Fidget obesity gene may cut obesity risk
By
Jonathan M. Gitlin | Published: June 06, 2007 - 10:20AM CT
With the problem of our ever-growing waistlines, you can be sure that a lot of time and money is being spent on understanding all the processes involved with obesity. Of course, we all know that if you eat too many calories and don’t expend enough, the excess gets stored as fat. We also know that being obese is a huge risk factor for any number of diseases, from type II diabetes to atherosclerosis, joint problems, sleep apnea, and so on.
A new paper published in
Cell Metabolism has identified a molecule that is important in controlling food-seeking behavior and spontaneous motor activity; both of which are important factors related to how much we eat and whether we gain weight. The hypothalamus is the region in the brain that controls both of these behaviors: the way you fidget subconsciously in your chair at work, or drum your fingers on the steering wheel when stuck in traffic, and also when you feel hungry enough to get up and forage for sustenance. Obviously a molecule that influences both of these behaviors would be a promising drug target for treating the obesity epidemic.
The study from a multinational team at the European Molecular Biology Laboratory, the German Institute for Nutrition, Potsdam, and the University of Cincinnati has identified a transcription factor called Bsx that is present in neurons within hypothalamus and regulates the production of a pair of neuropeptides, NPY and AgRP, which are involved in weight gain.
The researchers developed a strain of mice that lacked Bsx, and these mice were much lazier than their wild-type littermates, even when they had been fasted for an extended time period. They were the same weight as wild-type littermates, however. Normal mouse behavior would be to search for food in such conditions. In wild-type mice, fasting actually increases expression of Bsx, further underlining its role in regulating the way the brain processes hunger. The study also involved crossing the Bsx-deficient mice with another strain,
ob/ob, that lack a protein called leptin. Leptin is involved in weight loss, and ob/ob mice are obese as a result. The Bsx-deficient
ob/ob mice were much leaner and much lighter than the regular
ob/ob mice.
The gene that encodes for Bsx is highly conserved across species, from drosophila, through fish, all the way to mammals, including humans. This raises the possibility of drugs that target this pathway in the future, although such therapies will be many years away.
Fidget Obesity Gene 
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