Characterization of a Heart-specific Fatty Acid Transport Protein
Open accessAbstract
Fatty acids are a major source of energy for cardiac myocytes. Changes in fatty acid metabolism have been implicated as causal in diabetes and cardiac disease. The mechanism by which long chain fatty acids (LCFAs) enter cardiac myocytes is not well understood but appears to occur predominantly by protein-mediated transport. Here we report the cloning, expression pattern, and subcellular localization of a novel member of the fatty acid transport protein (FATP) family termed FATP6. FATP6 is principally expressed in the heart where it is the predominant FATP family member. Similar to other FATPs, transient and stable transfection of FATP6 into 293 cells enhanced uptake of LCFAs. FATP6 mRNA was localized to cardiac myocytes by in situ hybridization. Immunofluorescence microscopy of FATP6 in monkey and murine hearts revealed that the protein is exclusively located on the sarcolemma. FATP6 was restricted in its distribution to areas of the plasma membrane juxtaposed with small blood vessels. In these membrane domains FATP6 also colocalizes with another molecule involved in LCFA uptake, CD36. These findings suggest that FATP6 is involved in heart LCFA uptake, in which it may play a role in the pathogenesis of lipid-related cardiac disorders.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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?
The loss of FATP6 (SLC27A6) indicates that sugars replace fatty acids as the major energy source in the heart of fruit bats.
“For example, the loss of FATP6 (SLC27A6) that transports fatty acids into cardiac myocytes41 indicates that sugars replace fatty acids as the major energy source in the heart.”
From A genomics approach reveals insights into the importance of gene losses for mammalian adaptations (2018) · cites this paper as [41]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
No references could be resolved yet.
Research works printed but not linked: 3
- Hirsch, D., Stahl, A., and Lodish, H. F. (1998) Proc. Natl. Acad. Sci. U. S. A. 95, 8625-8629
- Slot, J. W., Geuze, H. J., Gigengack, S., James, D. E., and Lienhard, G. E. (1991) Proc. Natl. Acad. Sci. U. S. A. 88, 7815-7819
- Strauss, A. W., Powell, C. K., Hale, D. E., Anderson, M. M., Ahuja, A., Brackett, J. C., and Sims, H. F. (1995) Proc. Natl. Acad. Sci. U. S. A. 92, 10496 -10500
Cited by
Sorted by citations
A general introduction to the biochemistry of mitochondrial fatty acid β‐oxidation
Houten, S. M., & Wanders, R. J. A. (2010) · Journal of Inherited Metabolic Disease · doi:10.1007/s10545-010-9061-2 · Cited by 1,020 · see citing works
AMPK regulation of fatty acid metabolism and mitochondrial biogenesis: implications for obesity.
O’Neill, H. M., Holloway, G. P., & Steinberg, G. R. (2013) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2012.06.019 · Cited by 364 · see citing works
A genomics approach reveals insights into the importance of gene losses for mammalian adaptations
Sharma, V., Hecker, N., Roscito, J. G., Foerster, L., Langer, B. E., & Hiller, M. (2018) · Nature Communications · doi:10.1038/s41467-018-03667-1 · Cited by 237 · see citing works
Tissue-specific mRNA expression profiles of human solute carrier transporter superfamilies
Nishimura, M., & Naito, S. (2008) · Drug Metabolism and Pharmacokinetics · doi:10.2133/dmpk.23.22 · Cited by 190 · see citing works
Intramuscular lipid metabolism, insulin action, and obesity
Consitt, L. A., Bell, J. A., & Houmard, J. A. (2009) · IUBMB Life · doi:10.1002/iub.142 · Cited by 180 · see citing works
Targeting fatty acid metabolism to improve glucose metabolism
Stinkens, R., Goossens, G. H., Jocken, J. W. E., & Blaak, E. E. (2015) · Obesity Reviews · doi:10.1111/obr.12298 · Cited by 183 · see citing works
Talanian, J. L., Holloway, G. P., Snook, L. A., Heigenhauser, G. J. F., Bonen, A., & Spriet, L. L. (2010) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00073.2010 · Cited by 167 · see citing works
Fuel availability and fate in cardiac metabolism: a tale of two substrates
Pascual, F., & Coleman, R. A. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2016.03.014 · Cited by 125 · see citing works
Jain, S. S., Chabowski, A., Snook, L. A., Schwenk, R. W., Glatz, J. F. C., Luiken, J. J. F. P., & Bonen, A. (2009) · FEBS Letters · doi:10.1016/j.febslet.2009.06.020 · Cited by 96 · see citing works
Activation of AMPKα2 Is Not Required for Mitochondrial FAT/CD36 Accumulation during Exercise
Monaco, C., Whitfield, J., Jain, S. S., Spriet, L. L., Bonen, A., & Holloway, G. P. (2015) · PLOS ONE · doi:10.1371/journal.pone.0126122 · Cited by 27 · see citing works
- Authors
- Gimeno, R. E., Ortegon, A. M., Patel, S., Punreddy, S., Ge, P., Sun, Y., Lodish, H. F., & Stahl, A.
- Affiliations
- Palo Alto Medical Foundation (US)
- Whitehead Institute for Biomedical Research (US)
- Takeda Oncology (United States) (US)
- Corresponding author
- Stahl, Andreas
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2003-05
- Volume
- 278
- Issue
- 18
- Pages
- 16039-16044
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1992956691
- Cited by
- 218
- References
- 0
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 5 · 2023: 13 · 2022: 12 · 2021: 5 · 2020: 6 · 2019: 8 · 2018: 5 · 2017: 8 · 2016: 6 · 2015: 8 · 2014: 5 · 2013: 11 · 2012: 10
- FWCI
- 4.42
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- University of Pittsburgh
- National Institutes of Health
- Medical Center, University of Pittsburgh
- National Heart, Lung, and Blood Institute (HL41484, P01HL041484)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 47618)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- fatty acid transporters, long-chain fatty acid uptake, cardiomyocytes, sarcolemma, CD36, subcellular localization, gene expression patterns, lipid metabolism, heart disease, diabetes mellitus
- MeSH terms
- Carrier Proteins, Cell Membrane, Chromosome Mapping, Cloning, Molecular, Fatty Acids, Humans, Membrane Proteins, Myocardium, Membrane Transport Proteins, Myocytes, Cardiac, Fatty Acid Transport Proteins
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