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Adipose Mitochondrial Biogenesis Is Suppressed in db/db and High-Fat Diet–Fed Mice and Improved by Rosiglitazone
Abstract
The objective of this study was to further establish and confirm the relationship of adipose mitochondrial biogenesis in diabetes/obesity and the effects of rosiglitazone (RSG), a peroxisome proliferator-activated receptor (PPAR) gamma agonist, by systematically analyzing mitochondrial gene expression and function in two mouse models of obesity and type 2 diabetes. Using microarray technology, adipose mitochondrial gene transcription was studied in db/db, high-fat diet-fed C57BL/6 (HFD) and respective control mice with or without RSG treatment. The findings were extended using mitochondrial staining, DNA quantification, and measurements of citrate synthase activity. In db/db and HFD mice, gene transcripts associated with mitochondrial ATP production, energy uncoupling, mitochondrial ribosomal proteins, outer and inner membrane translocases, and mitochondrial heat-shock proteins were decreased in abundance, compared with db/+ and standard-fat diet-fed control mice, respectively. RSG dose-dependently increased these transcripts in both db/db and HFD mice and induced transcription of mitochondrial structural proteins and cellular antioxidant enzymes responsible for removal of reactive oxygen species generated by increased mitochondrial activity. Transcription factors, including PPAR coactivator (PGC)-1beta, PGC-1alpha, estrogen-related receptor alpha, and PPARalpha, were suppressed in both models and induced by RSG. The effects of RSG on adipose mitochondrial genes were confirmed by quantitative RT-PCR and further supported by mitochondrial staining, mitochondrial DNA quantification, and citrate synthase activity. Adipose mitochondrial biogenesis was overwhelmingly suppressed in both mouse models of diabetes/obesity and globally induced by RSG. These findings suggest an important role of adipose mitochondria in diabetes/obesity and the potential for new treatment approaches targeting adipose mitochondria.
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“Administration of thiazolidinediones induces changes in mitochondrial content and remodeling in white adipocytes concomitantly with an improvement in insulin sensitivity (170, 173, 177, 190, 194 -198).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [190]
In the citing paper
“Conversely, both genetic and dietinduced obesity result in decreased mitochondrial density and OXPHOS activity in adipose tissue (127, 177, 189 -191), potentially contributing to adipose tissue dysfunction and exacerbation of insulin resistance.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [190]
In the citing paper
“White adipocyte mitochondrial content is decreased in both rodent and human obesity (177, 188 -191) and correlates with insulin resistance that accompanies obesity.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [190]
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Metadata
- Authors
- Rong, J. X., Qiu, Y., Hansen, M. K., Zhu, L., Zhang, V., Xie, M., Okamoto, Y., Mattie, M. D., Higashiyama, H., Asano, S., Strum, J. C., & Ryan, T. E.
- Affiliations
- High Throughput Biology, Discovery Research, GlaxoSmithKline, Research Triangle Park, North Carolina
- GlaxoSmithKline (United States) (US)
- GlaxoSmithKline (Japan) (JP)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2007-07-01
- Volume
- 56
- Issue
- 7
- Pages
- 1751-1760
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2116872683
- Cited by
- 335
- References
- 48
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 14 · 2023: 16 · 2022: 17 · 2021: 13 · 2020: 21 · 2019: 19 · 2018: 16 · 2017: 23 · 2016: 27 · 2015: 23 · 2014: 27 · 2013: 23 · 2012: 17
- FWCI
- 9.58
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- rosiglitazone, type 2 diabetes, obesity, db/db mice, high-fat diet, PPARγ agonists, PGC-1α, PGC-1β, mitochondrial gene expression, mitochondrial DNA, citrate synthase, reactive oxygen species, antioxidant enzymes, mitochondrial uncoupling, mitochondrial heat shock proteins
- MeSH terms
- Rosiglitazone, Adipose Tissue, Animals, Diabetes Mellitus, Type 2, Dietary Fats, Disease Models, Animal, Hypoglycemic Agents, Male, Mice, Inbred C57BL, Mitochondria, Obesity, Transcription, Genetic, Gene Expression, Gene Expression Profiling, Thiazolidinediones, PPAR gamma, Mice
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