Induced Cre‐mediated knockdown of Brca1 in skeletal muscle reduces mitochondrial respiration and prevents glucose intolerance in adult mice on a high‐fat diet Article Swipe
Kathryn C. Jackson
,
Michael D. Tarpey
,
Ana P. Valencia
,
Melissa R. Iñigo
,
Stephen J. P. Pratt
,
Daniel J. Patteson
,
Joseph M. McClung
,
Richard M. Lovering
,
David M. Thomson
,
Espen E. Spangenburg
·
YOU?
·
· 2018
· Open Access
·
· DOI: https://doi.org/10.1096/fj.201700464r
YOU?
·
· 2018
· Open Access
·
· DOI: https://doi.org/10.1096/fj.201700464r
The breast cancer type 1 susceptibility protein (Brca1) is a regulator of DNA repair in mammary gland cells; however, recent cell culture evidence suggests that Brca1 influences other processes, including those in nonmammary cells. In this study, we sought to determine whether Brca1 is necessary for metabolic regulation of skeletal muscle using a novel in vivo mouse model. We developed an inducible skeletal muscle‐specific Brca1‐knockout (BRCA1KO smi ) model to test whether Brca1 expression is necessary for maintenance of metabolic function of skeletal muscle when exposed to a high‐fat diet (HFD). Our data demonstrated that deletion of Brca1 prevented HFD‐induced alterations in glucose and insulin tolerance. Irrespective of diet, BRCA1KO smi mice exhibited significantly lower ADP‐stimulated complex I mitochondrial respiration rates compared to age‐matched wild‐type (WT) mice. The data show that Brca1 has the ability to localize to the mitochondria in skeletal muscle and that BRCA1KO smi mice exhibit higher whole‐body CO 2 production, respiratory exchange ratio, and energy expenditure, compared with the WT mice. Our results demonstrate that loss of Brca1 in skeletal muscle leads to dysregulated metabolic function, characterized by decreased mitochondrial respiration. Thus, any condition that results in loss of Brca1 function could induce metabolic imbalance in skeletal muscle.—Jackson, K. C., Tarpey, M. D., Valencia, A. P., Iñigo, M. R., Pratt, S. J., Patteson, D. J., McClung, J. M., Lovering, R. M., Thomson, D. M., Spangenburg, E. E. Induced Cre‐mediated knockdown of Brca1 in skeletal muscle reduces mitochondrial respiration and prevents glucose intolerance in adult mice on a high‐fat diet. FASEB J. 32, 3070–3084 (2018). www.fasebj.org
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1096/fj.201700464r
- https://www.fasebj.org/doi/pdf/10.1096/fj.201700464R
- OA Status
- bronze
- Cited By
- 18
- References
- 23
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W2788550016
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Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W2788550016Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1096/fj.201700464rDigital Object Identifier
- Title
-
Induced Cre‐mediated knockdown of Brca1 in skeletal muscle reduces mitochondrial respiration and prevents glucose intolerance in adult mice on a high‐fat dietWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2018Year of publication
- Publication date
-
2018-01-26Full publication date if available
- Authors
-
Kathryn C. Jackson, Michael D. Tarpey, Ana P. Valencia, Melissa R. Iñigo, Stephen J. P. Pratt, Daniel J. Patteson, Joseph M. McClung, Richard M. Lovering, David M. Thomson, Espen E. SpangenburgList of authors in order
- Landing page
-
https://doi.org/10.1096/fj.201700464rPublisher landing page
- PDF URL
-
https://www.fasebj.org/doi/pdf/10.1096/fj.201700464RDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
bronzeOpen access status per OpenAlex
- OA URL
-
https://www.fasebj.org/doi/pdf/10.1096/fj.201700464RDirect OA link when available
- Concepts
-
Skeletal muscle, Endocrinology, Internal medicine, Gene knockdown, Biology, Respiration, Mitochondrion, Respiratory exchange ratio, Glucose uptake, Knockout mouse, Cell biology, Apoptosis, Insulin, Medicine, Anatomy, Biochemistry, Receptor, Heart rate, Blood pressureTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
18Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 1, 2022: 3, 2021: 5, 2020: 2, 2019: 3Per-year citation counts (last 5 years)
- References (count)
-
23Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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