Protein metabolism during nutrient deprivation and refeeding of neonatal heart cells.
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.
Schroedl
N A
NA
Research Department, Alfred I. duPont Institute of the Nemours Foundation, Wilmington, Delaware.
Bacon
C R
CR
Huang
Y C
YC
Hartzell
C R
CR
D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D003513:Cycloheximide / Q000494:pharmacology; D004591:Electrophoresis, Polyacrylamide Gel; D005502:Food; D006207:Half-Life; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism*; D013217:Starvation / Q000378:metabolism*
D011506:Proteins; D003513:Cycloheximide