title: Protein metabolism during nutrient deprivation and refeeding of neonatal heart cells.
abstract: 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.
authors.affiliation: Research Department, Alfred I. duPont Institute of the Nemours Foundation, Wilmington, Delaware.
authors.forename: N A
authors.initials: NA
authors.lastname: Schroedl
authors.forename: C R
authors.initials: CR
authors.lastname: Bacon
authors.forename: Y C
authors.initials: YC
authors.lastname: Huang
authors.forename: C R
authors.initials: CR
authors.lastname: Hartzell
mesh_terms: 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*
chemical_list: D011506:Proteins; D003513:Cycloheximide