Abstract

The migratory flights of birds are fuelled largely by fatty acids. Fatty acid transporters, including FAT/CD36, FABPpm and H-FABP, and enzymes involved in fatty acid oxidation (CPT, CS, HOAD) are seasonally up-regulated in flight muscle to meet the demands of this intense aerobic exercise. The mechanisms that control these biochemical changes in response to migration are mostly unknown. We studied the effects of a photoperiod-induced migratory state and a 7 day treatment with murine leptin (1 μg/g body mass, twice per day) on fatty acid metabolism in captive white-throated sparrows. Sparrows that were exposed to a long-day migratory photoperiod increased flight muscle FAT/CD36 and H-FABP mRNA by 154% and 589%, respectively, and had 32% higher H-FABP protein than birds kept on a short-day photoperiod that mimicked wintering conditions. Migrants increased activities of flight muscle CPT, CS and HOAD by 57%, 23% and 74%, respectively, and decreased LDH activity by 31%, reflecting an increase in aerobic relative to anaerobic capacity. The expression of fatty acid transporters and the activities of metabolic enzymes in cardiac muscle were unaffected by migratory state. Leptin had no effect on transport proteins or enzymes in either skeletal or cardiac muscle suggesting that other signaling pathways control fatty acid metabolism during migration. These data indicate that photoperiod alone is sufficient to prime flight muscles for migratory flights by promoting enhanced protein-mediated fatty acid transport and oxidation. However, the endocrine controls and other factors underlying these changes remain to be thoroughly investigated.

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