'Fat gene' could make you 'eat more and move less' "Do YOU have the fat gene?" the Mail Online asks, saying that, "90% of obese people could have mutation that means they're programmed to eat more and move less". Its report is based on a genetic analysis of a multigenerational Arab Israeli family in which it appeared that morbid obesity "ran in the family".
Researchers compared the DNA sequence of affected and unaffected family members, and found that those affected had an abnormal copy of the CEP19 gene, which codes for a protein present in many body tissues.
The researchers then genetically engineered mice to lack this CEP19 gene. They wanted to replicate the effects of the abnormal CEP19 gene found in the obese family members. They found that mice without the gene were heavier, had more body fat, ate more, moved less and had impaired glucose tolerance, suggesting they had or were at risk of diabetes.
The study furthers our understanding of the possible genes involved in the development of obesity, but it doesn't provide the whole answer to the problem. Despite the media headlines, it is not clear how many people in the general population could have this "obesity gene".
There are likely to be many other genetic and environmental factors involved. Even if your DNA makes it harder to lose weight, it certainly doesn't make it impossible. Why not try the NHS weight loss plan, a proven method of safe and sustainable weight loss.
Where did the story come from?
The study was carried out by researchers from the Mount Sinai School of Medicine and other institutions in the US and Israel, and was published in the peer-reviewed scientific journal, Cell. It has been published on an open access basis, so it is free to read online or download.
Individual researchers received funding from the National Institutes of Health, a March of Dimes award, and an American Heart Association grant.
The Mail's reporting of the study is confused. It claims that 90% of people could have the "fat gene", but this appears to be based on a reference in the introduction to the study, which suggests that some scientists estimate that 90% of obesity cases may be genetic. This unproven estimate does not mean that 90% of people have an abnormal copy of the CEP19 gene.
It is currently unclear how widespread this gene is. It could possibly be the case that it is only found in people of Arab Israeli ethnicity.
What kind of research was this?
Obesity is a major concern for the health of the population as it is associated with a large number of chronic diseases, including cardiovascular disease and cancer. Numerous past research studies in twins and other family groups have suggested various candidate genes that may be associated with obesity.
The current study involved both human and animal research. The researchers looked at a mutigenerational family group with genetically determined morbid obesity. They identified the gene abnormality present in those affected by morbid obesity, diabetes and cardiovascular disease, and compared them with unaffected family members. They then expanded their research by looking at what effect the absence of this gene would have in mice.
What did the research involve?
This cohort study involved members of a multigenerational Arab family living in the same village in the north of Israel.
People from this wide family seemed to fall into two groups (a bimodal distribution) – one with an average body mass index (BMI) around 28kg/m2 (which is considered overweight, but not obese) and the other with a BMI around 44kg/m2 (morbidly obese).
The researchers classed family members as "affected" if they had a BMI above 35, and "unaffected" if they had a BMI below this. There was a total of 15 affected family members, 11 of whom were currently alive.
All of those affected had a normal birth weight, but developed obesity by the age of three. They all had high blood pressure and all those tested using ultrasound scans had evidence of fatty liver disease. Ten of the 11 living members fulfilled clinical criteria for metabolic syndrome. Around a third of the family also had elevated blood fats, and a third had already developed cardiovascular disease.
The researchers took blood samples from 13 affected family members and from 31 unaffected family members. Laboratory techniques were used to analyse the genetic sequence of affected compared with unaffected individuals. DNA analysis revealed that those affected by obesity had a mutation in the CEP19 gene. The gene encodes for a ciliary protein that is expressed in lots of tissues of the body.
The researchers then genetically engineered mice so that they lacked a normal functioning CEP19 gene to see what effects this would have on them. The researchers observed their food intake and energy expenditure. They then carried out glucose and insulin tolerance tests when they were around three to five months old to see whether they were at risk of diabetes.
What were the basic results?
Mice lacking a functioning CEP19 gene appeared normal at birth, but differences then became apparent between the normal mice and mice lacking a functioning CEP19.
At the point of the greatest difference, mice lacking a functioning CEP19 gene were nearly twice the weight of age and sex-matched normal mice, and had twice as much total body fat. Their food consumption was much higher than the normal mice.
Movement was also reduced in the mice lacking the CEP19 gene. When they performed glucose tests on 12- and 18-week-old mice, they found that their glucose levels were increased at both times, more so for male than female mice.
By 18 weeks the male mice had developed impaired glucose tolerance. Female mice also had elevated blood fats when tested at both seven and 16 weeks; the males only at seven weeks. On insulin tolerance tests, the ability of insulin to lower glucose was compromised in both male and female mice.
How did the researchers interpret the results?
The researchers conclude that loss of the ciliary protein coded by the CEP19 gene causes obesity in both mice and humans, and "defines a target for investigating the molecular [development] of this disease and potential treatments for obesity and malnutrition".
Conclusion
The study furthers our understanding of the possible genes that may be involved in the development of obesity. It is of particular scientific interest as it involves a gene that seems to be well conserved across different animal species, with similar effects related to appetite control, energy expenditure and insulin signalling.
However, it doesn't provide the whole answer. Despite the media headlines, it is not apparent how many people in the general population could have this "obesity gene", or what contribution it could be making to the obesity epidemic. There are likely to be many other genetic factors involved in obesity.
In any case, while we can't change our genetic make-up, the best way to achieve a healthy weight is to eat a balanced diet high in fruit and vegetables and low in saturated fats and sugars, and stick to recommended activity levels. Read more about how to lose weight.
Links To The Headlines
Do you have the 'fat gene'? 90% of obese people could have mutation that means they're programmed to eat more and move less. Mail Online, November 21 2013
Found: The 'fat gene' that runs through generations. Metro, November 22 2013
Links To Science
Shalata A, Ramirez MC, Desnick RJ, et al. Morbid Obesity Resulting from Inactivation of the Ciliary Protein CEP19 in Humans and Mice. The American Journal of Human Genetics. Published online November 21 2013
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