EFFECTS OF PALMITOYL CARNITINE AND RELATED METABOLITES ON THE AVIAN CA2-ATPASE AND CA2+ RELEASE CHANNEL()

1. In birds, prolonged cold exposure induces the development of a non- shivering thermogenesis (NST) of muscular origin that may result from an increase in ATP-dependent cycling of Ca2+ between the sarcoplasmic reticulum (SR) and the cytosol. 2. Because fatty acids are thought to play a significant role in NST, we investigated the effects of palmiti c acid and related metabolites on skeletal SR Ca2+ uptake and release in ducklings. 3. Ca2+-ATPase activity, Ca-45(2+) release and [H-3]ryan odine-binding measurements indicated that palmitic acid was without ef fect on the Ca2+-ATPase and Ca2+ release channel. Palmitoyl carnitine and palmitoyl coenzyme A inhibited the Ca2+-ATPase at concentrations > 20 mu M whereas both activated the Ca2+ release channel at concentrat ions less than or equal to 20 mu M in a dose-dependent manner. 4. Palm itoyl carnitine stimulated [H-3]ryanodine binding to skeletal but not cardiac SR vesicles. Induction of Ca-45(2+) release was observed with long-chain (C greater than or equal to 14) but not with short-chain ac yl carnitines (C less than or equal to 12). 5. Long-chain acyl carniti nes accumulated significantly in duckling skeletal muscle during cold acclimation. Accordingly, these results suggest that long-chain acyl m etabolites may modulate SR Ca2+ cycling and its associated thermogenes is in vivo.