α1-Adrenergic receptors increase glucose oxidation under normal and ischemic conditions in adult mouse cardiomyocytes

• Published in: Journal of receptors and signal transduction 2021-03, Vol.41 (2), p.138-144
• Main Authors: Papay, Robert S., Perez, Dianne M.
• Format: Article
• Language: English
• Subjects: alpha1-adrenergic; G-protein coupled receptor; Glucose; metabolism; oxidation
• ISSN: 1079-9893; 1532-4281
• DOI: 10.1080/10799893.2020.1799291

The role of catecholamine receptors in cardiac energy metabolism is unknown. α 1 -adrenergic receptors (α 1 -ARs) have been identified to play a role in whole body metabolism but its role in cardiac energy metabolism has not been explored. We used freshly prepared primary adult mouse cardiomyocytes and incubated with either 14 C-palmitate or 14 C-glucose tracers to measure oxidation rates in the presence or absence of phenylephrine, an α 1 -AR agonist (with β and α 2 -AR blockers) under normal cell culture conditions. 14 CO 2 released was collected over a 10 min period in covered tissue culture plates using a 1 M hyamine hydroxide solution placed in well cups, counted by scintillation and converted into nmoles/hr. We found that phenylephrine stimulated glucose oxidation but not fatty acid oxidation in adult primary cardiomyocytes. α 1 -AR stimulated glucose oxidation was blocked by the AMPK inhibitor, dorsomorphin dihydrochloride, and the PKC inhibitor, rottlerin. Ischemic conditions were induced by lowering the glucose concentration from 22.5 mM to 1.375 mM. Under ischemic conditions, we found that phenylephrine also increased glucose oxidation. We report a direct role of α 1 -ARs in regulating glucose oxidation under normal and ischemic conditions that may lead to new therapeutic approaches in treating ischemia.