It is known that genetics plays a role in obesity, with genes directly causing obesity in disorders such as Bardet-Biedl syndrome and Prader-Willi syndrome. However, genes and behaviour may both be needed for a person to be overweight. Now, a study from researchers at the University of Helsinki identifies a genetic mutation which makes its bearers more likely to behave impulsively while intoxicated, which may also shield them from obesity and change the way testosterone impacts insulin resistance. The team state that their results also suggest men in their thirties with antisocial personalities may constitute a risk group for insulin resistance, and consequently type 2 diabetes later in life.
Earlier studies from the lab demonstrated that a point mutation in a gene of serotonin 2B receptor can render the carrier prone to impulsive behaviour, particularly when drunk. Over 100,000 Finns and more than 1,000 Finnish infants born every year are carriers of the point mutation in the serotonin 2B receptor. The current study shows that the genetic mutation may also shield its carriers from obesity and insulin resistance, both of which are associated with type 2 diabetes.
The current study investigates the insulin sensitivity, beta cell activity and BMI of 98 Finnish men between the ages of 25 and 30, all of whom had been diagnosed with antisocial personality disorder. Results show that carriers of a point mutation in a gene of serotonin 2B receptor had a lower BMI and higher insulin sensitivity than persons without the mutation. The group explain that normally men with low testosterone levels are more susceptible to metabolic disorders, however, among carriers of the point mutation, this tendency was reversed with lower levels of testosterone increasing insulin sensitivity.
Data findings show that the point mutation and testosterone predicted lower BMI independently, however, an interaction between the point mutation and testosterone leads to increased insulin sensitivity among point mutation carriers with low testosterone levels. Results show that the point mutation also predicted reduced beta cell activity and enhanced glucose metabolism. The lab conclude that reduced serotonin 2B receptor function at low or normal testosterone levels may be protective of obesity.
The team surmise that their findings show the serotonin 2B receptor and testosterone have a role in energy metabolism. For the future, the researchers state that as their results were observed among Finnish males with antisocial personality disorder, which limits the generality, more work is needed in the wider population.
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