Cellular thermogenic mechanisms : a comparative study of brown adipose tissue and skeletal muscle
TL;DRAbstract
Thermogenic mechanisms in homeotherms appear to be largely controlled by norepinephrine and the sympathetic nervous system. The thermogenic mechanism of brown adipose tissue (BAT) has been well characterized by other researchers and recent data from our laboratory have suggested a role for the vasculature in skeletal muscle thermogenesis. The aim of this thesis was to compare the thermogenic mechanisms of BAT and skeletal muscle. The contribution of the vasculature to BAT thermogenesis and the possibility of a mitochondria' uncoupling mechanism in skeletal muscle were investigated. To examine the vascular contribution to BAT thermogenesis a technique for the isolation and constant flow perfusion of the periaortic BAT deposit was developed and characterized. In this preparation, the thermogenic response was found to be entirely 0-adrenoreceptor mediated. Similar increases in oxygen consumption were induced by norepinephrine, isoproterenol and BRL 35135A (a specific 133-agonist). These i
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Thermogenic mechanisms in homeotherms appear to be largely controlled by norepinephrine and the sympathetic nervous system. The thermogenic mechanism of brown adipose tissue (BAT) has been well characterized by other researchers and recent data from our laboratory have suggested a role for the vasculature in skeletal muscle thermogenesis. The aim of this thesis was to compare the thermogenic mechanisms of BAT and skeletal muscle. The contribution of the vasculature to BAT thermogenesis and the possibility of a mitochondria' uncoupling mechanism in skeletal muscle were investigated. To examine the vascular contribution to BAT thermogenesis a technique for the isolation and constant flow perfusion of the periaortic BAT deposit was developed and characterized. In this preparation, the thermogenic response was found to be entirely 0-adrenoreceptor mediated. Similar increases in oxygen consumption were induced by norepinephrine, isoproterenol and BRL 35135A (a specific 133-agonist). These i
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