Obesity is generally considered the result of appetite control – or the lack of it. Obesity is a fast-growing global health problem. A vast amount of research has been undertaken to identify the molecular pathways in the brain that control eating behavior. Now scientists suggest an increase of brown fat cells to increase the metabolism could target obesity and its related diseases such as diabetes and heart disease.
By Sheila Collins
In early mammals including humans, adipose tissue, called white adipose tissue (WAT) evolved to store excess nutrient energy that could then be accessed in times of food scarcity. And while this storage bank is incredibly important, there were also other challenges to cope with.
Before we had clothes, brown fat kept us warm
Early humans and other mammals had to deal with environmental temperature fluctuations. Brown adipose tissue (BAT) evolved as a means of generating heat from stored calories as a special adaptation termed non-shivering thermogenesis. Non-shivering thermogenesis was particularly important for humans before the advent of houses and clothing.
In order to understand the importance of this evolutionary advance, it is important to know that brown adipocytes are highly enriched in mitochondria (the ‘powerhouse’ of the cell). These cells express a unique protein that serves to ‘uncouple’ the mitochondrial proton gradient from Adenosine triphosphate (ATP – the primary carrier of energy in cells) production, the by-product of which is heat.
Increase brown fat to target obesity
In order to sustain themselves, these cells are avid consumers of glucose and fatty acids, the net result being overall energy expenditure. Active brown fat is now appreciated to be present in humans throughout the lifespan. Moreover, its amount correlates with lower percent body fat and greater insulin sensitivity, an increase in brown fat cells and their metabolic activity could target obesity and its related diseases such as diabetes and heart disease.
In a review article from the journal Hormone Molecular Biology and Clinical Investigation, researchers from the SBP Medical Discovery Institute in Orlanda, Florida discuss two main hormonal mechanisms that regulate adipose tissue metabolism – the ‘sympathetic nervous system’ (SNS) that release adrenaline-type molecules – and heart hormones that control blood pressure, but also have an important role in adipose tissue metabolism.
The heart hormones appear to operate in tandem with the sympathetic nervous system, utilizing some common as well as some unique components. The authors describe the signals that are triggered inside the cell in response to these two hormonal systems.
Finally, they discuss a newer and exciting concept in the control of brown adipose tissue growth and metabolism; one that involves the existence of specialized ‘nucleic acid’ signals, about which more work is needed to integrate these fascinating signal transduction processes for the purpose of identifying therapeutically tractable targets for metabolic disease.
Appetite control – is this the key?
Obesity has traditionally been considered solely a consequence of appetite control, and tremendous efforts have been made to identify the molecular pathways in the brain that control eating behavior. However, there have been few drug successes that have resulted from this understanding, perhaps because the evolutionary mechanisms to eat are so fundamental that there are many redundant routes and workarounds. Targeting energy expenditure has also been a long standing approach – in the form of promoting exercise.
Obesity – a consequence of our modern lifestyles?
While there will always be a place for exercise and diet management in efforts to maintain metabolic health, our modern lifestyle requires barely the lifting of a finger to survive. Hence, we might benefit from a better understanding of the energy expending mechanisms that also arose in the ‘cave days’ – that of non-shivering thermogenesis in brown adipose tissue.
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