Hypomorphic mutation of PGC-1β causes mitochondrial dysfunction and liver insulin resistance.
Open accessAbstract
PGC-1beta is a transcriptional coactivator that potently stimulates mitochondrial biogenesis and respiration of cells. Here, we have generated mice lacking exons 3 to 4 of the Pgc-1beta gene (Pgc-1beta(E3,4-/E3,4-) mice). These mice express a mutant protein that has reduced coactivation activity on a subset of transcription factors, including ERRalpha, a major target of PGC-1beta in the induction of mitochondrial gene expression. The mutant mice have reduced expression of OXPHOS genes and mitochondrial dysfunction in liver and skeletal muscle as well as elevated liver triglycerides. Euglycemic-hyperinsulinemic clamp and insulin signaling studies show that PGC-1beta mutant mice have normal skeletal muscle response to insulin but have hepatic insulin resistance. These results demonstrate that PGC-1beta is required for normal expression of OXPHOS genes and mitochondrial function in liver and skeletal muscle. Importantly, these abnormalities do not cause insulin resistance in skeletal muscle but cause substantially reduced insulin action in the liver.
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PGC-1β-null mice have more striking hepatic phenotypes, with hepatic insulin resistance, even on normal chow, and steatosis with high-fat feeding.
“PGC-1-null mice have more striking hepatic phenotypes, with hepatic insulin resistance, even on normal chow, and steatosis with high-fat feeding (59,65,66).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [65]
Insulin sensitivity in PGC-1β-null mice is reported to be normal.
“Insulin sensitivity in these animals is reported to be normal.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [65]
PGC-1β-null mice display phenotypes similar to, but not identical to, those of PGC-1α knockouts, including reduced expression of OXPHOS genes, reduced ATP synthesis, reduced exercise capacity, and impaired thermogenesis.
“PGC-1-null mice (59, 62, 65, 66) display phenotypes similar to, but not identical to, those of PGC-1␣ knockouts, including reduced expression of OXPHOS genes, reduced ATP synthesis, reduced exercise capacity, and impaired thermogenesis (59,62).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [65]
PGC-1β whole-body hypomorph reduced mitochondrial DNA by 30% and OXPHOS mRNA by 20-30% (Vianna, 2006).
“Vianna, 2006 PGC-1 whole-body 2 30% 20 -30% 2 mRNA | (65) hypomorph”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [65]
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- Authors
- Vianna, C. R., Huntgeburth, M., Coppari, R., Choi, C. S., Lin, J., Krauss, S., Barbatelli, G., Tzameli, I., Kim, Y.-B., Cinti, S., Shulman, G. I., Spiegelman, B. M., & Lowell, B. B.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Yale University (US)
- Harvard University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Spiegelman, Bruce M.
- Lowell, Bradford B.
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2006-12
- Volume
- 4
- Issue
- 6
- Pages
- 453-464
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2006339456
- Cited by
- 181
- References
- 43
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 8 · 2023: 3 · 2022: 2 · 2021: 1 · 2020: 4 · 2019: 5 · 2018: 5 · 2017: 7 · 2016: 8 · 2015: 6 · 2014: 13 · 2013: 12 · 2012: 17
- FWCI
- 11.27
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 49569, R01DK040936, R01DK049569, U24DK059635, R01DK061562, DK 61562)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- PGC-1β, hypomorphic mutation, mitochondrial dysfunction, hepatic insulin resistance, mitochondrial biogenesis, OXPHOS genes, estrogen-related receptor alpha, transcriptional coactivator, skeletal muscle insulin sensitivity, hepatic triglycerides, mitochondrial respiration
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, ERRalpha Estrogen-Related Receptor, Animals, Gene Expression Regulation, Hypoglycemic Agents, Insulin, Insulin Resistance, Liver, Mitochondria, Liver, Mitochondria, Muscle, Mutation, Organ Specificity, Receptors, Estrogen, Transcription Factors, Glucose Clamp Technique, Trans-Activators, Mice, Knockout, Muscle, Skeletal, Mitochondrial Proteins, Mice
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