Regulatory, cellular and molecular aspects of avian muscle nonshivering thermogenesis

Regulatory, cellular and molecular aspects of muscle avian nonshivering thermogenesis are reviewed. The endocrine control of muscle NST may involve an interaction between several hormones including glucagon, catecholamines and thyroid hormones. The metabolic, central, vascular or genomic actions of these hormones have been investigated at several levels, in vivo and in vitro using perfused avian muscle preparations. Two main thermogenic processes may account for avian muscle NST. The first one, which is based on an uncoupling of mitochondrial oxidations and phosphorylations, is supported by experimental data using isolated mitochondria, perfused skeletal muscle and efficiency of locomotor activity in vivo. The second mechanism, which involves an increased ATP-dependent sarcoplasmic reticulum Ca 2+-cycling, is supported by biochemical analysis of the activity and expression of SR proteins. The molecular basis of the two processes have been investigated and fatty acids or their derivatives may play an important role in their control. Muscle NST is fuelled by coordinated increases in fatty acid supply from adipose tissue, cellular uptake by lipoprotein lipase, and intracellular fatty acid transport capacity by small cytosolic proteins fatty acid-binding protein (FABP). The control at the gene level of the functional adaptations of skeletal muscle during cold acclimation should now be investigated