Myocardial gene expression of type 2 diabetic mice with and without treatment with glucokinase activator
Chronic inflammation is a hallmark of obesity type II diabetes (T2D) accompanied by increased circulating inflammatory T-cells. Diabetic cardiomyopathy (dbCM) is characterised by systemic inflammation, disrupted metabolism and impaired cardiac function. However, whether T-cell mediated cardiac autoimmunity is present in dbCM and causally linked to cardiac metabolic remodelling remains unknown. We used db/db transgenic mouse model of dbCM and an integrated in vivo and ex vivo experimental approach to examine the impact of T-cell mediated inflammation on cardiac function and metabolic disturbances in T2D. Furthermore, we used  glucokinase activator AZD1656 drug intervention for six weeks in db/db mice to examine whether we can improve metabolic remodeling and cardiac inflammation in dbCM. This drug has been previously shown to target metabolism of T cells and with anti-inflammatory effect.  In this data set, we used RNA extracted from the snap-frozen hearts (control, db/db and AZD1656-treated db/db hearts, n=5/group) analysed by massive analysis of cDNA End (MACE-Seq, 1x75 bps Illumina; MACE: 5 Million reads / library).