Search: onr:"swepub:oai:prod.swepub.kib.ki.se:124259333" >
Tissue-specific con...
Tissue-specific control of mitochondrial respiration in obesity-related insulin resistance and diabetes
-
Holmstrom, MH (author)
-
Iglesias-Gutierrez, E (author)
-
- Zierath, JR (author)
- Karolinska Institutet
-
show more...
-
Garcia-Roves, PM (author)
-
show less...
-
(creator_code:org_t)
- American Physiological Society, 2012
- 2012
- English.
-
In: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 1522-1555 .- 0193-1849. ; 302:6, s. E731-E739
- Related links:
-
http://kipublication...
-
show more...
-
https://doi.org/10.1...
-
show less...
Abstract
Subject headings
Close
- The tissue-specific role of mitochondrial respiratory capacity in the development of insulin resistance and type 2 diabetes is unclear. We determined mitochondrial function in glycolytic and oxidative skeletal muscle and liver from lean (+/ ?) and obese diabetic ( db/db) mice. In lean mice, the mitochondrial respiration pattern differed between tissues. Tissue-specific mitochondrial profiles were then compared between lean and db/db mice. In liver, mitochondrial respiratory capacity and protein expression, including peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), was decreased in db/db mice, consistent with increased mitochondrial fission. In glycolytic muscle, mitochondrial respiration, as well as protein and mRNA expression of mitochondrial markers, was increased in db/db mice, suggesting increased mitochondrial content and fatty acid oxidation capacity. In oxidative muscle, mitochondrial complex I function and PGC-1α and mitochondrial transcription factor A (TFAM) protein levels were decreased in db/db mice, along with increased level of proteins related to mitochondrial dynamics. In conclusion, mitochondrial respiratory performance is under the control of tissue-specific mechanisms and is not uniformly altered in response to obesity. Furthermore, insulin resistance in glycolytic skeletal muscle can be maintained by a mechanism independent of mitochondrial dysfunction. Conversely, insulin resistance in liver and oxidative skeletal muscle from db/db mice is coincident with mitochondrial dysfunction.
Publication and Content Type
- ref (subject category)
- art (subject category)
Find in a library
To the university's database