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)

Seven young, healthy subjects performed bicycle exercise with a working load leading to exhaustion after one hour of work. The tests were done in the afternoon in the fed state. The serum insulin concentrations decreased from 22 to 4 mU/l and plasma glucagon increased from 241 to 340 pg/l already after 30 min of work. The level of adipose tissue lipoprotein lipase activity (LPLA) did not fall as had been expected, but increased. The skeletal muscle LPLA was unchanged. The results indicate that during the first hour of heavy exercise the heparin-releasable LPLA in tissues is not influenced by the work induced changes in serum hormone levels.
 ...
PMID:Lipoprotein-lipase activity of human skeletal-muscle and adipose tissue after intensive physical exercise. 44 62

In the present study, we investigated possible mechanisms behind exogenous phospholipase C-induced glycerol production in irreversibly damaged myocytes. Rat ventricular myocytes were preincubated for 60 min in substrate-free Krebs-Henseleit bicarbonate buffer equilibrated with 95% N2-5% CO2 (37 degrees C, pH = 7.4), resulting in exhaustion of cellular high energy phosphates and loss of rod-shaped morphology. At the end of the preincubation period, the incubation vials were divided into two groups; one receiving 10 mU/ml phospholipase C (PC-PLC), whereas the other received an equivalent volume of buffer (control incubations). Incubation was then continued for another 60 min under 95% air-5% CO2 atmosphere. Samples for measurement of metabolite levels were taken immediately after cell isolation, at the end of the preincubation period and at the end of the normoxic incubation period. During the 60 min incubation period following reoxygenation, glycerol output was markedly higher from PC-PLC treated than from control myocytes. However, the elevated glycerol output from these cells was not accompanied by a simultaneous rise in glycerol-3-phosphate, nor was it inhibited by inclusion of pyruvate in the incubation buffer. On the other hand, glycerol output from PC-PLC treated myocytes was effectively inhibited by a diacylglycerol lipase inhibitor (U-57908, The Upjohn Company). Analysis of cellular lipids revealed a 22% reduction of phospholipid in PC-PLC treated myocytes (P < 0.02), while the content of triacylglycerol, diacylglycerol and unesterified fatty acids increased by 76, 261 and 103%, respectively (P < 0.02). No significant changes were observed for these parameters in control myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Phospholipid degradation in hypoxic/reoxygenated cardiomyocytes in response to phospholipase C from Bacillus cereus. 760 7

The utilization of muscle triacylglycerols was studied during and after prolonged bicycle ergometer exercise to exhaustion in eight healthy young men. Two days before exercise and in the postexercise recovery period, subjects were fed a carbohydrate-rich diet (65-70% of energy from carbohydrates). Exercise decreased muscle glycogen concentrations from 533 +/- 18 to 108 +/- 10 mmol/kg dry wt, whereas muscle triacylglycerol concentrations were unaffected (49 +/- 5 before vs. 49 +/- 8 mmol/kg dry wt after exercise). During the first 18 h after exercise, muscle glycogen concentrations were restored to 409 +/- 20 mmol/kg dry wt. In contrast, muscle triacylglycerol concentrations decreased (P < 0.05) to a nadir of 38 +/- 5 mmol/kg dry wt, and muscle lipoprotein lipase activity increased by 72% compared with values before exercise. Pulmonary respiratory exchange ratio values of 0.80-0.82 indicated a relatively high fractional lipid combustion despite the high carbohydrate intake. From 18 to 42 h of recovery, muscle glycogen synthesis was slow and muscle triacylglycerol concentrations and lipoprotein lipase activity were restored to the preexercise values. It is concluded that muscle triacylglycerol concentrations are not diminished during exhaustive glycogen-depleting exercise. However, in the postexercise recovery period, muscle glycogen resynthesis has high metabolic priority, resulting in postexercise lipid combustion despite a high carbohydrate intake. It is suggested that muscle triacylglycerols, and probably very low density lipoprotein triacylglycerols, are important in providing fuel for muscle metabolism in the postexercise recovery period.
 ...
PMID:Utilization of skeletal muscle triacylglycerol during postexercise recovery in humans. 968 36

Dyslipoproteinemia in patients on hemodialysis is characterized by a decrease in high density lipoprotein (HDL), cholesterol, hypertriglyceridemia, increased triglyceride-rich lipoproteins, such as very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL), a higher proportion of the small dense low density lipoprotein (small dense LDL) subfraction, and higher lipoprotein(a) concentration. The reason for the changes in triglyceride metabolism is an increase in the production of apolipoprotein B, and a decrease in the metabolism of VLDL as a consequence of decreased endothelial cell delipidation. The endothelial lipoprotein lipase, which plays a major role in this process, is released by heparin, which is essential for the function of the enzyme. Repeated administration of heparin for anticoagulation during hemodialysis apparently leads to an LPL depletion in the endothelium. This results in further exhaustion of lipolysis. Clinical studies in hemodialysis patients with high triglyceride and cholesterol levels indicate that a change from standard heparin to low-molecular-weight heparin improves the lipid profile by lowering triglycerides and cholesterol.
 ...
PMID:[When lipids increase in dialysis: the role of heparin! Standard heparin increases, low-molecular-weight heparin lowers triglycerides]. 1091 18

We report the case of a 17-year-old woman with anorexia nervosa (AN) who developed an abetalipoproteinemia-like lipid profile and acanthocytosis. These abnormalities resolved slowly as her nutritional status improved. We considered 3 possible causes of an abetalipoproteinemia-like lipid profile in AN: (1) depletion of hepatic substrate for apolipoprotein B synthesis, (2) lack of exogenous fatty acids with exhaustion of endogenous stores of triglycerides in adipose tissue, and (3) preservation of the lipoprotein lipase (LPL) mass. This unusual case provides important clues that enhance our understanding of lipid metabolism under exogenous and endogenous fat deprivation and highlights the pivotal role of LPL as a gatekeeper of the energy source.
 ...
PMID:Abetalipoproteinemia-like lipid profile and acanthocytosis in a young woman with anorexia nervosa. 1244 51