CoChat
Sign Up
Cited by 324Fatty Acid Research and HealthLipid metabolism and biosynthesisCardiovascular Function and Risk Factors

Saturated but not mono-unsaturated fatty acids induce apoptotic cell death in neonatal rat ventricular myocytes

Open access
de Vries, J E, Vork, M M, Roemen, T H, de Jong, Y F, Cleutjens, J P, van der Vusse, G J, van Bilsen, M·1997·Journal of Lipid Research
DOI 10.1016/s0022-2275(20)37421-6
Open this paper in CoChat — free account

Abstract

The energy need of cardiac muscle cells in vivo is largely covered by the oxidation of saturated and mono-unsaturated fatty acids (FA). However, in vitro studies have shown that the saturated FA C16:0 at physiological concentrations exerts detrimental effects on primary cultures of neonatal rat ventricular myocytes by, as yet, unknown mechanisms. To evaluate the noxious effects of FA in more detail, neonatal cardiomyocytes were exposed to saturated (C16:0; C18:0) or mono-unsaturated (C16:1; cis-C18:1; trans-C18:1) FA, or combinations thereof for up to 48 h. FA (0.5 mM) complexed to bovine serum albumin (BSA) (0.15 mM) were added to a glucose-containing defined medium. Irrespective of the length and degree of unsaturation of the aliphatic chain, FA supplied to the cells were readily incorporated in the phospholipid pool. In the presence of mono-unsaturated FA, cardiomyocytes remained healthy and accumulated substantial amounts of triacylglycerol. In contrast, within 24 h after application of the saturated FA C16:0 or C18:0, cells had become irreversibly damaged, as evidenced by the presence of pyknotic nuclei and massive release of the cytosolic markers lactate dehydrogenase (LDH) and fatty acid-binding protein (FABP). Moreover, the occurrence of DNA-laddering indicated that apoptosis was involved. Induction of apoptotic cell death by C16:0 was counteracted by the co-administration of equimolar amounts of cis-C18:1, whereas trans-C18:1 delayed, but did not prevent, loss of cardiomyocyte viability. The present findings suggest that the incorporation of saturated, but not mono-unsaturated, fatty acids induces alterations in the phospholipid membrane, which initiate apoptotic cell death in neonatal cardiomyocytes.

Integrity signals

Registry

Crossref · 10.1016/s0022-2275(20)37421-6

Cites

47 of 47 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Diets with increased saturated fat content, or exposure of cultured cells to saturated FA, promote apoptosis, which can be reversed by the addition of mono- or polyunsaturated FA.

    “Studies examining the effects of altering dietary FA composition have suggested that diets with increased saturated fat content, or exposure of cultured cells to saturated FA promote apoptosis, which can be reversed by the addition of mono- or polyunsaturated FA (PUFA) (74, 212, 236, 260).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [74]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
de Vries, J. E., Vork, M. M., Roemen, T. H., de Jong, Y. F., Cleutjens, J. P., van der Vusse, G. J., & van Bilsen, M.
Affiliations
Maastricht University (NL)
ORCID
Cleutjens, J P
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
1997-07
Volume
38
Issue
7
Pages
1384-1394
ISSN
0022-2275 (ISSN-L)
DOI
10.1016/s0022-2275(20)37421-6
OpenAlex
W2407618083
Cited by
324
References
47
Citations by year
2026: 2 · 2025: 3 · 2024: 8 · 2023: 3 · 2022: 7 · 2021: 12 · 2020: 8 · 2019: 8 · 2018: 9 · 2017: 9 · 2016: 14 · 2015: 9 · 2014: 7 · 2013: 21 · 2012: 16
FWCI
6.75
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Lipid Research (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Research Publications (Maastricht University) (publishedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords
saturated fatty acids, monounsaturated fatty acids, palmitic acid, stearic acid, cardiomyocyte apoptosis, neonatal rat ventricular myocytes, membrane damage, triglyceride accumulation, fatty acid oxidation, cardiotoxicity
MeSH terms
Fatty Acid-Binding Protein 7, Animals, Animals, Newborn, Carrier Proteins, Cells, Cultured, Culture Media, Fatty Acids, Fatty Acids, Monounsaturated, Glucose, Kinetics, L-Lactate Dehydrogenase, Myocardium, Neoplasm Proteins, Nerve Tissue Proteins, Phospholipids, Rats, Inbred WKY, Serum Albumin, Bovine, Triglycerides, Apoptosis, Myelin P2 Protein, Fatty Acid-Binding Proteins, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review