QBI Neuroscience Seminar: Considering obesity as a chronic brain disease
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- Dr Giles Yeo, University of Cambridge Metabolic Research Labs, welcomes Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK
Title: Considering obesity as a chronic brain disease
Abstract:
It is an inescapable fact that the underlying cause of obesity is a result of consuming more energy than you burn. The question that is more complex to answer is why some people eat more than others. Over the past 20 years, insights from human and mouse genetics have illuminated multiple pathways within the hypothalamus, brainstem and higher brain regions that play a key role in the control of food intake. We now know for example, that the brain leptin-melanocortin signalling pathway is central to the control of mammalian food intake. Intriguingly, it is becoming clear that in addition to engaging classical “neuropeptide/receptor” systems within the brain, leptin also rapidly modifies synaptic connections between neurons. There is also evidence for neurotrophins, which are critical in the development and maintenance of neuronal connections, playing a role in the control of energy homeostasis. However, although monogenic alterations in these pathways result in extreme Mendelian obesity, these remain incredibly rare. The major burden of disease is carried by those of us with “common obesity,” which to date has resisted yielding meaningful biological insights. Progress however, has been made with genome-wide association studies, which have now revealed more than 100 different candidate genes, most of which are highly expressed or known to act in the CNS. In and amongst these are components of leptin-melanocortin signalling, emphasizing, as in rare monogenic forms of obesity, the role of melanocortin signalling and, more broadly, the brain in predisposition to obesity.
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