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Expression profiling following local muscle inactivity in humans provides new perspective on diabetes-related genes
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2006 (English)In: Genomics, ISSN 0888-7543, Vol. 87, no 1, 165-172 p.Article in journal (Refereed) Published
Abstract [en]

Physical activity enhances muscle mitochondrial gene expression, while inactivity and mitochondrial dysfunction are both risk factors for developing diabetes. Defective activation of the transcriptional coactivator PGC-1 may contribute to the gene expression pattern observed in diabetic and insulin-resistant skeletal muscle. We proposed that greater insight into the mitochondrial component of skeletal muscle “diabetes” would be possible if the clinical transcriptome data were contrasted with local muscle inactivity-induced modulation of mitochondrial genes in otherwise healthy subjects. We studied PPARGC1A (PGC-1), PPARGC1B (PGC-1β), NRF1, and a variety of mitochondrial DNA (mtDNA) and nuclear-encoded mitochondrial genes critical for oxidative phosphorylation in soleus muscle biopsies obtained from six healthy men and women before and after 5 weeks of local muscle inactivity. Muscle inactivity resulted in a coordinated down-regulation of PGC-1 and genes involved with mitochondrial metabolism, including muscle substrate delivery genes. Decreased expression of the mtDNA helicase Twinkle was related to the decline in mitochondrial RNA polymerase (r = 0.83, p < 0.04), suggesting that mtDNA transcription and replication are coregulated in human muscle tissue. In contrast to the situation in diabetes, PGC-1β expression was not significantly altered, while NRF1 expression was actually up-regulated following muscle inactivity. We can conclude that reduced PGC-1 expression described in Type 2 diabetes may be partly explained by muscle inactivity. Further, although diabetes patients are typically inactive, our analysis indicates that local muscle inactivity may not be expected to contribute to the decreased NRF1 and PGC-1β expression noted in insulin-resistant and Type 2 diabetes patients, suggesting these changes may be more disease specific.

Place, publisher, year, edition, pages
2006. Vol. 87, no 1, 165-172 p.
Keyword [en]
gene expression, human skeletal muscle, unloading
Keyword [sv]
Idrottsvetenskap
National Category
Sport and Fitness Sciences
Identifiers
URN: urn:nbn:se:miun:diva-4651DOI: 10.1016/j.ygeno.2005.09.007Local ID: 5849OAI: oai:DiVA.org:miun-4651DiVA: diva2:29683
Available from: 2008-09-30 Created: 2008-09-30Bibliographically approved

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CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf