Nov 15, 2010 Greg Philp
Mice eat more and get fatter with FTO - Rama
Obesity is a significant health risk, increasing the likelihood of heart disease and diabetes- and it is on the rise. It is estimated that over half of the world's adult population will be obese by 2030. As such, lots of research has been conducted into the causes of obesity and what can be done to prevent and treat this condition. As with most medical conditions, there are contributions from both genetic and environmental factors (nature and nurture).
The big story has been the identification of the FTO gene (delightfully referred to as 'fatso' among researchers). A new study published in Nature Genetics has shown that mice with a version of this gene eat more and have higher levels of bodily fat (Church et al., 2010). But, what do the results actually show? And what are the implications for this finding in humans?
FTO leads to fat mice
The study had a fairly simple premise: look at what happens to the weight of mice when the FTO gene is expressed more than normal. To do this the researchers looked at 'normal' mice, without any extra FTO genes and compared them to mice with one or two extra copies of the FTO gene. These mice were treated in the same way and allowed to live until 20 weeks old.
The researchers found that mice with extra copies of FTO were heavier than the normal mice. Most of this extra weight came from increased levels of fat in their body, particularly in females. In addition, these mice ate greater amounts of food than the normal mice. There is also some evidence that mice with extra copies of FTO had developed glucose intolerance (an early predictor of diabetes) when fed a high fat diet.
Not the whole story
These results might seem pretty convincing, but there are some key points that need to be considered...
1. The increase in body weight was 9% with one extra gene and 18% with two extra genes in female mice, this was lower in male mice.
2. The increased food intake noted in the mice with extra FTOs was not clear cut in the female mice when other variables were considered
3. Glucose intolerance was not shown when mice were fed a regular diet, only on a high-fat diet
What it means for humans
Humans gain weight when they have the FTO gene (on average an increase of 3.4%), but this is much lower than seen in the mice. Adding extra copies of FTO may be the reason for this, as it would increase the level of any proteins to a level that is normally not found in 'real life'. So it is difficult to say that these results reflect what is happening in people who are obese.
Interpreting results on energy intake and expenditure in obesity can be difficult because intake and expenditure are both increased in the obese. Although this study took that into account, this caused differences in results between male and female mice, clouding the picture. Previous data has been conflicting on the role of FTO in controlling food intake in mice, so perhaps further studies are needed.
It is estimated that 16% of Europeans have two copies of FTO- but the rate of obesity is rising faster than can be predicted if FTO is responsible. Therefore, FTO will only ever be part of the picture. The researchers suggest that drugs targeting FTO would help tackle obesity, however clearly further work is required before this claim can be substantiated.
Clearly the environmental aspect of obesity cannot be ignored and those wishing to control their weight can usually do so through effective diet and exercise.
Sources
Church C, Moir L, McMurray F et al. (2010) Overexpression of Fto leads to increased food intake and results in obesity. Nature Genetics epub
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