Post-Heparin Lipolytic Activity and Tissue Lipoprotein Lipase Activity in the Alloxan-Diabetic Rat

1974 ◽  
Vol 46 (5) ◽  
pp. 661-664
Author(s):  
R. S. Elkeles ◽  
E. Williams
Keyword(s):  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Lipolytic Activity ◽  
Diabetic Rats ◽  
Plasma Triglyceride ◽  
Diabetic Rat ◽  
Lipoprotein Lipase Activity ◽  
Post Heparin Lipolytic Activity ◽  
Adipose Tissue Lipoprotein Lipase

1. Alloxan-diabetic rats showed raised plasma triglyceride levels and low adipose tissue lipoprotein lipase activity compared with controls. Heart lipoprotein lipase activity appeared unaltered by the diabetic state. 2. Plasma post-heparin lipolytic activity was slightly but not significantly increased in the diabetic group. The significance of these findings is discussed.

Modifications of Plasma Post-Heparin Lipolytic Activity and Tissue Lipoprotein Lipase Activity Induced in the Rat by Acute Administration of Ethanol or Propan-2-ol

1975 ◽  
Vol 48 (2) ◽  
pp. 153-156
Author(s):  
Y. Giudicelli ◽  
R. Nordmann ◽  
J. Nordmann
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Lipolytic Activity ◽  
Ethanol Administration ◽  
Acute Administration ◽  
Post Heparin Lipolytic Activity ◽  
Adipose Tissue Lipoprotein Lipase ◽  
Made In

1. The oral administration of propan-2-ol [isopropanol; 100 mmol (6 g)/kg body weight] or ethanol [130 mmol (6 g)/kg body weight] to starved rats produced no change in plasma post-heparin lipase activity (PHLA) compared with that observed in 154 mmol/l sodium chloride (saline)-treated rats. 2. An increase of adipose tissue lipoprotein lipase (LLA) and a decrease of heart LLA occurred in isopropanol-treated animals, whereas no significant changes were found in these activities after ethanol administration. 3. Since administration of isopropanol produces hyperglycaemia, observations were also made in rats receiving glucose infusion rather than saline. In these animals a rise in PHLA and adipose tissue LLA, and a fall in heart LLA, occurred. 4. It is suggested that the changes in tissue LLA produced by isopropanol are mediated by the rise in blood glucose.

scholarly journals Post-translational regulation of lipoprotein lipase activity in adipose tissue

1978 ◽  
Vol 176 (3) ◽  
pp. 865-872 ◽  
Author(s):  
P Ashby ◽  
D P Bennett ◽  
I M Spencer ◽  
D S Robinson
Keyword(s):  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Translational Regulation ◽  
Progressive Increase ◽  
Lipoprotein Lipase Activity ◽  
Dependent Part ◽  
Adipose Tissue Lipoprotein Lipase ◽  
Energy Dependent

Changes in adipose-tissue lipoprotein lipase activity that are independent of protein synthesis were investigated in an incubation system in vitro. Under appropriate conditions at 25 degrees C a progressive increase in the enzyme activity occurs that is energy-dependent. Part of the enzyme is rapidly inactivated when the tissue is incubated with adrenaline or adrenaline plus theophylline. The mechanism of this inactivation appears to be distinct from, and to follow, the activation of the enzyme. A hypothesis is presented to account for the results in terms of an activation of the enzyme during obligatory post-translational processing and a catecholamine-regulated inactivation of the enzyme as an alternative to secretion from the adipocyte.

Lipoprotein lipase activity in rat heart and adipose tissue during endotoxic shock

1980 ◽  
Vol 238 (3) ◽  
pp. H325-H330 ◽  
Author(s):  
G. J. Bagby ◽  
J. A. Spitzer
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipoprotein Lipase ◽  
Endotoxic Shock ◽  
Plasma Triglyceride ◽  
Lipoprotein Lipase Activity ◽  
Fat Pad ◽  
E Coli ◽  
Adipose Tissue Lipoprotein Lipase ◽  
Observation Period

The present studies were designed to delineate changes in heart and adipose tissue lipoprotein lipase (LPL) activity following the administration of E. coli endotoxin. Plasma triglyceride levels were elevated in animals given endotoxin compared to saline-injected controls. Heart LPL activity decreased from 126.4 mumol fatty acid released per gram wet wt per hour in control rats to less than 22.5 mumol . g-1 . h-1 by 7 h following the injection of endotoxin. Although endotoxin was administered in doses producing 0-100% mortalities in a 24-h period, myocardial LPL activity was depressed to the same extent (75-80%) regardless of dose. The response of adipose tissue was less pronounced. Epididymal fat pad LPL activity fell significantly over the 24-h observation period in control and endotoxin-treated rats with the latter group somewhat more depressed 7 h after treatment. The findings are consistent with the suggestion that hypertriglyceridemia often observed during endotoxic shock may be related to depressed LPL activity; the degree of depression is probably tissue dependent.

Regulation of lipoprotein lipase activity in cardiac myocytes from control and diabetic rat hearts by plasma lipids

1992 ◽  
Vol 70 (9) ◽  
pp. 1271-1279 ◽  
Author(s):  
Brian Rodrigues ◽  
Janice E. A. Braun ◽  
Michael Spooner ◽  
David L. Severson
Keyword(s):  
Lipoprotein Lipase ◽  
Cardiac Myocytes ◽  
Lipase Activity ◽  
Plasma Lipids ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Lipoprotein Lipase Activity ◽  
Triton Wr 1339 ◽  
Plasma Triacylglycerol

The objective of this investigation was to test the hypothesis that the diabetes-induced reduction in lipoprotein lipase activity in cardiac myocytes may be due to hypertriglyceridemia. Administration of 4-aminopyrazolopyrimidine (50 mg/kg) to control rats for 24 h reduced plasma triacylglycerol levels and increased the heparin-induced release of lipoprotein lipase into the incubation medium of cardiac myocytes. The acute (3–5 days) induction of diabetes by streptozotocin (100 mg/kg) produced hypertriglyceridemia and reduced heparin-releasable lipoprotein lipase activity in cardiac myocytes. Treatment of diabetic rats with 4-aminopyrazolopyrimidine resulted in a fall in plasma triacylglycerol content and increased heparin-releasable lipoprotein lipase activity. Administration of Triton WR-1339 also resulted in hypertriglyceridemia, but the heparin-induced release of lipoprotein lipase from control cardiac myocytes was not reduced in the absence of lipolysis of triacylglycerol-rich lipoproteins. Treatment with Triton WR-1339 did, however, increase the heparin-induced release of lipoprotein lipase from diabetic cardiac myocytes. Preparation of cardiac myocytes with 0.9 mM oleic acid resulted in a decrease in both total cellular and heparin-releasable lipoprotein lipase activities. These results suggest that the diabetes-induced reduction in heart lipoprotein lipase activity may, at least in part, be due to an inhibitory effect of free fatty acids, derived either from lipoprotein degradation or from adipose tissue lipolysis, on lipoprotein lipase activity in (and (or) release from) cardiac myocytes.Key words: diabetes, plasma triacylglycerols, cardiac myocytes, lipoprotein lipase.

scholarly journals Adipose-tissue lipoprotein lipase activity and cellularity in the genetically obese Zucker rat (fa/fa) (Short Communication)

1973 ◽  
Vol 132 (3) ◽  
pp. 633-635 ◽  
Author(s):  
P. de Gasquet ◽  
E. Péquignot ◽  
D. Lemonnier ◽  
A. Alexiu
Keyword(s):  
Adipose Tissue ◽  
Surface Area ◽  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Enzyme Activities ◽  
Short Communication ◽  
Zucker Rat ◽  
Lipoprotein Lipase Activity ◽  
Obese Zucker Rat ◽  
Adipose Tissue Lipoprotein Lipase

The lipoprotein lipase activity per adipocyte was increased in the genetically obese rat (fa/fa). However, there was no difference between obese and lean animals when the enzyme activities were related to adipocyte surface area. The possible implications of the findings are discussed.

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