Advances in Nutritional Research 1980
DOI: 10.1007/978-1-4757-4448-4_8
|View full text |Cite
|
Sign up to set email alerts
|

The Metabolism of Long-Chain Monoenoic Fatty Acids in Heart Muscle and Their Cardiopathogenic Implications

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2

Citation Types

0
2
0

Year Published

1982
1982
2016
2016

Publication Types

Select...
3
3

Relationship

0
6

Authors

Journals

citations
Cited by 9 publications
(2 citation statements)
references
References 94 publications
0
2
0
Order By: Relevance
“…The mode of action for cardiac lipidosis outlined for rats exposed to erucic acid is also consistent with observations made with structurally related fatty acids and with other species of experimental animals. Oils containing other monounsaturated fatty acids with 20 or more carbon atoms also induce transient cardiac lipidosis in rats and are poor substrates for mitochondrial b-oxidation (Sauer and Kramer, 1980). Based on in vitro data, the pig heart appears to be somewhat more efficient in the b-oxidation of erucic acid compared to the rat heart.…”
Section: Cardiac Lipidosismentioning
confidence: 99%
See 1 more Smart Citation
“…The mode of action for cardiac lipidosis outlined for rats exposed to erucic acid is also consistent with observations made with structurally related fatty acids and with other species of experimental animals. Oils containing other monounsaturated fatty acids with 20 or more carbon atoms also induce transient cardiac lipidosis in rats and are poor substrates for mitochondrial b-oxidation (Sauer and Kramer, 1980). Based on in vitro data, the pig heart appears to be somewhat more efficient in the b-oxidation of erucic acid compared to the rat heart.…”
Section: Cardiac Lipidosismentioning
confidence: 99%
“…It regresses after termination but also upon continuation of the high erucic acid diet. Numerous studies suggest that the major reason for this adaptation resides in the induction of the peroxisomal b-oxidation system of the liver and also in the heart, whereas the mitochondrial b-oxidation systems appear not to be induced in both organs (Sauer and Kramer, 1980;Bremer and Norum, 1982). As a high proportion of the dietary fat (estimated to be at least 50%) passes through the liver, an enhanced hepatic peroxisomal b-oxidation of erucic acid would lower the influx of this fatty acid to the heart and eventually lead to the regression of cardiac lipidosis, facilitated by the rapid turnover (estimated to be about 5 h) of cardiac triacylglycerols.…”
Section: Cardiac Lipidosismentioning
confidence: 99%