Molecular mechanisms regulating myocardial glucose oxidation.
In heart muscle regulation of pyruvate dehydrogenase (PDH) complex activity by reversible phosphorylation is the major determinant of glucose oxidation under physiological conditions and in diabetes. Altered mitochondrial concentrations of effectors of PDH kinase and phosphatase (metabolites, Ca2+, H+) appear to explain effects of oxidation of lipid fuels, myocardial contraction and ischaemia on PDH complex activity. The effects of diabetes and starvation are mediated in addition by protein(s) which increase the activity of PDH kinase. End product inhibition by NADH may be important in ischaemia.
D000818:Animals; D003327:Coronary Disease / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism*; D000860:Hypoxia / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010766:Phosphorylation; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism; D051381:Rats; D013217:Starvation / Q000378:metabolism; D013997:Time Factors
D011768:Pyruvate Dehydrogenase Complex; D005947:Glucose