Lipoprotein Lipase Activities in Heart Muscle of Streptozotocin-Induced Diabetic Rats

1984 ◽  
Vol 16 (02) ◽  
pp. 67-70 ◽  
Author(s):  
T. Nakai ◽  
K. Oida ◽  
T. Tamai ◽  
S. Yamada ◽  
T. Kobayashi ◽  
...  
Keyword(s):  
Lipoprotein Lipase ◽  
Heart Muscle ◽  
Diabetic Rats

scholarly journals Suppression of Hyperlipidemia-Associated Cataracts in Diabetic Rats with the Lipoprotein Lipase Activator NO-1886.

1996 ◽  
Vol 19 (12) ◽  
pp. 1570-1573 ◽  
Author(s):  
Kazuhiko TSUTSUMI ◽  
Yasuhide INOUE ◽  
Chieko YOSHIDA
Keyword(s):  
Lipoprotein Lipase ◽  
Diabetic Rats

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.

Oscillatory changes in muscle lipoprotein lipase activity of fed and starved rats.

1977 ◽  
Vol 233 (4) ◽  
pp. E316
Author(s):  
T J Kotlar ◽  
J Borensztajn
Keyword(s):  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Feeding Habits ◽  
Quadriceps Muscle ◽  
Diabetic Rats ◽  
Lipoprotein Lipase Activity ◽  
Nocturnal Feeding ◽  
Ad Libitum ◽  
Short Time ◽  
Fast Twitch

Lipoprotein lipase activity was measured at short time intervals in cardiac and skeletal muscles of normal and streptozotocin-treated diabetic rats fed ad libitum or deprived of food. In normal animals fed ad libitum, lipoprotein lipase activities of heart, diaphragm, soleus, and fast-twitch red fibers of the quadriceps muscle showed rhythmic oscillations that appeared to coincide with the nocturnal feeding habits of the animals. During the day (7 A.M. to 7 P.M.), when food consumption by the rats was greatly reduced, lipoprotein lipase activity in all muscles increased, followed by a decline to basal levels during the night. Similar oscillatory changes in lipoprotein lipase activity were observed in the muscles of diabetic rats fed ad libitum. In normal rats deprived of food, however, the oscillatory changes in muscle lipoprotein lipase activity were not abolished and persisted for at least 48 h. In diabetic rats starved during a 48-h period, the oscillatory changes in muscle lipoprotein lipase activity were markedly altered. In all animals, muscle lipoprotein lipase activities were not correlated to plasma glucagon levels.

Response of lipoprotein lipase to calorie intake in streptozotocin-induced diabetic rats

1992 ◽  
Vol 52 (8) ◽  
pp. 797-802 ◽  
Author(s):  
H. Inadera ◽  
J. Tashiro ◽  
Y. Okubo ◽  
Y. Ishikawa ◽  
K. Shirai ◽  
...  
Keyword(s):  
Lipoprotein Lipase ◽  
Diabetic Rats ◽  
Calorie Intake

Diabetes reduces heparin- and phospholipase C-releasable lipoprotein lipase from cardiomyocytes

1991 ◽  
Vol 260 (3) ◽  
pp. E477-E485 ◽  
Author(s):  
J. E. Braun ◽  
D. L. Severson
Keyword(s):  
Cell Surface ◽  
Phospholipase C ◽  
Lipoprotein Lipase ◽  
Cardiac Myocytes ◽  
Myocardial Cell ◽  
Diabetic Rats ◽  
Capillary Endothelium ◽  
Rat Hearts ◽  
Isolated Cardiac Myocytes ◽  
Covalently Linked

Incubation of isolated cardiac myocytes from rat hearts with heparin or phosphatidylinositol-specific phospholipase C (PLC) resulted in the release of lipoprotein lipase (LPL) into the medium. The release of LPL by the combination of heparin and PLC was not additive, and preincubation of cardiac myocytes with heparin eliminated the release of LPL in a subsequent incubation with PLC. This evidence suggests that LPL may be bound ionically to heparan sulfate proteoglycans that are covalently linked to the cell surface of cardiac myocytes by a phosphatidylinositol-glycan membrane anchor; a second pool of LPL may also be bound to proteoglycans attached directly to the myocardial cell surface. The induction of diabetes by the administration of streptozotocin (100 mg/kg for 3-4 days) to rats resulted in a decrease in the initial cellular activity of LPL and a marked reduction in the heparin-induced secretion of LPL into the medium of cardiac myocytes. The intravenous administration of insulin (5 U for 1 h) in diabetic rats reversed the effects of diabetes on cellular and heparin-releasable LPL activities. Diabetes also reduced the PLC-induced release of LPL. The reduction in the release of LPL from diabetic cardiac myocytes could result in a decrease in functional LPL activity at the capillary endothelium of whole hearts.

Olive cake reduces glycaemia and lipemia and increases antioxidant enzymes in STZ-induced diabetes in rat erythrocytes and tissues

2019 ◽  
Vol 50 (2) ◽  
pp. 360-372
Author(s):  
Hayet Cherrad ◽  
Sherazede Bouderbala ◽  
Yahiaoui Zidan ◽  
Djamil Krouf
Keyword(s):  
Antioxidant Enzymes ◽  
Heart Muscle ◽  
Design Methodology ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Thiobarbituric Acid Reactive Substances ◽  
Olive Cake ◽  
Sod Activity ◽  
Content Type ◽  
Antioxidant Enzymes Activities

Purpose The purpose of this study is to determine the effect of olive cake (CO) on glycaemia and lipemia and lipid peroxidation and antioxidant enzymes activities in erythrocytes and tissues, in streptozotocin (STZ)-induced diabetic rats. Design/methodology/approach Diabetes was induced by a single intraperitoneal injection of STZ (55 mg/kg BW). In total, 12 diabetic D rats, weighing 260 ± 20 g, were divided into two groups fed a casein diet supplemented (D-OC) or not (D) with OC (7.5 per cent), for four weeks. Findings In D-OC compared with D, glycaemia, total cholesterol and triglycerides values (−40 per cent; p = 0.007, 27 per cent; p = 0.007 and −27 per cent; p = 0.0019). In erythrocyte, liver, kidney, heart, muscle and brain, thiobarbituric acid reactive substances contents were respectively, (−19 per cent; p = 0.03, −32 per cent; p = 0.002, −20 per cent; p = 0.04, −68 per cent; p = 0.003, −74 per cent; p = 0.0003 and −38 per cent; p = 0.04). In erythrocyte, SOD, GSH-Px and CAT activities were respectively, (+14 per cent; p = 0.01, +74 per cent; p = 0.012 and +34 per cent; p = 0.0009). In the liver, kidney, heart and muscle, SOD activity was respectively, (+31 per cent; p = 0.004, +12 per cent; p = 0.038, +43 per cent; p = 0.001 and +23 per cent; p = 0.18). GSH-Px activity was respectively, (+121 per cent; p = 0.0009, 89 per cent; p = 0.0006, + 95 per cent; p = 0.008, +71 per cent; p = 0.02 and +26 per cent; p = 0.01), in the liver, kidney, heart, muscle and brain. Catalase activity was (+21 per cent; p = 0.008) in the liver, (+88 per cent; p = 0.0002 in the kidney, +53 per cent; p = 0,002 in the heart and 83 per cent; p = 0.00004 in the muscle). Originality/value In diabetic rats, OC reduces hyperglycaemia induced by STZ and attenuates triglyceridemia and cholesterolemia. This residue is able to decrease the oxidative stress by increasing the antioxidant enzymes activity in erythrocytes and tissues. The high contents of phytoconstituents present in OC are considered to be responsible for this effect.

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