Effects of glucocorticoid treatment on cardiac protein synthesis and degradation.
We treated rats with dexamethasone (DEX, 1 mg . kg-1 . day-1) and examined the effects of this glucocorticoid on heart protein metabolism using atrial explant and Langendorff perfusion preparations. Fasted rats treated with DEX for 2 days had significantly lower body weights (92% of control, P less than 0.001) and larger hearts (106% of control, P less than 0.005) than fasted control animals. Protein and RNA concentrations remained constant. In atrial explants, DEX treatment produced a 19% increase in protein synthesis (P less than 0.001) and a 13% increase in protein degradation (P less than 0.002). In Langendorff-perfused hearts, DEX treatment caused a 36% increase in protein synthesis (P less than 0.02), while protein degradation was 8% above control (P greater than 0.05). Thus, in contrast to their catabolic effects on skeletal muscle, glucocorticoids are anabolic on the heart. The increased accumulation of total cardiac protein during early glucocorticoid administration is mediated entirely via increased rates of synthesis.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D003345:Corticosterone / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology*; D006321:Heart / Q000033:anatomy & histology / Q000187:drug effects; D007328:Insulin / Q000097:blood; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009929:Organ Size / Q000187:drug effects; D014176:Protein Biosynthesis; D011506:Proteins / Q000378:metabolism*; D012313:RNA / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013217:Starvation / Q000378:metabolism
D007328:Insulin; D011506:Proteins; D012313:RNA; D003907:Dexamethasone; D003345:Corticosterone