Skip to main content
Fig. 2 | Clinical Epigenetics

Fig. 2

From: The role of myocardial energy metabolism perturbations in diabetic cardiomyopathy: from the perspective of novel protein post-translational modifications

Fig. 2

Metabolic perturbations in cardiomyocytes in DbCM and acyl donor formation of novel PTMs. Insulin resistance leads to reduced extracellular glucose uptake and glycolysis in diabetic cardiomyocytes. Additionally, aerobic oxidation of pyruvate within the mitochondria is inhibited, resulting in increased lactate levels in cardiomyocytes. Free fatty acids and ketone β-HB serve as alternative energy sources to glucose, enhancing their supply to cardiomyocytes and promoting the uptake of fatty acids and β-oxidation. However, the metabolism of ketone bodies in cardiomyocytes is bidirectional, with acyl-CoA being both formed and consumed during energy metabolism, thereby influencing the corresponding PTMs. DbCM, diabetic cardiomyopathy; β-HB, β-hydroxybutyrate; GLUT, glucose transporter; TCA cycle, tricarboxylic acid cycle; BDH1, β-hydroxybutyrate dehydrogenase 1; SCOT, succinyl-CoA:3-ketoacid CoA transferase; SCS, succinyl-CoA synthetase; AcAc, acetoacetic acid; FACS, fatty acyl-CoA synthetase; NADH, nicotinamide adenine dinucleotide; FADH2, flavin adenine dinucleotide hydrogen transmitter 2

Back to article page

Clinical Epigenetics

ISSN: 1868-7083

Contact us