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Influence of Starvation and Refeeding on Cardiac Protein Degradation in Rats¹

Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Departments of Physiology and Internal Medicine, University of Texas Health Science Center at Dallas, Dallas, TX 75235

To assess the effects of starvation and refeeding on cardiac proteolytic capacity, hearts from age-matched rats fed ad libitum, starved 1 day, starved 5 days and refed 1 day after 5 days of starvation were studied in vitro using a modified Langendorff perfusion apparatus. The release ofphenylalanine into the perfusate while protein synthesis was inhibited by cycloheximide was measured as a reflection of p rotein degradation. All hearts were perfused with identical, insulin-free perfusate. Phenylalanine release was 0.17 ± 0.008 nmole/mg heart per hour (mean ± SEM) for control hearts and 0.14 ± 0.006, 0.12 ± 0.004 and 0.12 ± 0.004 for hearts of rats starved 1 day, starved 5 days and refed 1 day after 5 days of starvation, respectively. Thus, the capacity for cardiac protein degradation in vitro under controlled, insulin-free conditions was decreased 18% after 1 day and 29% after 5 days of starvation (P < 0.001). After 1 day of refeeding, the rate of cardiac proteolysis remained 29% less than that of control hearts (P < 0.001). Effects on proteolysis were opposite in direction from those which one would predict from simultaneous changes in cathepsin D, suggesting that the cardiac lysosomal alterations that accompany starvation are not important in regulating the rate of protein breakdown. Starvation caused alterations in the release of some amino acids which are metabolized by the heart (e.g., alanine and the branched-chain amino acids), that were not identical to changes in the release of amino acids such as phenylalanine and tyrosine which are neither synthesized nor catabolized by heart.

KEY WORDS: • phenylalanine • cardiac proteolysis • lysosomal enzymes • cardiac atrophy • starvation

¹ This work was supported by grants from the Moss Heart Fund and the National Heart, Lung and Blood Institute (HL 06296 and HL 18087).

² Address reprint requests to Dr. Kern Wildenthal, Dean, Graduate School of Biomedical Sciences, 5323 Harry Hines Boulevard, Dallas, TX 75235.

Manuscript received 27 April 1979.

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