Green Tea Modulates α₁-Adrenergic Stimulated Glucose Transport in Cultured Rat Cardiomyocytes

α₁-Adrenergic stimulation triggers glucose transport in the heart through the translocation of glucose transporter (GLUT) 1 and GLUT4 to plasma membranes, mediated by protein kinase C (PKC) isoforms. Evidence is emerging that dietary polyphenolic compounds may act not only as antioxidants but also by modulating PKC-mediated signaling. This study evaluated the ability of a green tea extract (GTE) to modulate α₁-adrenoceptor-mediated glucose transport in rat cardiomyocytes. GTE supplementation decreased phenylephrine (PhE)-stimulated glucose uptake and GLUT4 recruitment. PhE stimulation activated PKC α, β, δ, and ε, while GTE supplementation decreased the translocation of β and δ isoforms, but not α and ε, supporting the notion that GTE directly affects PKC activation and is a β and δ isoform-selective PKC inhibitor. Due to reactive oxygen species (ROS) involvement in pathological heart alterations, the observation that GTE is able to both inhibit effects originated by some PKC isoforms and counteract ROS deleterious effects could be important in the prevention/counteraction of these diseases.

Keywords: Green tea; cardiomyocytes; α₁-adrenergic stimulation; glucose transport; PKC isoforms