The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Liver-specific deletion of acetyl-CoA carboxylase 1 reduces hepatic triglyceride accumulation without affecting glucose homeostasis
Abstract
In animals, liver and white adipose are the main sites for the de novo fatty acid synthesis. Deletion of fatty acid synthase or acetyl-CoA carboxylase (ACC) 1 in mice resulted in embryonic lethality, indicating that the de novo fatty acid synthesis is essential for embryonic development. To understand the importance of de novo fatty acid synthesis and the role of ACC1-produced malonyl-CoA in adult mouse tissues, we generated liver-specific ACC1 knockout (LACC1KO) mice. LACC1KO mice have no obvious health problem under normal feeding conditions. Total ACC activity and malonyl-CoA levels were ≈70–75% lower in liver of LACC1KO mice compared with that of the WT mice. In addition, the livers of LACC1KO mice accumulated 40–70% less triglycerides. Unexpectedly, when fed fat-free diet for 10 days, there was significant up-regulation of PPARγ and several enzymes in the lipogenic pathway in the liver of LACC1KO mice compared with the WT mice. Despite the significant up-regulation of the lipogenic enzymes, including a >2-fold increase in fatty acid synthase mRNA, protein, and activity, there was significant decrease in the de novo fatty acid synthesis and triglyceride accumulation in the liver. However, there were no significant changes in blood glucose and fasting ketone body levels. Hence, reducing cytosolic malonyl-CoA and, therefore, the de novo fatty acid synthesis in the liver, does not affect fatty acid oxidation and glucose homeostasis under lipogenic conditions.
Overview
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
Verification
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?
Mice with liver ablation of Acaca and Scd1 have reduced liver TG levels.
“Furthermore, genetic studies have also demonstrated that mice with liver ablation of Acaca and Scd1 have reduced liver TG levels ( 57,58 ).”
From KSRP is critical in governing hepatic lipid metabolism through controlling Per2 expression (2015) · cites this paper as [57]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Molecular mediators of hepatic steatosis and liver injury
Browning, J. D., & Horton, J. D. (2004) · Journal of Clinical Investigation · doi:10.1172/jci200422422 · Cited by 1,772
The Mitochondrial Carnitine Palmitoyltransferase System — From Concept to Molecular Analysis
McGarry, J. D., & Brown, N. F. (1997) · European Journal of Biochemistry · doi:10.1111/j.1432-1033.1997.00001.x · Cited by 1,616
Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2
Abu-Elheiga, L., Matzuk, M. M., Abo-Hashema, K. A. H., & Wakil, S. J. (2001) · Science · doi:10.1126/science.1056843 · Cited by 903
Self-citationA possible role for malonyl-CoA in the regulation of hepatic fatty acid oxidation and ketogenesis.
McGarry, J. D., Mannaerts, G. P., & Foster, D. W. (1977) · Journal of Clinical Investigation · doi:10.1172/jci108764 · Cited by 736
An, J., Muoio, D. M., Shiota, M., Fujimoto, Y., Cline, G. W., Shulman, G. I., Koves, T. R., Stevens, R., Millington, D., & Newgard, C. B. (2004) · Nature Medicine · doi:10.1038/nm995 · Cited by 450
Savage, D. B. (2006) · Journal of Clinical Investigation · doi:10.1172/jci27300 · Cited by 447
Flagged first, then by citations
Research works printed but not linked: 26
- 10.1021/bi00437a001 · DOI
- 10.1096/fasebj.8.15.8001737 · DOI
- 10.1152/physrev.1995.75.1.47 · DOI
- 10.1146/annurev.nutr.17.1.325 · DOI
- 10.1146/annurev.bi.52.070183.002541 · DOI
- 10.1126/science.288.5475.2379 · DOI · Paper page
- 10.1006/bbrc.1996.1868 · DOI
- 10.1016/S0898-6568(97)00070-3 · DOI
- 10.1016/S0021-9258(19)84614-8 · DOI
- 10.1073/pnas.92.9.4011 · DOI
- 10.1074/jbc.272.16.10669 · DOI
- 10.1073/pnas.93.21.11466 · DOI
- 10.1073/pnas.85.16.5784 · DOI
- 10.1016/S0021-9258(18)69116-1 · DOI
- 10.1073/pnas.97.4.1444 · DOI
- 10.1073/pnas.0505714102 · DOI
- 10.1073/pnas.1733877100 · DOI · Paper page
- 10.1073/pnas.0409451102 · DOI
- 10.1073/pnas.0931394100 · DOI
- 10.1016/j.cmet.2005.04.002 · DOI
- 10.1172/JCI22422 · DOI · Paper page
- 10.1073/pnas.201524598 · DOI · Paper page
- 10.1101/gad.891301 · DOI · Paper page
- 10.1016/j.cmet.2004.11.004 · DOI
- 10.1146/annurev.biochem.73.011303.074027 · DOI
- 10.1194/jlr.M300094-JLR200 · DOI
Cited by
Sorted by citations
Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease
Ipsen, D. H., Lykkesfeldt, J., & Tveden-Nyborg, P. (2018) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-018-2860-6 · Cited by 1,471
De novo fatty acid synthesis controls the fate between regulatory T and T helper 17 cells
Berod, L., Friedrich, C., Nandan, A., Freitag, J., Hagemann, S., Harmrolfs, K., Sandouk, A., Hesse, C., Castro, C. N., Bähre, H., et al. (2014) · Nature Medicine · doi:10.1038/nm.3704 · Cited by 927
Fullerton, M. D., Galic, S., Marcinko, K., Sikkema, S., Pulinilkunnil, T., Chen, Z.-P., O'Neill, H. M., Ford, R. J., Palanivel, R., O'Brien, M., et al. (2013) · Nature Medicine · doi:10.1038/nm.3372 · Cited by 893
SIRT1 Regulates Hepatocyte Lipid Metabolism through Activating AMP-activated Protein Kinase
Hou, X., Xu, S., Maitland-Toolan, K. A., Sato, K., Jiang, B., Ido, Y., Lan, F., Walsh, K., Wierzbicki, M., Verbeuren, T. J., et al. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m802187200 · Cited by 778
Nonalcoholic fatty liver disease as a nexus of metabolic and hepatic diseases
Samuel, V. T., & Shulman, G. I. (2018) · Cell Metabolism · doi:10.1016/j.cmet.2017.08.002 · Cited by 745
“Mice lacking hepatic FGF21 are prone to developing glucose intolerance when placed on a high-fat diet (Markan et al., 2014), whereas FGF21 transgenic mice have enhanced glucose tolerance (Zhang et al.”
Fatty acid metabolism: Target for metabolic syndrome
Wakil, S. J., & Abu-Elheiga, L. A. (2009) · Journal of Lipid Research · doi:10.1194/jlr.r800079-jlr200 · Cited by 731
Self-citationRole of Dietary Fructose and Hepatic De Novo Lipogenesis in Fatty Liver Disease
Softic, S., Cohen, D. E., & Kahn, C. R. (2016) · Digestive Diseases and Sciences · doi:10.1007/s10620-016-4054-0 · Cited by 709
Kim, C.-W., Addy, C., Kusunoki, J., Anderson, N. N., Deja, S., Fu, X., Burgess, S. C., Li, C., Ruddy, M., Chakravarthy, M., et al. (2017) · Cell Metabolism · doi:10.1016/j.cmet.2017.07.009 · Cited by 419
Zhu, L., Brown, W. C., Cai, Q., Krust, A., Chambon, P., McGuinness, O. P., & Stafford, J. M. (2013) · Diabetes · doi:10.2337/db11-1718 · Cited by 326
Bates, J., Vijayakumar, A., Ghoshal, S., Marchand, B., Yi, S., Kornyeyev, D., Zagorska, A., Hollenback, D., Walker, K., Liu, K., et al. (2020) · Journal of Hepatology · doi:10.1016/j.jhep.2020.04.037 · Cited by 230
Alkhouri, N., Lawitz, E., Noureddin, M., DeFronzo, R., & Shulman, G. I. (2020) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2020.1668374 · Cited by 162
Regulation of Lipogenesis by Glucocorticoids and Insulin in Human Adipose Tissue
Gathercole, L. L., Morgan, S. A., Bujalska, I. J., Hauton, D., Stewart, P. M., & Tomlinson, J. W. (2011) · PLoS ONE · doi:10.1371/journal.pone.0026223 · Cited by 150
Dual mode action of mangiferin in mouse liver under high fat diet
Lim, J., Liu, Z., Apontes, P., Feng, D., Pessin, J. E., Sauve, A. A., Angeletti, R. H., & Chi, Y. (2014) · PLoS ONE · doi:10.1371/journal.pone.0090137 · Cited by 64
Insulin Regulation of Hepatic Lipid Homeostasis
Uehara, K., Santoleri, D., Whitlock, A. E. G., & Titchenell, P. M. (2023) · Comprehensive Physiology · doi:10.1002/cphy.c220015 · Cited by 49
KSRP is critical in governing hepatic lipid metabolism through controlling Per2 expression
Chou, C.-F., Zhu, X., Lin, Y.-Y., Gamble, K. L., Garvey, W. T., & Chen, C.-Y. (2015) · Journal of Lipid Research · doi:10.1194/jlr.m050724 · Cited by 20
Metadata
- Authors
- Mao, J., DeMayo, F. J., Li, H., Abu-Elheiga, L., Gu, Z., Shaikenov, T. E., Kordari, P., Chirala, S. S., Heird, W. C., & Wakil, S. J.
- Affiliations
- Molecular and Cell Biology and
- Pediatrics-Nutrition, Children’s Nutrition Research Center, Baylor College of Medicine, Houston, TX 77030
- *The Verna and Marrs McLean Department of Biochemistry and Molecular Biology and Departments of
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2006-05-30
- Volume
- 103
- Issue
- 22
- Pages
- 8552-8557
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 285
- References
- 6
- Language
- en
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
