Something needs to be done about the obesity epidemic. Experts are predicting obesity rates of between 43 and 48% among men and women in both the US and the UK by 2030 if we continue along our current trajectory. These figures are particularly alarming in terms of healthcare costs and life expectancy. Because hand-in-hand with obesity go obesity-related diseases such as type 2 diabetes, heart disease, dyslipidemia, and high blood pressure. For the first time, our current generation may have a shorter life span than previous generations.
In the search for more effective and safer weight loss treatments, the spotlight is on adipose tissue (fat storage sites). White adipose tissue (WAT) stores excess energy from food in the form of triglycerides, noticeable as the extra lumps and bumps we get when we are overweight. Brown adipose tissue (BAT) contains abundant levels of mitochondria that consume excess energy and dissipate it in the form of heat. BAT is vital for the survival of newborns and small animals in cold environments. A third type, referred to as induced BAT or beige adipocytes, has a similar function to BAT but develops in white fat in response to various stimuli (eg, severe cold). Higher levels of BAT and induced BAT correlate with leanness in humans, and researchers are keen to determine the genetic factors that influence this.
The focus of researchers from the Harvard Medical School in their article published in The New England Journal of Medicine was the FTO gene; located on chromosome 16 and previously identified as having a strong association with body mass index. They identified a specific variant of the gene (RS1421085) that prevents the formation of induced BAT, instead favouring fat storage and body weight gain.
Despite elucidating the contribution this variant makes to obesity, formulating an anti-obesity drug from this research is not a simple task. But what this study does demonstrate is how data from DNA mapping studies may be used to develop more individual- and target-specific treatments.