AJP - Cell Physiology, Vol 257, Issue 5 C913-C919, Copyright © 1989 by American Physiological Society
Protein metabolism during nutrient deprivation and refeeding of neonatal heart cells
N. A. Schroedl, C. R. Bacon, Y. C. Huang and C. R. Hartzell
Research Department, Alfred I. duPont Institute of the Nemours Foundation, Wilmington, Delaware.
Pathological conditions or nutrient deprivation in the heart cause an
imbalance between rates of protein synthesis and degradation, often
resulting in a severe depletion of cardiac protein. We used cultured
neonatal rat heart cells, a model system exhibiting positive nitrogen
balance, to examine the effects of 10 h of starvation on myocardial glucose
and protein metabolism. Cellular capacity for glucose utilization was
depressed after starvation, as evidenced by lower hexokinase and other
glycolytic enzyme activities and a 21% decrease in glucose usage. A 21.0%
decrease in protein synthetic rate and an increase in protein degradation
rate combined to yield a 29.5% decrease in total cellular protein during
starvation. Degradation rates increased 29.0, 46.7, and 59.6% in 2-, 24-,
and 96-h prelabeled cells, respectively, indicating that lability increased
with half-life of proteins. During refeeding of starved, cultured cells, at
least three proteins were synthesized at a lower rate. At the same time,
proteins with approximate molecular masses of 45, 84, 92, and 174 kDa
exhibited increased synthesis.
