Increased chain shortening of erucic acid in perfused heart from rats fed rapeseed oil

Norseth, John; Christiansen, Erling N.; Christophersen, Bjørn O.

doi:10.1016/0014-5793(79)80075-7

Cited by 23 publications

(8 citation statements)

References 8 publications

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“…Utilization of erucic acid by heart cells is likely preceded by a shortening step (PINSON & PADIEU, 1974) which is stimulated by continuous erucic acid feeding (NORSETH, 1979;NORSETH et al, 1979;BREMER & NORUM, 1982;CHRISTOPHERSEN et al, 1982) leading to regression of steatosis.…”

Section: Introductionmentioning

confidence: 97%

Erucic acid metabolism in rat heart. A combined biochemical and radioautographical study

Caselli¹,

Carlier²,

Bézard

1990

Archives Internationales de Physiologie et de Biochimie

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Section: Introductionmentioning

confidence: 97%

Erucic acid metabolism in rat heart. A combined biochemical and radioautographical study

Caselli¹,

Carlier²,

Bézard

1990

Archives Internationales de Physiologie et de Biochimie

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“…Our data agree with previous findings in mitochondrial preparations isolated from hearts of rats fed rapeseed oil (50). Therefore, the events leading to a decline in TG content are: (a) increased chain shortening of 22:1 by a peroxisomal, cyanide insensitive, 13-oxidation system in the liver, resulting in a decreased 22:1 content in the blood lipids and concomitantly to a reduced 22:1 delivery to the heart (3,17,51), (b) increased capacity for chain shortening of 22:1 in hearts from HEAR-and TE-fed rats (16) and (c) increased TG hydrolysis.…”

Section: Myocardial Lipidosis Lipolysis and Erucate Oxidationmentioning

confidence: 99%

“…This high fatty acid: BSA molar ratio was used to assure a high palmitate uptake by the heart (see 57 for a review). Since fatty acids do not affect myocardial adenyl cyclase activity (49), the inhibitory action of 16:0 is probably directly caused by feedback regulation of the tissue lipase activity. In previous reports (28,29) we showed mechanisms leading to enhanced fatty acid oxidation (increased contractility, uncoupling of oxidative phosphorylation) lead to stimulated glycerol release (lipase activity) in hearts from TE-fed rats.…”

Section: Regulation Of Triglyceride Hydrolysismentioning

confidence: 99%

“…During prolonged feeding of 22:l-enriched diets, intracellular cardiac TG levels decrease and may almost reach a normal value (14). In this process, a role of increased chain shortening of 22:1 by a peroxisomal /3-oxidation system in liver and heart has been considered (15)(16)(17). Recent studies from our laboratory (17)(18) have shown dietary erucic acid-induced cardiac lipidosis alters the rate of basal-and hormone-stimulated lipolysis.…”

Section: Introductionmentioning

confidence: 99%

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Erucic acid‐induced alteration of cardiac triglyceride hydrolysis

Stam

Geelhoed-Mieras

Hülsmann

1980

Lipids

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Male Wistar rats were fed for 3 or l 0 days with high erucic acid rapeseed oil (HEAR) or trierucate (TE). These diets produced increased myocardial triglyceride (TG) levels. Cardiac lipid accumulation was related to basal-and hormone-(glucagon, norepinephrine) stimulated lipolysis, determined as glycerol release, which proved to be enhanced in isolated, perfused hearts from HEAR-and TE-fed rats. Endogenous TG levels in isolated hearts from rats fed the stock and the sunflowerseed oil (SSO) diet were low and probably rate-limiting for tissue lipolytic activities. HEAR feeding of rats did not modify the rate of erucic acid (22: 1) oxidation in heart. Prolonged HEAR and TE feeding led to a decrease in the endogenous TG level, a process in which the increased rate of TG hydrolysis might play an important role. The enhanced breakdown of tissue TG in hearts from TE-and HEAR-fed rats was accompanied by an increased release of fatty acids into the coronary effluent. Erucic acid was a major constituent of the perfusate fatty acids. Evidence is presented that the site of the intracellular TG breakdown is associated with lysosomes, since a subcellular fraction enriched in acid lipase, N-acetyl-t3-glucosaminidase and TG could be isolated from heart homogenates of TE-fed rats. Fatty acids seemed to be an important regulator of tissue lipase activity: palmitate inhibited glucagon-stimulated lipolysis, which suggests the tissue lipase is subject to product inhibition by fatty acids.

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“…The intracellular triglycerides are present as cytosolic lipid droplets (35) and membrane-bound particles (3), probably of lysosomal origin (5,8,9,38,39). Cell fractionation studies have revealed the presence of a lysosomal fraction enriched in triglycerides (1,19,34). Sevcral lipases have been demonstrated in heart tissue but the lipase responsible for basal and glucagonstimulated endogenous lipolysis is still a matter of dispute, although the inhibition of lipolysis in isolated perfused rat hearts in the presence of methylamine (11,12,22) and other lysosomotropic agents (8) favors a distinctive role of the acid lysosomal lipase in the lipolysis of endogenous triglycerides.…”

Section: Introductionmentioning

confidence: 99%

Involvement of lysosome-like particles in the metabolism of endogenous myocardial triglycerides during ischemia/reperfusion. Uptake and degradation of triglycerides by lysosomes isolated from rat heart

et al. 1990

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The hormonal regulation and enzymatic basis of endogenous lipolysis in heart are not yet completely elucidated. The lysosomal fraction from rat heart appeared to be markedly enriched in triglycerides and a significant reduction in triglycerides in this fraction was found after prolonged perfusion or stimulation of lipolysis with glucagon. The enhanced rate of lipolysis, measured as glycerol release from the isolated perfused rat heart, was abolished 10-15 min after continuous glucagon administration. Omission of glucagon for another 60 min restored the ability of glucagon to stimulate lipolysis, indicating the limited availability of endogenous triglycerides and the presence of a transfer-system for triglycerides from a non-metabolically active pool to a metabolically active pool. The enhanced lipolysis induced by low-flow ischemia was found to be inhibited by the lysosomotropic agent methylamine (5 mM). Methylamine-perfusion during low-flow ischemia was accompanied by an increased recovery of myocardial triglycerides in the lysosomal fraction. The possible role of lysosome-like particles in myocardial triglyceride homeostasis was further investigated by studying the kinetics of uptake and degradation of labeled triglycerides by membrane-particles recovered in the subcellular fraction enriched with lysosomal marker enzymes. It appeared that isolated lysosomal membranes take up added triglycerides at an average rate of 30 nmoles/min/g protein. The bulk of these triglycerides taken up is stored whereas 20% is degraded to diglycerides and free fatty acids. More than 90% of the free fatty acids formed were released from the lysosomes into the supernatant. The uptake and degradation of triglyceride-filled liposomes by isolated myocardial lysosomes was inhibited during incubation with methylamine (5 mM). On the other hand, a lowering of pH during in vitro incubation increased the rate of uptake and degradation of added triglycerides by isolated lysosomes. These results indicate that lysosomes or lysosome-like particles are involved in the enhanced lipolysis during myocardial ischemia.

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Increased chain shortening of erucic acid in perfused heart from rats fed rapeseed oil

Cited by 23 publications

References 8 publications

Erucic acid metabolism in rat heart. A combined biochemical and radioautographical study

Erucic acid metabolism in rat heart. A combined biochemical and radioautographical study

Erucic acid‐induced alteration of cardiac triglyceride hydrolysis

Involvement of lysosome-like particles in the metabolism of endogenous myocardial triglycerides during ischemia/reperfusion. Uptake and degradation of triglycerides by lysosomes isolated from rat heart

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