is offset by another change that occurs during this form of therapy. It also suggests that other forms of therapy will be required to improve these cardiovascular risk factors in type 2 diabetes.
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PMID:The effects of glibenclamide on glucose homeostasis and lipoprotein metabolism in poorly controlled type 2 diabetes. 845 16

Cortisol is known to increase whole body lipolysis, yet chronic hypercortisolemia results in increased fat mass. The main aim of the study was to explain these two apparently opposed observations by examining the acute effects of hypercortisolemia on lipolysis in subcutaneous adipose tissue and in the whole body. Six healthy subjects were studied on two occasions. On one occasion hydrocortisone sodium succinate was infused i.v. to induce hypercortisolemia (mean plasma cortisol concentrations, 1500 +/- 100 vs. 335 +/- 25 nmol/L; P < 0.001); on the other occasion (control study) no intervention was made. Lipolysis in the s.c. adipose tissue of the anterior abdominal wall was studied by measurement of arterio-venous differences, and lipolysis in the whole body was studied by constant infusion of [1,2,3-2H5]glycerol for measurement of the systemic glycerol appearance rate. Hypercortisolemia led to significantly increased arterialized plasma nonesterified fatty acid (NEFA; P < 0.01) and blood glycerol concentrations (P < 0.05), with an increase in systemic glycerol appearance (P < 0.05). However, in s.c. abdominal adipose tissue, hypercortisolemia decreased veno-arterialized differences for NEFA (P < 0.05) and reduced NEFA efflux (P < 0.05). This reduction was attributable to decreased intracellular lipolysis (P < 0.05), reflecting decreased hormone-sensitive lipase action in this adipose depot. Hypercortisolemia caused a reduction in arterialized plasma TAG concentrations (P < 0.05), but without a significant change in the local extraction of TAG (presumed to reflect the action of adipose tissue lipoprotein lipase). There was no significant difference in plasma insulin concentrations between the control and hypercortisolemia study. Site-specific regulation of the enzymes of intracellular lipolysis (hormone-sensitive lipase) and intravascular lipolysis (lipoprotein lipase) may explain the ability of acute cortisol treatment to increase systemic glycerol and NEFA appearance rates while chronically promoting net central fat deposition.
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PMID:Effects of physiological hypercortisolemia on the regulation of lipolysis in subcutaneous adipose tissue. 946 84

Postprandial lipaemic responses to two test meals were investigated in 30 Northern (15 British and 15 Irish), and 30 Southern (Greeks from Crete) healthy male Europeans. The meals were a saturated fatty acid (SFA) meal, which resembled the fatty acid composition of an average UK diet, and a monounsaturated fatty acid (MUFA) meal in which the fat consisted of olive oil. Habitual diets of the two groups differed, with higher total fat, (P < 0.03) and MUFA (P < 0.0001) and lower polyunsaturated fatty acid (PUFA) (P < 0.0001) intakes in Southern than Northern Europeans. Levels of total MUFA (P < 0.02) and oleic acid (P < 0.004) were also higher in adipose tissue of Southern in comparison to Northern Europeans. In both European groups there were no significant differences in postprandial triglyceride response between the two meal types, SFA or MUFA. However, Northern and Southern Europeans showed significant differences in their patterns of postprandial response in plasma triglycerides (P < 0.0001), apolipoprotein B-48 (P < 0.0001), NEFA (P < 0.0001), insulin (P < 0.0007), and factor VII activity (P-0.03). In the case of NEFA, areas under the response curve were higher following the SFA than the MUFA meal for both groups, (P < 0.003) and were greater in Southern than Northern Europeans (P < 0.002) and apo B-48 responses were lower (P < 0.005). Some of these differences may reflect differences in fasting levels since fasting apolipoprotein B-48 levels were lower (P < 0.01) and fasting NEFA (P < 0.02) and insulin (P < 0.005) were higher in the Southern than in the Northern Europeans. In addition, 9 h postprandial post-heparin lipoprotein lipase activity was lower in the Southern than in the Northern Europeans (P < 0.0006). This is the first report of differences in postprandial lipid, factor VII and insulin responses in Southern and Northern Europeans which may be of importance in explaining the different susceptibilities of these two populations to risk of coronary artery disease.
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PMID:Differences in postprandial lipaemic response between Northern and Southern Europeans. 969 95

Non-esterified fatty acids (NEFA, or free fatty acids) are an important metabolic fuel. Both the concentration of NEFA and their flux through the circulation vary widely from hour to hour, reflecting nutritional state and physical activity. Inappropriately elevated plasma NEFA concentrations may have a number of adverse effects on both carbohydrate and lipid metabolism. These adverse effects are likely to be most marked in the postprandial period, when NEFA release from adipose tissue is usually suppressed. Although the regulation of NEFA release in the postabsorptive state is well understood in molecular terms, the predominant pathway for release of NEFA in the postprandial state is the action of lipoprotein lipase (LPL) in adipose tissue capillaries on chylomicron-triacylglycerol (TG). Fatty acids released by LPL may either be sequestered in the adipocytes by esterification, or released as NEFA into the plasma. The regulation of this branch-point, which may be of crucial significance for postprandial metabolism, is not well understood. Factors stimulating tissue retention of fatty acids include insulin and acylation stimulating protein. There is considerable indirect evidence that impaired regulation of this step occurs in insulin resistance and other conditions collectively recognised by an elevated concentration of apolipoprotein B (hyper-apo B). Inappropriate release of NEFA in the postprandial period is likely both to reduce the sensitivity of glucose metabolism to insulin and to accentuate postprandial lipaemia. Further study of the regulation of this pathway is much needed.
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PMID:Non-esterified fatty acid metabolism and postprandial lipaemia. 988 41

Because pigs are fatter when they are heat-stressed, it was hypothesized that lipid metabolism is enhanced in heat-stressed pigs. To test this hypothesis, an experiment was conducted to determine the influence of a high ambient temperature on the level of plasma lipids, thyroid hormones, lipoprotein lipase activity, and on the composition of very low density lipoproteins (VLDL) and chylomicrons in the growing pig. Twelve Large White x Landrace castrated male pigs with an initial weight of 20 +/- 0.6 kg were allotted to one of the following treatments: 1) ambient temperature of 31 degrees C, with ad libitum access to feed or 2) ambient temperature of 20 degrees C and fed the amount consumed by those kept at 31 degrees C until 35 kg BW. Ambient temperature did not affect piglet performance. Compared to that in pigs kept at 20 degrees C, in pigs kept at 31 degrees C the lipid content of backfat was 26% higher and the proportion of flare fat was increased by more than twofold (P < 0.001). Lipoprotein lipase activity was increased more than twofold in backfat and nearly twofold in leaf fat at 31 vs 20 degrees C (P < 0.001). In warmth-exposed (31 degrees C), feed-restricted pigs, the plasma level of triiodothyronine was 30% lower than at 20 degrees C (P < 0.001), whereas VLDL-lipid concentration was more than fourfold higher, and plasma concentrations of NEFA and triglycerides were 2.6- and 3.6-fold higher, respectively (P < 0.001). In conclusion, the chronic exposure of growing pigs to a high ambient temperature enhances lipid metabolism in both the liver (VLDL production) and the adipose tissue (lipoprotein lipase activity). Consequently, plasma triglyceride uptake and storage are facilitated in the adipose tissue, which results in greater fatness.
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PMID:Influence of a high ambient temperature on lipid metabolism in the growing pig. 1120 19


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