The control of sugar uptake by metabolic demand in isolated adult rat heart cells.
To investigate the control of sugar uptake by metabolic demand, we used isolated quiescent adult rat heart cells in suspension, under conditions similar to those found during anoxia. Metabolic demand was varied by exposing cells to rotenone plus various levels of p-trifluoromethoxyphenylhydrazone. Without glucose, the time taken for half of the cells to undergo contracture was inversely proportional to the metabolic demand as measured by the rate of lactate production. For any metabolic demand, the onset of contracture was preceded by a sudden drop in adenosine triphosphate. The permeability of contracted cells to glucose was investigated using 3-O-methylglucose. The rate of 3-O-methylglucose uptake by such cells was strongly dependent on the time taken for half the cells to undergo contracture, with low rates at low times to half contracture, and insulin-like rates at high times to half contracture. This suggests that the full induction of glucose transport by metabolic demand can be prematurely curtailed by the loss of adenosine triphosphate. This phenomenon appeared to limit glucose utilization in cells with a high metabolic demand when glucose was present: such cells underwent contracture unless insulin was also present, the rate of glucose uptake as measured with 2-deoxyglucose was inhibited, and the rate of lactate production was inhibited. Isoproterenol depressed glucose transport by two mechanisms. First, by stimulating the basal metabolic demand of the cell it reduced the time taken for half the cells to undergo contracture and, hence, the level of induced sugar transport. Second, it significantly delayed the onset of sugar permeability with respect to the contracture event.(ABSTRACT TRUNCATED AT 250 WORDS)
- Copyright © 1986 by American Heart Association