IL-10 prevents aging-associated inflammation and insulin resistance in skeletal muscle
Authors
Dagdeviren, SezinJung, Dae Young
Friedline, Randall H.
Noh, Hye Lim
Kim, Jong Hun
Patel, Payal R.
Tsitsilianos, Nicholas
Inashima, Kunikazu
Tran, Duy A.
Hu, Xiaodi
Loubato, Marilia M.
Craige, Siobhan M.
Kwon, Jung Yeon
Lee, Ki Won.
Kim, Jason K.
UMass Chan Affiliations
UMass Metabolic NetworkDepartment of Medicine, Division of Cardiovascular Medicine
Program in Molecular Medicine
Document Type
Journal ArticlePublication Date
2016-11-03Keywords
cytokinesinterleukins
aging
type 2 diabetes
glucose metabolism
Cellular and Molecular Physiology
Endocrinology
Endocrinology, Diabetes, and Metabolism
Metadata
Show full item recordAbstract
Altered energy balance and insulin resistance are important characteristics of aging. Skeletal muscle is a major site of glucose disposal, and the role of aging-associated inflammation in skeletal muscle insulin resistance remains unclear. To investigate, we examined glucose metabolism in 18-mo-old transgenic mice with muscle-specific overexpression of IL-10 (MIL10) and in wild-type mice during hyperinsulinemic-euglycemic clamping. Despite similar fat mass and energy balance, MIL10 mice were protected from aging-associated insulin resistance with significant increases in glucose infusion rates, whole-body glucose turnover, and skeletal muscle glucose uptake ( approximately 60%; P < 0.05), as compared to age-matched WT mice. This protective effect was associated with decreased muscle inflammation, but no changes in adipose tissue inflammation in aging MIL10 mice. These results demonstrate the importance of skeletal muscle inflammation in aging-mediated insulin resistance, and our findings further implicate a potential therapeutic role of anti-inflammatory cytokine in the treatment of aging-mediated insulin resistance.Source
FASEB J. 2016 Nov 3. pii: fj.201600832R. Link to article on publisher's siteDOI
10.1096/fj.201600832RPermanent Link to this Item
http://hdl.handle.net/20.500.14038/28805PubMed ID
27811060Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1096/fj.201600832R