Mitochondrial remodeling in adipose tissue associated with obesity and treatment with rosiglitazone.
Open accessAbstract
Adipose tissue plays a central role in the control of energy homeostasis through the storage and turnover of triglycerides and through the secretion of factors that affect satiety and fuel utilization. Agents that enhance insulin sensitivity, such as rosiglitazone, appear to exert their therapeutic effect through adipose tissue, but the precise mechanisms of their actions are unclear. Rosiglitazone changes the morphological features and protein profiles of mitochondria in 3T3-L1 adipocytes. To examine the relevance of these effects in vivo, we studied white adipocytes from ob/ob mice during the development of obesity and after treatment with rosiglitazone. The levels of approximately 50% of gene transcripts encoding mitochondrial proteins were decreased with the onset of obesity. About half of those genes were upregulated after treatment with rosiglitazone, and this was accompanied by an increase in mitochondrial mass and changes in mitochondrial structure. Functionally, adipocytes from rosiglitazone-treated mice displayed markedly enhanced oxygen consumption and significantly increased palmitate oxidation. These data reveal mitochondrial remodeling and increased energy expenditure in white fat in response to rosiglitazone treatment in vivo and suggest that enhanced lipid utilization in this tissue may affect whole-body energy homeostasis and insulin sensitivity.
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Higher mitochondrial density and even UCP1 can be induced in response to pharmacological or genetic alterations of white adipocytes, suggesting that white adipose tissue could potentially be induced to acquire more oxidative metabolic phenotypes, promoting increased fuel consumption and thus energy expenditure.
“Higher mitochondrial density and even UCP1 can be induced in response to pharmacological or genetic alterations of white adipocytes (170 -177), suggesting that white adipose tissue could potentially be induced to acquire more oxidative metabolic phenotypes, promoting increased fuel consumption and thus energy expenditure.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [177]
Both genetic and diet-induced obesity result in decreased mitochondrial density and OXPHOS activity in adipose tissue, potentially contributing to adipose tissue dysfunction and exacerbation of insulin resistance.
“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 [177]
Administration of thiazolidinediones induces changes in mitochondrial content and remodeling in white adipocytes concomitantly with an improvement in insulin sensitivity.
“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 [177]
White adipocyte mitochondrial content is decreased in both rodent and human obesity and correlates with insulin resistance that accompanies obesity.
“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 [177]
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- Authors
- Wilson-Fritch, L., Nicoloro, S., Chouinard, M., Lazar, M. A., Chui, P. C., Leszyk, J., Straubhaar, J., Czech, M. P., & Corvera, S.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- University of Pennsylvania (US)
- Corresponding author
- Corvera, Silvia
- Venue
- Journal of Clinical Investigation
- Published
- 2004-11-01
- Volume
- 114
- Issue
- 9
- Pages
- 1281-1289
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC524228
- OpenAlex
- W2022473709
- Cited by
- 616
- References
- 32
- Citations by year
- 2026: 4 · 2025: 13 · 2024: 21 · 2023: 19 · 2022: 23 · 2021: 17 · 2020: 34 · 2019: 22 · 2018: 28 · 2017: 32 · 2016: 32 · 2015: 36 · 2014: 42 · 2013: 44 · 2012: 33
- FWCI
- 15.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (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 (DK60837-02)
- Topics
- Health Sciences › Medicine › Physiology › 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 › Mitochondrial Function and Pathology
- Keywords
- mitochondrial remodeling, adipose tissue, obesity, rosiglitazone, white adipocytes, ob/ob mice, insulin sensitivity, energy homeostasis, mitochondrial mass, mitochondrial structure, oxygen consumption, palmitate oxidation, lipid utilization, 3T3-L1 adipocytes, mitochondrial gene expression
- MeSH terms
- Rosiglitazone, Adipose Tissue, Animals, Blood Glucose, Fatty Acids, Insulin, Mice, Inbred C57BL, Mice, Obese, Mice, Transgenic, Microscopy, Fluorescence, Mitochondria, Obesity, Oxygen, RNA, Messenger, Mass Spectrometry, Time Factors, Vasodilator Agents, Blotting, Northern, Blotting, Western, Adipocytes, RNA, Complementary, Chaperonin 60, Palmitic Acid, Oligonucleotide Array Sequence Analysis, 3T3-L1 Cells, Thiazolidinediones, PPAR gamma, Mice
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