期刊
DIABETES
卷 68, 期 3, 页码 515-526出版社
AMER DIABETES ASSOC
DOI: 10.2337/db18-0470
关键词
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资金
- Strategic Diabetes Program at Karolinska Institute
- European Research Council Ideas Program (ICEBERG) [ERC-2008-AdG23285]
- Vetenskapsradet (Swedish Research Council) [2011-3550, 2012-1760, 2015-165]
- Swedish Diabetes Foundation [DIA2015-032, DIA2015-052]
- Stiftelsen for Strategisk Forskning (Swedish Foundation for Strategic Research) [SRL10-0027]
- Diabetes Wellness Sweden
- Novo Nordisk Foundation [NNF14OC0009941]
- Swedish Research Council for Sport Science [FO2016-0005]
- Swedish Heart Lung Foundation [20150423]
- Stockholm Lans Landsting (Stockholm County Council)
- Swedish Foundation for Strategic Research (SSF) [SRL10-0027] Funding Source: Swedish Foundation for Strategic Research (SSF)
miRNAs are noncoding RNAs representing an important class of gene expression modulators. Extracellular circulating miRNAs are both candidate biomarkers for disease pathogenesis and mediators of cell-to-cell communication. We examined the miRNA expression profile of total serum and serum-derived exosome-enriched extracellular vesicles in people with normal glucose tolerance or type 2 diabetes. In contrast to total serum miRNA, which did not reveal any differences in miRNA expression, we identified differentially abundant miRNAs in patients with type 2 diabetes using miRNA expression profiles of exosome RNA (exoRNA). To validate the role of these differentially abundant miRNAs on glucose metabolism, we transfected miR-20b-5p, a highly abundant exoRNA in patients with type 2 diabetes, into primary human skeletal muscle cells. miR-20b-5p overexpression increased basal glycogen synthesis in human skeletal muscle cells. We identified AKTIP and STAT3 as miR-20b-5p targets. miR-20b-5p overexpression reduced AKTIP abundance and insulin-stimulated glycogen accumulation. In conclusion, exosome-derived extracellular miR-20b-5p is a circulating biomarker associated with type 2 diabetes that plays an intracellular role in modulating insulin-stimulated glucose metabolism via AKT signaling.
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