Sökning: id:"swepub:oai:prod.swepub.kib.ki.se:127866724" >
Autocrine role of i...
Autocrine role of interleukin-13 on skeletal muscle glucose metabolism in type 2 diabetic patients involves microRNA let-7
-
- Jiang, LQ (författare)
- Karolinska Institutet
-
Franck, N (författare)
-
Egan, B (författare)
-
visa fler...
-
Sjogren, RJO (författare)
-
- Katayama, M (författare)
- Karolinska Institutet
-
Duque-Guimaraes, D (författare)
-
- Arner, P (författare)
- Karolinska Institutet
-
- Zierath, JR (författare)
- Karolinska Institutet
-
- Krook, A (författare)
- Karolinska Institutet
-
visa färre...
-
(creator_code:org_t)
- American Physiological Society, 2013
- 2013
- Engelska.
-
Ingår i: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 1522-1555 .- 0193-1849. ; 305:11, s. E1359-E1366
- Relaterad länk:
-
http://kipublication...
-
visa fler...
-
https://doi.org/10.1...
-
visa färre...
Abstract
Ämnesord
Stäng
- Low-grade inflammation associated with type 2 diabetes (T2DM) is postulated to exacerbate insulin resistance. We report that serum levels, as well as IL-13 secreted from cultured skeletal muscle, are reduced in T2DM vs. normal glucose-tolerant (NGT) subjects. IL-13 exposure increases skeletal muscle glucose uptake, oxidation, and glycogen synthesis via an Akt-dependent mechanism. Expression of microRNA let-7a and let-7d, which are direct translational repressors of the IL-13 gene, was increased in skeletal muscle from T2DM patients. Overexpression of let-7a and let-7d in cultured myotubes reduced IL-13 secretion. Furthermore, basal glycogen synthesis was reduced in cultured myotubes exposed to an IL-13-neutralizing antibody. Thus, IL-13 is synthesized and released by skeletal muscle through a mechanism involving let-7, and this effect is attenuated in skeletal muscle from insulin-resistant T2DM patients. In conclusion, IL-13 plays an autocrine role in skeletal muscle to increase glucose uptake and metabolism, suggesting a role in glucose homeostasis in metabolic disease.
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
Hitta via bibliotek
Till lärosätets databas