The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Muscle wasting in insulinopenic rats results from activation of the ATP-dependent, ubiquitin-proteasome proteolytic pathway by a mechanism including gene transcription.
Open accessAbstract
In normal subjects and diabetic patients, insulin suppresses whole body proteolysis suggesting that the loss of lean body mass and muscle wasting in insulinopenia is related to increased muscle protein degradation. To document how insulinopenia affects organ weights and to identify the pathway for accelerated proteolysis in muscle, streptozotocin-treated and vehicle-injected, pair-fed control rats were studied. The weights of liver, adipose tissue, and muscle were decreased while muscle protein degradation was increased 75% by insulinopenia. This proteolytic response was not eliminated by blocking lysosomal function and calcium-dependent proteases at 7 or 3 d after streptozotocin. When ATP synthesis in muscle was inhibited, the rates of proteolysis were reduced to the same level in insulinopenic and control rats suggesting that the ATP-dependent, ubiquitin-proteasome pathway is activated. Additional evidence for activation of this pathway in muscle includes: (a) an inhibitor of proteasome activity eliminated the increased protein degradation; (b) mRNAs encoding ubiquitin and proteasome subunits were increased two- to threefold; and (c) there was increased transcription of the ubiquitin gene. We conclude that the mechanism for muscle protein wasting in insulinopenia includes activation of the ubiquitin-proteasome pathway with increased expression of the ubiquitin gene.
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Cites
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Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy
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Self-citationSkeletal muscle atrophy and the E3 ubiquitin ligases MuRF1 and MAFbx/atrogin-1
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Metadata
- Authors
- Price, S. R., Bailey, J. L., Wang, X., Jurkovitz, C., England, B. K., Ding, X., Phillips, L. S., & Mitch, W. E.
- Venue
- Journal of Clinical Investigation
- Published
- 1996-10-15
- Volume
- 98
- Issue
- 8
- Pages
- 1703-1708
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2102615617
- Cited by
- 349
- References
- 37
- FWCI
- 4.33
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Muscle wasting in insulinopenic rats results from activation of the ATP-dependent, ubiquitin-proteasome proteolytic pathway by a mechanism including gene transcription. https://app.cochat.ai/papers/10.1172/jci118968
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- Price, S. R., Bailey, J. L., Wang, X., Jurkovitz, C., England, B. K., Ding, X., Phillips, L. S., & Mitch, W. E. (1996). Muscle wasting in insulinopenic rats results from activation of the ATP-dependent, ubiquitin-proteasome proteolytic pathway by a mechanism including gene transcription. Journal of Clinical Investigation. https://doi.org/10.1172/jci118968
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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