ABSTRACT
AIM:To investigate the serum miRNA-101 expression level in patients with newly diagnosed type 2 diabetes mellitus (T2DM),and to evaluate the clinical implications of miRNA-101 expression level variation.METHODS:qRT-PCR was used to determine the serum miRNA-101 expression level.Pearson correlation analysis was performed to observe the relationship between two variables.Multiple stepwise linear regression analysis was used to assess the association of serum miRNA-101 level and other parameters.RESULTS:Serum miRNA-101 level in patients with newly diagnosed T2DM was significantly higher than that in control subjects (P ＜ 0.05).The serum level of miRNA-101 was positively correlated with the glycosylated hemoglobin A1c (HbA1c,P ＜0.05).Multiple linear regression analysis revealed that the circulating miRNA-101 was in significant positive correlation with HbA1c (P ＜ 0.05) after adjustment for age,sex and body weight.CONCLUSION:Enhanced circulating miRNA-101 level in newly diagnosed T2DM patients may be associated with elevation of HbA1 c.
ABSTRACT
ObjectiveTo explore the relationship between hypoxia induced by cobalt chloride( CoCl2 ) and inflammation in 3T3-LI adipocytes, and the underlying molecular mechanism. Methods3T3-L1 pre-adipocytes were induced under standard differentiation process. Differentiated 3T3-L1 adipocytes were incubated with CoCl2 to induce hypoxia. The mRNA and protein expressions of hypoxia inducible factor-1 α ( HIF-1 α ), glucose transporter 1 ( Glut1 ), adipocytokines, and inflammatory cytokines, as well as the related signaling pathways were determined with quantitative realtime-PCR and Western-blot in this cell model. ResultsCoCl2 at the concentration of 200 μmol/L significantly up-regulated HIF-1 α and Glut1 expressions. After adipocytes were treated with CoCl2, the mRNA levels of endoplasmic reticulum stress marker genes, such as C/EBP homologous protein (CHOP) and glucose-regulated protein78 (GRP78) were markedly increased, adiponectin mRNA expression was significantly decreased, while resistin and leptin mRNA expressions were significantly increased.In addition, the mRNA expressions of cyclooxygenase 2, interleukin-6, and other inflammatory factors were also increased. The phosphorylation of IκBα,which could inhibit the activation of NF-κB, was stimulated by CoCl2.ConclusionsThe results indicate that hypoxia may induce inflammatory response via NF-κB activiation in adipocytes.