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Cited by 184

The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.

Overexpression of uncoupling protein 3 in skeletal muscle protects against fat-induced insulin resistance

Open access
Choi, Cheol Soo, Fillmore, Jonathan J., Kim, Jason K., Liu, Zhen-Xiang, Kim, Sheene, Collier, Emily F., Kulkarni, Ameya, Distefano, Alberto, Hwang, Yu-Jin, Kahn, Mario, Chen, Yan, Yu, Chunli, Moore, Irene K., Reznick, Richard M., Higashimori, Takamasa, Shulman, Gerald I.·2007·Journal of Clinical Investigation
DOI 10.1172/jci13579
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Abstract

Insulin resistance is a major factor in the pathogenesis of type 2 diabetes and is strongly associated with obesity. Increased concentrations of intracellular fatty acid metabolites have been postulated to interfere with insulin signaling by activation of a serine kinase cascade involving PKCtheta in skeletal muscle. Uncoupling protein 3 (UCP3) has been postulated to dissipate the mitochondrial proton gradient and cause metabolic inefficiency. We therefore hypothesized that overexpression of UCP3 in skeletal muscle might protect against fat-induced insulin resistance in muscle by conversion of intramyocellular fat into thermal energy. Wild-type mice fed a high-fat diet were markedly insulin resistant, a result of defects in insulin-stimulated glucose uptake in skeletal muscle and hepatic insulin resistance. Insulin resistance in these tissues was associated with reduced insulin-stimulated insulin receptor substrate 1- (IRS-1-) and IRS-2-associated PI3K activity in muscle and liver, respectively. In contrast, UCP3-overexpressing mice were completely protected against fat-induced defects in insulin signaling and action in these tissues. Furthermore, these changes were associated with a lower membrane-to-cytosolic ratio of diacylglycerol and reduced PKCtheta activity in whole-body fat-matched UCP3 transgenic mice. These results suggest that increasing mitochondrial uncoupling in skeletal muscle may be an excellent therapeutic target for type 2 diabetes mellitus.

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Metadata

Authors
Choi, C. S., Fillmore, J. J., Kim, J. K., Liu, Z.-X., Kim, S., Collier, E. F., Kulkarni, A., Distefano, A., Hwang, Y.-J., Kahn, M., Chen, Y., Yu, C., Moore, I. K., Reznick, R. M., Higashimori, T., & Shulman, G. I.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2007-07-02
Volume
117
Issue
7
Pages
1995-2003
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci13579
OpenAlex
W1975982666
Cited by
184
References
33
FWCI
8.02
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Overexpression of uncoupling protein 3 in skeletal muscle protects against fat-induced insulin resistance. https://app.cochat.ai/papers/10.1172/jci13579
The paper
Choi, C. S., Fillmore, J. J., Kim, J. K., Liu, Z.-X., Kim, S., Collier, E. F., Kulkarni, A., Distefano, A., Hwang, Y.-J., Kahn, M., Chen, Y., Yu, C., Moore, I. K., Reznick, R. M., Higashimori, T., & Shulman, G. I. (2007). Overexpression of uncoupling protein 3 in skeletal muscle protects against fat-induced insulin resistance. Journal of Clinical Investigation. https://doi.org/10.1172/jci13579

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.