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Mitochondrial biogenesis and remodeling during adipogenesis and in response to the insulin sensitizer rosiglitazone.
Open accessAbstract
White adipose tissue is an important endocrine organ involved in the control of whole-body metabolism, insulin sensitivity, and food intake. To better understand these functions, 3T3-L1 cell differentiation was studied by using combined proteomic and genomic strategies. The proteomics approach developed here exploits velocity gradient centrifugation as an alternative to isoelectric focusing for protein separation in the first dimension. A 20- to 30-fold increase in the concentration of numerous mitochondrial proteins was observed during adipogenesis, as determined by mass spectrometry and database correlation analysis. Light and electron microscopy confirmed a large increase in the number of mitochondrion profiles with differentiation. Furthermore, mRNA profiles obtained by using Affymetrix GeneChips revealed statistically significant increases in the expression of many nucleus-encoded mitochondrial genes during adipogenesis. Qualitative changes in mitochondrial composition also occur during adipose differentiation, as exemplified by increases in expression of proteins involved in fatty acid metabolism and of mitochondrial chaperones. Furthermore, the insulin sensitizer rosiglitazone caused striking changes in mitochondrial shape and expression of selective mitochondrial proteins. Thus, although mitochondrial biogenesis has classically been associated with brown adipocyte differentiation and thermogenesis, our results reveal that mitochondrial biogenesis and remodeling are inherent to adipose differentiation per se and are influenced by the actions of insulin sensitizers.
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“However, mitochondrial density increases dramatically, and mitochondrial remodeling occurs during white adipocyte differentiation (156 -158), suggesting that mitochondrial functions are required to support the multiple biological roles of mature white adipocytes.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [158]
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Metadata
- Authors
- Wilson-Fritch, L., Burkart, A., Bell, G., Mendelson, K., Leszyk, J., Nicoloro, S., Czech, M., & Corvera, S.
- Affiliations
- Program in Molecular Medicine
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Corvera, Silvia
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2003-02-01
- Volume
- 23
- Issue
- 3
- Pages
- 1085-1094
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC140688
- OpenAlex
- W2114978842
- Cited by
- 459
- References
- 28
- Citations by year
- 2026: 3 · 2025: 17 · 2024: 13 · 2023: 15 · 2022: 8 · 2021: 13 · 2020: 29 · 2019: 23 · 2018: 22 · 2017: 24 · 2016: 23 · 2015: 28 · 2014: 18 · 2013: 26 · 2012: 25
- FWCI
- 8.24
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-60837, R01DK060837)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- mitochondrial biogenesis, mitochondrial remodeling, adipogenesis, 3T3-L1 cells, rosiglitazone, insulin sensitizers, white adipose tissue, mitochondrial proteins, fatty acid metabolism, mitochondrial chaperone, mitochondrial morphology, gene expression profiling
- MeSH terms
- Rosiglitazone, Animals, Cell Differentiation, Insulin, Microscopy, Electron, Mitochondria, Oxygen Consumption, RNA, Messenger, Thiazoles, 3T3 Cells, Adipocytes, Mitochondrial Proteins, Thiazolidinediones, Mice
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