The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
“New” hepatic fat activates PPARα to maintain glucose, lipid, and cholesterol homeostasis
Open accessAbstract
De novo lipogenesis is an energy-expensive process whose role in adult mammals is poorly understood. We generated mice with liver-specific inactivation of fatty-acid synthase (FAS), a key lipogenic enzyme. On a zero-fat diet, FASKOL (FAS knockout in liver) mice developed hypoglycemia and fatty liver, which were reversed with dietary fat. These phenotypes were also observed after prolonged fasting, similarly to fasted PPARalpha-deficiency mice. Hypoglycemia, fatty liver, and defects in expression of PPARalpha target genes in FASKOL mice were corrected with a PPARalpha agonist. On either zero-fat or chow diet, FASKOL mice had low serum and hepatic cholesterol levels with elevated SREBP-2, decreased HMG-CoA reductase expression, and decreased cholesterol biosynthesis; these were also corrected with a PPARalpha agonist. These results suggest that products of the FAS reaction regulate glucose, lipid, and cholesterol metabolism by serving as endogenous activators of distinct physiological pools of PPARalpha in adult liver.
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Cites
SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver
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“Palmitate as well as laurate (12:0) and stearate (18:0) have been shown to transactivate PPARα using reporter gene constructs (Kliewer et al., 1997; Gottlicher et al., 1992).”
BackgroundInsulin-regulated hepatic gluconeogenesis through FOXO1–PGC-1α interaction
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Efficient in vivo manipulation of mouse genomic sequences at the zygote stage.
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PGC-1 promotes insulin resistance in liver through PPAR-α-dependent induction of TRB-3
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Skeletal muscle respiratory uncoupling prevents diet-induced obesity and insulin resistance in mice
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Self-citation
Cited by
Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications
Fabbrini, E., Sullivan, S., & Klein, S. (2010) · Hepatology · doi:10.1002/hep.23280 · Cited by 2,100
Human Fatty Liver Disease: Old Questions and New Insights
Cohen, J. C., Horton, J. D., & Hobbs, H. H. (2011) · Science · doi:10.1126/science.1204265 · Cited by 2,089
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Badman, M. K., Pissios, P., Kennedy, A. R., Koukos, G., Flier, J. S., & Maratos-Flier, E. (2007) · Cell Metabolism · doi:10.1016/j.cmet.2007.05.002 · Cited by 1,495
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
Metadata
- Authors
- Chakravarthy, M. V., Pan, Z., Zhu, Y., Tordjman, K., Schneider, J. G., Coleman, T., Turk, J., & Semenkovich, C. F.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2005-05
- Volume
- 1
- Issue
- 5
- Pages
- 309-322
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W1972744939
- Cited by
- 545
- References
- 8
- FWCI
- 8.18
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Chakravarthy, M. V., Pan, Z., Zhu, Y., Tordjman, K., Schneider, J. G., Coleman, T., Turk, J., & Semenkovich, C. F. (2005). “New” hepatic fat activates PPARα to maintain glucose, lipid, and cholesterol homeostasis. Cell Metabolism. https://doi.org/10.1016/j.cmet.2005.04.002
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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