Scientists have discovered a “greedy” gene which appears to make us over eat even when we are full!  Hooray, we all cry, at last we can blame it on something other than our own weak wills!

However, a word of caution!  This research has been undertaken in mice, not humans so don’t go for the chocolate and biscuits just yet!

Scientists have looked at the role of a mutated gene called BDNF “brain-derived neurotrophic factor” and the effect it has on feeling full.  In normal circumstances, our hormones tell our brain when we are full.  However, when mice carried a mutant version of the BDNF hormone, the signal to tell the brain when they were full was blocked and they became over eaters and therefore gained weight.  In fact male mice became twice as heavy as the mice without the “greedy” gene and female mice were 2.7 times as fat.

This research is indeed interesting and will hopefully lead to a greater understanding of obesity in humans but more work needs to be done.  We don’t know how many humans may carry a mutated gene such as this and it can’t be the case that all obese people are that way due to genetics.  People are overweight and obese for a vast array of reasons.  Even if this study is replicated in humans, it will be many years before a suitable treatment is developed.

The study was carried out by researchers from Georgetown University Medical Center and the University of Colorado in the US and was funded by the US National Institutes of Health and the American Diabetes Association.

The study was published in the scientific journal Nature Medicine.

The researchers took two groups of mice, one with a mutated version of the BDNF gene and the other with a normal version of the gene. They then looked at the weight of the mice, how much food they consumed and then how much weight they gained.  The researchers also looked at the role of Leptin in the mice which is a hormone which suppresses the appetite.  Leptin was injected into the mice 3 times a day and then their eating habits were monitored. 

The results that the researchers found were quite remarkable.  When the mice were 5-6 weeks old, and had the mutated gene, they were found to be severely obese compared to the mice without the mutate gene.

By 16 weeks of age, female mice with the mutation were 171% heavier than their non-BDNF mutation counterparts, and male mice were 90% heavier. Importantly, the researchers reported that this weight gain was not due to inactivity but directly due to over eating.  They were eating 69-80% more than the mice without the “greedy” gene.

It was also discovered that the role of Leptin became redundant in the mice with the mutated gene and appeared to switch itself off and therefore was unable to make the mice feel full as it’s supposed to do.  The mice injected with Leptin who did not carry the mutant gene ate 26% less food than their counterparts after being injected. 

So, in conclusion, the BDNF “brain-derived neurotrophic factor” caused obesity and also stopped the key role of Leptin in suppressing appetite.

Researchers were keen to stress that this work is in the very early stages and more work needs to be done to understand the way in which the brain effects eating habits and energy balance.  However, this research may give a different avenue to look at in the pursuit of a treatment for obesity.  This work is very informative at a time when obesity rates are soaring in the UK and so any insight into why this is happening is welcome.  Obesity is a complex issue with many factors such as an abundance of food, convenience foods, leisure, sedentary lifestyles and socio economic factors all play a role.  Given the vast array of illnesses associated with obesity such as heart disease and diabetes, a better scientific understanding of why obesity occurs and a cure can’t come fast enough!

James.