Convertible adipose tissue in mice.
Abstract
Ability to express uncoupling protein (UCP) and establish UCP-dependent thermogenesis was analyzed in anatomical areas of mice that are generally considered to be white adipose tissue: mesenterial, perimetral, epididymal, inguinal, and superficial layer of interscapular white adipose tissue. The mice were acclimatized for 1 week to 4 degrees C; the following week they were exposed to cold stress (1 h at -20 degrees C, 2-3 times daily). In such conditions in inguinal adipose tissue, slot-blot analysis detected significant amount of UCP mRNA and lipoprotein lipase mRNA. Immuno-electron-microscopic localization of UCP showed that developed mitochondria of cold-stressed inguinal adipocytes contained UCP in the same amount as uncoupled (UC)-mitochondria of brown adipocytes. Morphological and morphometrical analysis showed that such inguinal adipose tissue appeared as brown adipose tissue. Since in control mice, inguinal adipose tissue was UCP-negative and tissue appeared as white adipose tissue, the duration of this white-to-brown adipose tissue conversion was analyzed. Mice, cold stressed for 1 week, were rewarmed at 28 degrees C and their inguinal adipose tissue was analyzed in comparison with interscapular brown adipose tissue and epididymal white adipose tissue for another 37 days. During that time inguinal adipocytes ceased expressing UCP mRNA; UC-mitochondria in inguinal adipocytes were destroyed and replaced with common, C-mitochondria; and UCP was undetectable immunohistochemically. Adipocytes accumulated lipids, and the tissue morphologically once again resembled white adipose tissue. Described changes showed that besides typical brown and white adipose tissue in mice, there existed a third type of adipose tissue described as convertible adipose tissue.
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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 [172]
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- Authors
- Lončar, D.
- Venue
- Cell and Tissue Research
- Published
- 1991-10
- Volume
- 266
- Issue
- 1
- Pages
- 149-161
- ISSN
- 0302-766X (ISSN-L)
- 1432-0878
- OpenAlex
- W2041068624
- Cited by
- 187
- References
- 55
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 7 · 2023: 5 · 2022: 6 · 2021: 10 · 2020: 7 · 2019: 6 · 2018: 14 · 2017: 7 · 2016: 14 · 2015: 9 · 2014: 10 · 2013: 9 · 2012: 7
- FWCI
- 1.49
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell and Tissue Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- uncoupling proteins, thermogenesis, cold stress, inguinal adipose tissue, brown adipose tissue, white adipose tissue, lipoprotein lipase
- MeSH terms
- Uncoupling Protein 1, Adipose Tissue, Animals, Adipose Tissue, Brown, Carrier Proteins, Cell Differentiation, Cold Temperature, Female, Ion Channels, Lipoprotein Lipase, Male, Membrane Proteins, Mitochondria, RNA, Messenger, Stress, Physiological, Mitochondrial Proteins, Mice
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