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J Biol Chem, Vol. 273, Issue 45, 29530-29539, November 6, 1998
From the Division of Cardiology, Department of Internal Medicine,
University of Texas-Houston Medical School, Houston, Texas 77030
We determined the contribution of all major
energy substrates (glucose, glycogen, lactate, oleate, and
triglycerides) during an acute increase in heart work (1 µM epinephrine, afterload increased by 40%) and
the involvement of key regulatory enzymes, using isolated working rat
hearts exhibiting physiologic values for contractile performance and
oxygen consumption. We accounted for oxygen consumption quantitatively
from the rates of substrate oxidation, measured on a minute-to-minute
basis. Total 
-oxidation (but not exogenous oleate oxidation) was
increased by the work jump, consistent with a decrease in the level of
malonyl-CoA. Glycogen and lactate were important buffers for carbon
substrate when heart work was acutely increased. Three mechanisms
contributed to high respiration from glycogen: 1) carbohydrate
oxidation was increased selectively; 2) stimulation of glucose
oxidation was delayed at glucose uptake; and 3) glycogen-derived
pyruvate behaved differently from pyruvate derived from extracellular
glucose. Despite delayed activation of pyruvate dehydrogenase relative
to phosphorylase, glycogen-derived pyruvate was more tightly coupled to
oxidation. Also, glycogen-derived lactate plus pyruvate contributed to
an increase in the relative efflux of lactate versus
pyruvate, thereby regulating the redox. Glycogen synthesis resulted
from activation of glycogen synthase late in the protocol but was timed
to minimize futile cycling, since phosphorylase a became
inhibited by high intracellular glucose.
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