UCP1 expression is increased specifically in adipose tissue. During glucagon signaling in adipose, what would be the fuel source for the adipose cell and what happens to the fuel normally and then with irisin signaling? What do you expect would happen to the level of oxygen consumption, electron transport, and ATP production PER FATTY ACID in adipose cells when UCP1 expression increases?

Brown adipose tissue (BAT) mitochondria are distinct from their counterparts in other tissues in that ATP production is not their primary physiologic role. BAT mitochondria are equipped with a specialized protein known as uncoupling protein 1 (UCP1). UCP1 short–circuits the electron transport chain, allowing mitochondrial membrane potential to be transduced to heat, making BAT a tissue capable of altering energy expenditure and fuel metabolism in mammals without increasing physical activity.

The recent discovery that adult humans have metabolically active BAT has rekindled an interest in this intriguing tissue, with the overarching aim of manipulating BAT function to augment energy expenditure as a countermeasure for obesity and the metabolic abnormalities it incurs. Subsequently, there has been heightened interest in quantifying BAT function and more specifically, determining UCP1-mediated thermogenesis in BAT specimens – including in those obtained from humans.

In this article, BAT mitochondrial bioenergetics will be described and compared with more conventional mitochondria in other tissues. The biochemical methods typically used to quantify BAT mitochondrial function will also be discussed in terms of their specificity for assaying UCP1 mediated thermogenesis. Finally, recent data concerning BAT UCP1 function in humans will be described and discussed.

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