Circulating levels of microRNA from children with newly diagnosed type 1 diabetes and healthy controls: Evidence that miR‐25 associates to residual beta‐cell …
LB Nielsen, C Wang, K Sørensen… - Journal of Diabetes …, 2012 - Wiley Online Library
LB Nielsen, C Wang, K Sørensen, CH Bang-Berthelsen, L Hansen, MLM Andersen…
Journal of Diabetes Research, 2012•Wiley Online LibraryThis study aims to identify key miRNAs in circulation, which predict ongoing beta‐cell
destruction and regeneration in children with newly diagnosed Type 1 Diabetes (T1D). We
compared expression level of sera miRNAs from new onset T1D children and age‐matched
healthy controls and related the miRNAs expression levels to beta‐cell function and
glycaemic control. Global miRNA sequencing analyses were performed on sera pools from
two T1D cohorts (n= 275 and 129, resp.) and one control group (n= 151). We identified …
destruction and regeneration in children with newly diagnosed Type 1 Diabetes (T1D). We
compared expression level of sera miRNAs from new onset T1D children and age‐matched
healthy controls and related the miRNAs expression levels to beta‐cell function and
glycaemic control. Global miRNA sequencing analyses were performed on sera pools from
two T1D cohorts (n= 275 and 129, resp.) and one control group (n= 151). We identified …
This study aims to identify key miRNAs in circulation, which predict ongoing beta‐cell destruction and regeneration in children with newly diagnosed Type 1 Diabetes (T1D). We compared expression level of sera miRNAs from new onset T1D children and age‐matched healthy controls and related the miRNAs expression levels to beta‐cell function and glycaemic control. Global miRNA sequencing analyses were performed on sera pools from two T1D cohorts (n = 275 and 129, resp.) and one control group (n = 151). We identified twelve upregulated human miRNAs in T1D patients (miR‐152, miR‐30a‐5p, miR‐181a, miR‐24, miR‐148a, miR‐210, miR‐27a, miR‐29a, miR‐26a, miR‐27b, miR‐25, miR‐200a); several of these miRNAs were linked to apoptosis and beta‐cell networks. Furthermore, we identified miR‐25 as negatively associated with residual beta‐cell function (est.: −0.12, P = 0.0037), and positively associated with glycaemic control (HbA1c) (est.: 0.11, P = 0.0035) 3 months after onset. In conclusion this study demonstrates that miR‐25 might be a “tissue‐specific” miRNA for glycaemic control 3 months after diagnosis in new onset T1D children and therefore supports the role of circulating miRNAs as predictive biomarkers for tissue physiopathology and potential intervention targets.
