Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 305, Issue 11, Pages E1359-E1366Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00236.2013
Keywords
cytokines; diabetes; glucose metabolism; lipid metabolism; gene expression
Categories
Funding
- Swedish Research Council
- European Foundation for the Study of Diabetes
- European Research Council
- Swedish Diabetes Association
- Strategic Research Foundation
- Knut and Alice Wallenberg Foundation
- Novo Nordisk Research Foundation
- Johan and Jakob Soderbergs Foundation
- Diabetes Wellness Foundation
- Stockholm County Council Swedish Heart and Lung Foundation
- Diabetes Research Programme at Karolinska Institutet
- Swedish Society of Medicine
- Novo Nordisk Fonden [NNF12OC1016320] Funding Source: researchfish
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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.
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