Fat Fighting Undermined By Over Active Eating Pacemaker
- Date:
- May 13, 2004
- Source:
- University Of Warwick
- Summary:
- Researchers at the University of Warwick have for the first time been able to detail how and why specific neurons in the brain control the hunger response. They have revealed a set of pacemaker nerve cells in the brain that appear to underlie the drive to feed which itself feeds on a complex web of signals.
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Researchers at the University of Warwick have for the first time been able to detail how and why specific neurons in the brain control the hunger response. They have revealed a set of pacemaker nerve cells in the brain that appear to underlie the drive to feed which itself feeds on a complex web of signals. The level of complexity they have found is such that the system could be much more at risk of serious repercussions from a single error in how those signals are processed than anyone had previously thought. Any number of a range of errors could lead to over activity of these pacemaker cells and explain why many people find difficulty in eating less.
In the research, published in the May Issue of Nature Neuroscience, Dr David Spanswick and his research team in the University of Warwick's Department of Biological Sciences, looked at a part of the brain called the hypothalamic arcuate nucleus which was known to deal with hunger and satiety signals but how it achieves this is poorly understood. The University of Warwick team have identified very specific neurons that act as feeding "pacemakers".
This specific group of neurons- which they have dubbed the "ARC pacemaker" produce regular bursts of electrical activity. However these cells integrate and process a wide variety of signals indicating the energy needs of the body signals most often transmitted by the use of chemical messengers such as hormones like ghrelin, released from the gut and leptin from fat cells.
The combination of these signals and their integration by the ARC pacemaker is such a finely balanced mechanism that one small error or mutation leading to any inappropriate communication in these pathways could produce a significant untoward affect on human eating or feeding patterns.
The high number of potential ways that this delicately balanced hunger pacemaker can go wrong could explain why many overweight people are unable to address their weight problems by a combination of diet and exercise. In the past people with a weight problem have faced scepticism and doubts as to how hard they were really trying to stick to diet and exercise regimes. This research shows that there may indeed be very good reasons why they seem unable to solve their weight problems simply by employing the usual methods, - eating less may be a more difficult and complicated problem than we currently anticipate.
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Full text of research paper on Nature Neuroscience web site at: http://www.nature.com/cgi-taf/DynaPage.taf?file=/neuro/journal/v7/n5/full/nn1226.html
This research was supported by the Biotechnology and Biological Sciences Research Council (BBSRC), The Foundation for Prader-Willi Research (USA) and British Heart Foundation (BHF).
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Materials provided by University Of Warwick. Note: Content may be edited for style and length.
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