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)

Two men aged 48 and 35 years with severe hypertriglyceridaemia, glucose intolerance, and a secondary anaemia had more apolipoprotein C-III-2 and less apo C-III-1 on their triglyceride-rich lipoproteins (d less than 1.006) than did types IV or V lipaemic controls. Although the patients' abnormal lipoproteins seemed to produce normal activation of lipoprotein lipase, they did not serve as an efficient substrate for purified lipoprotein lipase. Adipose tissue of case 1 had considerable lipoprotein-lipase activity and the hypertriglyceridaemia responded to dietary therapy (carbohydrate 180 g, fat 80 g, protein 60 g per day, and no alcohol). The haemolytic anaemia improved, but the patient remained glucose intolerant. The abnormal content of apo C-III-2 on the triglyceride-rich lipoproteins, rendering them resistant to clearance by lipoprotein lipase, is believed to have contributed to the patients' severe hypertriglyceridaemia.
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PMID:Hypertriglyceridaemia associated with an abnormal triglyceride-rich lipoprotein carrying excess apolipoprotein C-III-2. 9 Jul 60

In order to elucidate the mechanism(s) of hyperlipidemia following glucocorticoid administration, dexamethasone (0.125 mg/Kg) was administered daily intramuscularly for 2 wk to male Sprague-Dawley rats and the effects on plasma triglyceride (TG) and cholesterol (Chol), lipoprotein neutral lipids, hepatic triglyceride secretion rates (TGSR; Triton), and epididymal fat lipoprotein lipase (LPL) were determined. Special measures were taken to maintain positive caloric balance and keep the weights of control and dexamethasone-treated animals comparable. Significant increases (p less than 0.001) in TG and very-low density lipoprotein (VLDL) triglyceride associated with no change in Chol and actual reduction in both triglyceride and cholesterol in low density lipoprotein (ldl) were observed in the steroid-treated animals. Dexamethasone treatment was associated with increased basal insulin and glucose levels, an insignificant increment in TGSR, and a highly significant reduction (p less than 0.001) in LPL. These findings suggest that glucocorticoid treatment increases splanchnic triglyceride production rates, but the resulting hypertriglyceridemia is primarily a consequence of impaired VLDL removal due to low adipose tissue LPL activity.
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PMID:Glucocorticoids and triglyceride transport: effects on triglyceride secretion rates, lipoprotein lipase, and plasma lipoproteins in the rat. 17 40

The hypolipidaemic effect of a new drug, gemfibrozil (CI-719), was studied for 20 weeks in 20 patients with primary type IIb, III, IV or V hyperlipoproteinaemia. Baseline recordings of serum cholesterol (9.1 mmol/l), triglyceride (3.79 mmol/l) and ultra-centrifugally isolated lipoproteins were obtained during a six-week pretreatment period with stable diet and body weight. With 800 mg of gemfibrozil per day given in two divided doses, the mean serum triglyceride and cholesterol levels were decreased by 44.6% and 10.5% respectively, during 20 treatment weeks. Only 2 patients were completely resistant to the hypolipidaemic action of the drug. Serum triglyceride was brought down to normal levels in 9 subjects. After 12 weeks of treatment the mean VLDL-triglyceride, VLDL-cholesterol, and LDL-triglyceride were reduced by 48.5%, 57.6%, and 22.7% respectively, while the HDL-cholesterol rose by 16%. The LDL-cholesterol increased slightly but significantly during treatment in type IV patients and decreased in type IIb patients. The change of LDL-cholesterol showed an inverse correlation with the initial LDL-cholesterol level (r=-0.87). The postheparin plasma lipoprotein lipase and hepatic lipase activities, determined separately by an immunochemical method, increased during four weeks of gemfibrozil treatment (+18.1% and +20.6% respectively), but neither of these changes was significantly correlated with the changes in any of the serum lipid or lipoprotein levels. Oral glucose tolerance was not influenced by the treatment, but one-hour plasma insulin increased slightly during administration of the drug. One patient discontinued the drug after eight weeks because of generalized allergic eczema, but no other side effects were recorded. It is concluded that gemfibrozil is highly effective in reducing elevated serum VLDL levels. The simultaneous elevation of LDL in type IV patients needs more attention and study. The mechanism of the hypolipidaemic action of the drug is so far obscure, but it might partly be due to an increased efficiency in VLDL removal by an increased activity of lipoprotein lipase.
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PMID:Gemfibrozil: effect on serum lipids, lipoproteins, postheparin plasma lipase activities and glucose tolerance in primary hypertriglyceridaemia. 19 Jun 8

To identify cells developing into adipocytes by accumulation of triglyceride, rat epididymal fat pad cells from small rats were exposed to (3)H-labeled chylomicron fatty acids in vivo and then liberated with collagenase. Tissue remnants were removed by filtration and mature fat cells by flotation. Aggregating cells were then removed by filtration through a 25- micro m nylon screen. Further purification of cells labeled in vivo was obtained by removing floating cells from those adhering to the bottom of a culture dish. The adhering cells multiplied to a confluent monolayer when cultured in Medium 199 containing serum, glucose, insulin, and a triglyceride emulsion. The cells then gradually enlarged due to granulation of the cytoplasm by a lipid-staining material. After about 2 weeks these granules had coalesced forming mature adipocytes of typical signet-ring appearance. Free adipocytes could then be recovered from the cultures by collagenase treatment. After about 2 weeks of culture these cells had the same size (about 30 micro m) as adipocytes recovered in the original collagenase preparation of the rat epididymal fat pad. They contained triglyceride lipase activity and incorporated glucose into triglycerides to the same extent as cells developed in vivo but had higher lipoprotein lipase activity. In vitro, heparin in a low concentration, prostaglandin E(1), isobutylmethylxanthine, and cholera toxin markedly promoted the development of these cells into adipocytes. This could be shown to occur almost completely indicating that this fraction of cells was homogeneous and consisted of cells with the capacity to form adipocytes. The duplication time was about 2 days and did not change with subculturing. Preadipocytes could be obtained by density gradient centrifugation, isolating triglyceride-containing cells either directly from the pad or after 3 days in culture. All of these cells developed into adipocytes as described above but did not multiply as readily. It was concluded that cells from the epididymal fat pad from small rats can be isolated in a homogenous fraction that develops in culture into cells of identical morphology and function as adipocytes formed in vivo. The differentiation of these cells into adipocytes may be manipulated in vitro.
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PMID:Isolation and characterization of cells from rat adipose tissue developing into adipocytes. 20 38

Healthy, nonobese, young rats developed hypertriglyceridemia (mean triglyceride levels of 250 mg/dl) following consumption of a sucrose-lard diet. The hypertriglyceridemia was apparent three days after start of the diet and persisted throughout the 4-week experimental period. Body weight, liver weight, and serum glucose levels were similar in animals eating either the sucrose-lard diet or standard rat chow. On the other hand, serum free fatty acid levels were slightly increased and serum insulin levels were substantially increased in animals eating the sucrose-lard diet. Determination of very low density lipoprotein turnover revealed that total triglyceride secretion in rats eating the sucrose-lard diet was significantly (P < 0.01) increased over that of rats eating standard chow. Direct measurement of hepatic and intestinal very low density lipoprotein secretion indicated that the observed rise in total triglyceride secretion was secondary to increased secretion of very low density lipoproteins by the liver. Finally, lipoprotein lipase activity of adipose tissue from rats eating the sucrose-lard diet was equal to, or greater than (depending upon sampling time), the activity of the enzyme from adipose tissue of rats eating the control diet. These data indicate that young, nonobese, rats develop hypertriglyceridemia when they ingest a sucrose-lard diet, and that the rise in plasma triglyceride levels results from an increase in hepatic very low density lipoprotein secretion. The dietary-induced hypertriglyceridemia is associated with elevated serum insulin levels, and, as such, may provide a useful animal model to use in studies aimed at defining the pathogenesis of endogenous hypertriglyceridemia in man.-Reaven, G. M., T. R. Risser, Y-D. I. Chen, and E. P. Reaven. Characterization of a model of dietary-induced hypertriglyceridemia in young, nonobese rats.
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PMID:Characterization of a model of dietary-induced hypertriglyceridemia in young, nonobese rats. 22 4

The major effects of glucocorticoids on white fat are shown in Fig. 1. The glucocorticoid diffuses into the cytosol of fat cells where it binds to a soluble receptor. The steroid-receptor complex then enters the nucleus where RNA synthesis is increased. The next step may be a selective increase in synthesis of protein(s). In any event, there is an inhibition of the membrane-bound glucose transport system and an increase in the ability of lipolytic agents to activate triglyceride lipolysis. There is also a decrease in phosphoenolpyruvate carboxykinase, lipoprotein lipase, and fatty acid synthetase that occurs after a somewhat longer lag period than is required for inhibition of glucose transport or lipolysis activation. Whether these effects are independent or secondary to the glucose transport inhibition and lipolysis activation remains to be established.
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PMID:Inhibition of glucose transport in fat cells and activation of lipolysis by glucocorticoids. 22 73

The capacity of para-aminosalicylic acid (PAS) to lower initially high serum lipoprotein lipid concentrations was tested in a double-blind crossover study. Thirty patients who were on a lipid-lowering diet were treated with PAS (6 gm daily) for 4 wk. There was an average reduction of the serum triglyceride concentration of 28% (p less than 0.001) and of 12% of the serum cholesterol concentration (p less than 0.001) corresponding to a reduction of very low density lipoprotein (VLDL) triglycerides of 40% (p less than 0.001) and low density lipoprotein (LDL) cholesterol of 6% (p less than 0.05). In hypercholesterolemic patients, the LDL cholesterol reduction was 14% (p less than 0.001). In patients with hypertriglyceridemia type IV, the mean reduction of the VLDL triglyceride concentration was 47% (p less than 0.01), corresponding to a serum triglyceride reduction by 37% (p less than 0.01). In spite of the decrease of VLDL concentration, there was an unexpected reduction of the lipoprotein lipase activity in adipose tissue of 16% (p less than 0.02). The glucose tolerance and the serum insulin concentrations at fasting and after glucose injection were not changed.
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PMID:Para-aminosalicylic acid as a lipid-lowering agent. 34 78

Biopsies of human adipose tissue were maintained for 1 wk in vitro with physiologic (1.5-30 X 10(-8) M) or pharmacologic (300 X 10(-8) M) concentrations of hydrocortisone or 1000 muU/ml insulin, or both. After this period, the explants were washed and incubated for 2 hr according to techniques generally used to study fat cell metabolism. Physiologic concentrations of hydrocortisone mainly exert an insulin antagonistic effect. Thus, the long-term effects of insulin in increasing lipolysis, as well as glucose metabolism to triglycerides, were reduced, as were the acute effects of insulin on these parameters. At these concentrations, the glucocorticoid itself did not influence the basal metabolic rates when due consideration was given to simultaneous changes in mean fat cell size. At higher concentrations, which may easily be reached during nonspecific glucocorticoid therapy, the glucose metabolism was reduced. Hydrocortisone decreased the number of insulin receptors. However, this cannot solely explain the insulin-antagonistic effect, since it was not overcome by a supramaximal concentration of insulin. Insulin and hydrocortisone together increased the lipoprotein lipase (lpl) activity several times. The resultant changes in LPL appear to depend upon the insulincorticosteroid ratio.
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PMID:Human adipose tissue in culture. VIII. Studies on the insulin-antagonistic effect of glucocorticoids. 44 90

The activity of lipoprotein lipase (E.C.3.1.1.3.) has been measured in adipose tissue from insulin-independent diabetics with hypertriglyceridaemia, non-diabetics with hypertriglyceridaemia and control patients, all of whom were obese. Although all groups showed an increase of plasma insulin after oral glucose, both the diabetic and nondiabetic hypertriglyceridaemics had impaired activities of lipoprotein lipase in adipose tissue compared to the obese normals (p less than 0.02, p less than 0.03, respectively). A course of insulin therapy (20 u.o.d.) for one week increased the activity of lipoprotein lipase extracted from adipose tissue, lowered plasma triglycerides and improved triglyceride clearance from plasma in a group of diabetics with hypertriglyceridaemia (mean plasma triglyceride 8.7 mmol/l). Our results suggest that a feature in the development of insulin resistance in adult diabetics may be a failure of maintenance of key intracellular enzyme activities involved in lipid metabolism.
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PMID:Insulin-independent diabetes: a defect in the activity of lipoprotein lipase in adipose tissue. 45 74

The acute effect of feeding high concentration carbohydrate meals containing equicaloric amounts of dextrose or sucrose on the activity of adipose tissue lipoprotein lipase and the concentration of plasma triglyceride was assessed in 11 hemodialysis patients. Dextrose feeding resulted in higher postprandial glucose levels and a greater insulin response than sucrose. The relationship between the postprandial change in the activity of adipose tissue lipoprotein lipase and the insulin response to feeding almost reached statistical significant (rs = 0.40, P = 0.08, n = 20), and the increase in the activity of the enzyme after dextrose feeding was greater than after sucrose (P less than 0.01). There was a significant decrease in plasma triglyceride levels after dextrose feeding (P less than 0.01), but no change was observed after the ingestion of sucrose. These results indicate that the inability of the administered sucrose to raise the plasma insulin concentration to the same level as isocaloric amounts of dextrose probably accounts for the smaller increase in the activity of adipose tissue lipoprotein lipase after sucrose. The failure of plasma triglyceride levels to fall after sucrose feeding suggests that the extent to which the activity of adipose tissue lipoprotein lipase increases postprandially may be important in the regulation of triglyceride metabolism in hemodialysis patients.
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PMID:Effect of high carbohydrate feeding with dextrose or sucrose on adipose tissue lipoprotein lipase activity and plasma triglyceride levels in hemodialysis patients. 46 2


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