Research data for article – SCD4 deficiency decreases cardiac steatosis and prevents cardiac remodeling in mice fed a high-fat diet

Results collected as part of the project titled “Stearoyl-CoA desaturase as a novel regulator of cardiomyocyte maturation” financed by the National Science Center. The study showed that the stearoyl-CoA deaturase 4 (SCD4) gene knockout did not affect the beating rate and rise time of contraction, but increased the amplitude of contraction and decreased the relaxation time after contraction of neonatal cardiomyocytes (P0). Treatment of neonatal cardiomyocytes with stearic acid (18:0), an SCD substrate, increased the beating rate of SCD4-silenced cardiomyocytes compared to wild-type (WT) control cells. In contrast, stearic acid had no effect on contraction amplitude or rise time in both WT cardiomyocytes and cardiomyocytes lacking SCD4. Treatment of cardiomyocytes with 18:0 impaired the relaxation of WT cells, as evidenced by prolonged fall time after contraction, while it had no effect on this parameter in SCD4 knockout cardiomyocytes. In conclusion, the absence of SCD4 preserved the contractile function of neonatal cardiomyocytes treated with 18:0. SCD4 knockout increased the activity of adipocyte-specific triacylglycerol lipase (ATGL) in primary neonatal cardiomyocytes (P0), indicating an increased rate of lipolysis in these cells. This may have influenced the reduced number and size of lipid droplets observed in SCD4-deficient primary cardiomyocytes treated with 18:0. Therefore, SCD4 gene knockout reduces fatty acid-stimulated lipid accumulation in SCD4-knockout neonatal cardiomyocytes, which may affect energy metabolism and cardiac maturation at later stages.