Cited by 36Muscle Physiology and DisordersMitochondrial Function and PathologyAdipose Tissue and Metabolism

Expression of uncoupling protein 3 is upregulated in skeletal muscle during sepsis

Sun, Xiaoyan, Wray, Curtis, Tian, Xintian, Hasselgren, Per-Olof, Lu, James·2003·American Journal of Physiology-Endocrinology and Metabolism

Abstract

Uncoupling protein 3 (UCP3) is a member of the mitochondrial transporter superfamily that is expressed primarily in skeletal muscle. UCP3 is upregulated in various conditions characterized by skeletal muscle atrophy, including hyperthyroidism, fasting, denervation, diabetes, cancer, lipopolysaccharide (LPS), and treatment with glucocorticoids (GCs). The influence of sepsis, another condition characterized by muscle cachexia, on UCP3 expression and activity is not known. We examined UCP3 gene and protein expression in skeletal muscles from rats after cecal ligation and puncture and from sham-operated control rats. Sepsis resulted in a two- to threefold increase in both mRNA and protein levels of UCP3 in skeletal muscle. Treatment of rats with the glucocorticoid receptor antagonist RU-38486 prevented the sepsis-induced increase in gene and protein expression of UCP3. The UCP3 mRNA and protein levels were increased 2.4- to 3.6-fold when incubated muscles from normal rats were treated with dexamethasone (DEX) and/or free fatty acids (FFA ) ex vivo. In addition, UCP3 mRNA and protein levels were significantly increased in normal rat muscles in vivo with treatment of either DEX or FFA. The results suggest that sepsis upregulates the gene and protein expression of UCP3 in skeletal muscle, which may at least in part be mediated by GCs and FFA.

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Crossref · 10.1152/ajpendo.00446.2002

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  • UCP3 increases in skeletal muscle of mice during acute sepsis and inflammation as well as in skeletal muscle of NTIS patients, coinciding with increased DIO2 expression.

    “UCP3, which is a T3 target gene, increases in skeletal muscle of mice during acute sepsis [42] and inflammation [43] as well as in skeletal muscle of NTIS patients, coinciding with increased DIO2 expression [44].”

    From An update on non-thyroidal illness syndrome (2021) · cites this paper as [42]

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Authors
Sun, X., Wray, C., Tian, X., Hasselgren, P.-O., & Lu, J.
Affiliations
  • University of Cincinnati (US)
  • Harvard University (US)
Venue
American Journal of Physiology-Endocrinology and Metabolism
Published
2003-09
Volume
285
Issue
3
Pages
E512-E520
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
OpenAlex
W2086800162
Cited by
36
References
60
Citations by year
2026: 1 · 2025: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 4 · 2018: 1 · 2016: 1 · 2015: 2 · 2013: 2 · 2012: 2
FWCI
0.80
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of General Medical Sciences (T32GM008478)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 37908, R01DK037908)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
UCP3, sepsis, skeletal muscle, glucocorticoids, free fatty acids, dexamethasone, mifepristone, cecal ligation and puncture, gene expression, mitochondrial uncoupling
MeSH terms
Uncoupling Protein 3, Animals, Cachexia, Carrier Proteins, Dexamethasone, Fatty Acids, Nonesterified, Glucocorticoids, Ion Channels, Male, RNA, Messenger, Up-Regulation, Gene Expression, Rats, Sprague-Dawley, Muscle, Skeletal, Sepsis, Mitochondrial Proteins, Rats

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