The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
PPARγ coactivator 1β/ERR ligand 1 is an ERR protein ligand, whose expression induces a high-energy expenditure and antagonizes obesity.
Open accessAbstract
A well balanced body energy budget controlled by limitation of calorie uptake and/or increment of energy expenditure, which is typically achieved by proper physical exercise, is most effective against obesity and diabetes mellitus. Recently, peroxisome proliferator-activated receptor (PPAR) gamma, a member of the nuclear receptor, and its cofactors have been shown to be involved in lipid metabolism and in the control of energy expenditure. Here we show that PPARgamma coactivator 1 (PGC-1) beta functions as ERRL1 (for ERR ligand 1), which can bind and activate orphan ERRs (estrogen receptor-related receptors) in vitro. Consistently, PGC-1beta/ERRL1 transgenic mice exhibit increased expression of the medium-chain acyl CoA dehydrogenase, a known ERR target and a pivotal enzyme of mitochondrial beta-oxidation in skeletal muscle. As a result, the PGC-1beta/ERRL1 mice show a state similar to an athlete; namely, the mice are hyperphagic and of elevated energy expenditure and are resistant to obesity induced by a high-fat diet or by a genetic abnormality. These results demonstrate that PGC-1beta/ERRL1 can function as a protein ligand of ERR, and that its level contributes to the control of energy balance in vivo, and provide a strategy for developing novel antiobesity drugs.
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“In addition, PGC-1␣ and PGC-1 coactivate different nuclear receptors (272).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [272]
In the citing paper
“Taken together, these studies suggest that modest overexpression of PGC-1␣ (261, 262) and transgenic overexpression of PGC-1 (271, 272) increase oxidative metabolism and insulin sensitivity.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [272]
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“Consistent with these findings, whole-body transgenic overexpression of PGC-1 resulted in increased oxidative metabolism, protection from obesity induced by high-fat diet or hyperphagia, and enhanced insulin sensitivity (272).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [272]
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Cites
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Research works printed but not linked: 1
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Sorted by citations
Wallace, D. C. (2005) · Annual Review of Genetics · doi:10.1146/annurev.genet.39.110304.095751 · Cited by 3,185
Metabolic control through the PGC-1 family of transcription coactivators
Lin, J., Handschin, C., & Spiegelman, B. M. (2005) · Cell Metabolism · doi:10.1016/j.cmet.2005.05.004 · Cited by 2,130
“…+ ND fatty-acid oxidation Wang et al., 2003 PPARγ + + UCP1/GyK induction Guan et al., 2005; Puigserver et al., 1998 Huss et al., 2002; Huss et al., 2004; Kamei et al., 2003; ERRα,β,γ + + mitochondrial genes Mootha et al., 2004; Schreiber et al., 2004 TRβ + + cpt-1 induction Wu et al., 2002; Zhang…”
BackgroundInfluentialPGC-1 coactivators: inducible regulators of energy metabolism in health and disease
Finck, B. N. (2006) · Journal of Clinical Investigation · doi:10.1172/jci27794 · Cited by 1,461
Transcriptional regulatory circuits controlling mitochondrial biogenesis and function
Kelly, D. P., & Scarpulla, R. C. (2004) · Genes & Development · doi:10.1101/gad.1177604 · Cited by 1,243
The Human Obesity Gene Map: The 2005 Update
Rankinen, T., Zuberi, A., Chagnon, Y. C., Weisnagel, S. J., Argyropoulos, G., Walts, B., Pérusse, L., & Bouchard, C. (2006) · Obesity · doi:10.1038/oby.2006.71 · Cited by 1,119
Metadata
- Authors
- Kamei, Y., Ohizumi, H., Fujitani, Y., Nemoto, T., Tanaka, T., Takahashi, N., Kawada, T., Miyoshi, M., Ezaki, O., & Kakizuka, A.
- Affiliations
- Kyoto University (JP)
- Corresponding author
- Kakizuka, Akira
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2003-10-06
- Volume
- 100
- Issue
- 21
- Pages
- 12378-12383
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC218766
- OpenAlex
- W1965989272
- Cited by
- 357
- References
- 26
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 11 · 2023: 8 · 2022: 6 · 2021: 12 · 2020: 11 · 2019: 12 · 2018: 14 · 2017: 10 · 2016: 9 · 2015: 16 · 2014: 11 · 2013: 15 · 2012: 16
- FWCI
- 8.04
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- PGC-1β, orphan nuclear receptor, protein ligands, energy expenditure, obesity resistance, high-fat diet, medium-chain acyl-CoA dehydrogenase, mitochondrial beta-oxidation, skeletal muscle, hyperphagia, energy balance, anti-obesity drugs
- MeSH terms
- ERRalpha Estrogen-Related Receptor, Amino Acid Sequence, Animals, Base Sequence, DNA, Energy Metabolism, Ligands, Mice, Transgenic, Molecular Sequence Data, Obesity, Receptors, Estrogen, Recombinant Proteins, Transcription Factors, Gene Expression, Receptors, Cytoplasmic and Nuclear, Mice
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