Hormone-stimulated lipolysis in cardiac myocytes

Palmer, W. K.; Kane, Teruyuki

doi:10.1042/bj2160241

Cited by 34 publications

(12 citation statements)

References 12 publications

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“…LPL activity was measured both in sonicated preparations and in acetone/ether-dried-powder preparations, and the myocardial cells were sensitive to the catecholamine, as evidenced by an increase in the phosphorylase a activity ratio. Thus we cannot confirm the report ofPalmer & Kane [15] that a 15 min incubation of myocytes with adrenaline could increase the serumstimulated lipase activity that has the characteristics of LPL. The reason for this discrepancy is not apparent.…”

Section: Discussioncontrasting

confidence: 50%

“…Our objective, therefore, was to determine the effect of isoprenaline and other interventions that increase cyclic AMP on heparin-releasable LPL activity, using cardiac myocytes isolated from adult rat hearts. Palmer & Kane [15] have shown that incubation of cardiac myocytes with adrenaline for 15 min resulted in a 35 % increase in an intracellular lipase activity that has the characteristics of LPL, and so the effect of isoprenaline on cellular LPL activity was also investigated.…”

Section: Introductionmentioning

confidence: 99%

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Short-term incubation of cardiac myocytes with isoprenaline has no effect on heparin-releasable or cellular lipoprotein lipase activity

Severson

Carroll

Kryski

et al. 1987

Biochemical Journal

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Heparin (5 units/ml) produced a rapid (5-10 min) release of lipoprotein lipase (LPL) into the incubation medium of cardiac myocytes. Preincubation of myocytes for 30 min with 0.01-10 microM-isoprenaline, 100 microM-forskolin or 500 microM-8-(4-chlorophenylthio)adenosine 3′,5′-cyclic monophosphate did not increase heparin-releasable LPL activity. Incubation with isoprenaline also did not change cellular LPL activity, even though the catecholamine did increase the phosphorylase a activity ratio.

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Section: Discussioncontrasting

confidence: 50%

Section: Introductionmentioning

confidence: 99%

Short-term incubation of cardiac myocytes with isoprenaline has no effect on heparin-releasable or cellular lipoprotein lipase activity

Severson

Carroll

Kryski

et al. 1987

Biochemical Journal

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“…This lipase exhibited all characteristics of lipoprotein lipase (stimulation by serum, inhibition by 1 M NaC1 and almost complete inhibition by anti-lipoprotein lipase antibodies). The presence of lipoprotein lipase in isolated myocytes and aorta confirms previous results (19)(20)(21)(22)(23)(24)(25)(26)(27)43). In addition, Ramirez et al (21) and Goldberg and Khoo (24) have recently described a very low and labile activity of a H. STAM ET AL.…”

Section: Distribution Of Acid and Neutral Cholesteryl Esterase Activisupporting

confidence: 86%

“…High acid and neutral triglyceride lipase and cholesteryl esterase activities have been described for aortic tissue and cultured macrophages, fibroblasts, lymphocytes and neutrophils (8,(10)(11)(12)(13)(14)(15)(16)(17)(18)(19). Furthermore, neutral triglyceride lipase activities, including lipoprotein lipase, have been described in isolated rat heart myocytes (20)(21)(22)(23).…”

mentioning

confidence: 99%

Cholesteryl esterase activities in ventricles, isolated heart cells and aorta of the rat

Stam

Broekhoven-Schokker

Schoonderwoerd

et al. 1987

Lipids

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Cholesteryl esterase activities were determined in homogenates of rat heart (ventricles), isolated, calcium-tolerant, cardiac myocytes and aortic tissue and were compared with acid and neutral triglyceride lipase activities in these fractions. Using cholesteryl oleate/phosphatidylcholine/taurocholate emulsions and digitonin pretreatment of the enzyme fractions, acid and neutral cholesteryl esterase activities were measured in all tissue preparations. In contrast to the acid and neutral triglyceridase and acid cholesteryl esterase activity, the neutral cholesteryl esterase activity was subject to substrate inhibition. Upon isolation of cardiac myocytes, and in contrast with the recovery of neutral triglyceride lipase activity, only a small portion of the neutral cholesteryl esterase (6%) was recovered, suggesting that nonmyocyte neutral cholesteryl esterase activity markedly contributes to the relatively high activity detectable in whole ventricular homogenates. The recovery of large amounts of neutral cholesteryl esterase activity in the supernatant of collagenase-digested heart tissue, obtained during the isolation of myocytes, which is also markedly enriched in activities of two endothelial marker enzymes (5'-nucleotidase and angiotensine-converting enzyme) may indicate the predominant contribution of neutral cholesteryl esterase activity from coronary endothelial cells to this activity detectable in ventricular homogenates. Relative to the activity in ventricular and myocyte homogenates, aorta homogenates possessed the highest specific neutral cholesteryl esterase activity. We propose that in addition to coronary endothelium, smooth muscle cells also contribute to the neutral cholesteryl esterase activity in ventricular homogenates.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Evidence also suggests that adrenaline affects LPL at a posttranslational level, changing the enzyme's secretion and activation (23). It has been observed that adrenaline decreases LPL activity in rat heart and in isolated cardiac myocytes (24). Others have observed that cAMP increases LPL synthesis within 2 h in isolated rat heart cells (25).…”

Section: Discussionmentioning

confidence: 95%

Failure of the nonselective β‐blocker propranolol to affect lipoprotein lipase gene expression in the rat

Gouni-Berthold

Oka

Berthold

et al. 1997

Lipids

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Treatment with beta-blockers has been reported to be associated with the development of hypertriglyceridemia. The etiology, even the existence, of this phenomenon is controversial. The purpose of our study was to examine whether the nonselective beta-blocker propranolol causes hypertriglyceridemia in the rat and whether its action is mediated by the modulation of lipoprotein lipase (LPL) messenger RNA (mRNA) accumulation or activity. LPL activity was assayed in fresh tissue by incubation with tritiated triglycerides. LPL mRNA was quantified in total RNA by slot-blot analysis using a mouse LPL complementary DNA probe. We have conducted three series of experiments in unanaesthetized rats in order to study the effects of different single doses of propranolol (1.5 to 6 mg i.p.) and different durations of treatment (15 min to 4 wk). We measured triglyceride and cholesterol levels in plasma as well as the LPL activity and mRNA levels in the heart and adipose tissue before and after propranolol administration. In these experiments we did not find any significant decrease in either the activity or the amount of mRNA of lipoprotein lipase nor was there any change in plasma lipids following treatment. Our results lead us to the conclusion that the nonselective beta-blocker propranolol affects neither the activity nor the mRNA level of LPL in the rat.

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Hormone-stimulated lipolysis in cardiac myocytes

Cited by 34 publications

References 12 publications

Short-term incubation of cardiac myocytes with isoprenaline has no effect on heparin-releasable or cellular lipoprotein lipase activity

Short-term incubation of cardiac myocytes with isoprenaline has no effect on heparin-releasable or cellular lipoprotein lipase activity

Cholesteryl esterase activities in ventricles, isolated heart cells and aorta of the rat

Failure of the nonselective β‐blocker propranolol to affect lipoprotein lipase gene expression in the rat

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