For the first time ever, scientists have uncovered a direct link between a specific gene and the the production of body fat — a discovery that may one day hold the key to tackling obesity.
Obesity remains a global health issue, particularly in the U.S. According to the Centers for Disease Control and Prevention (CDC), more than two thirds of Americans are either overweight or obese, leading to an estimated $200 billion in direct medical costs each year — more than 20 percent of all annual healthcare expenditures nationwide.
The causes of obesity are complex and not entirely understood; researchers agree that a combination of biological, environmental, and behavioral factors contribute to the disease, but the nature-nurture debate continues.
While diet and exercise certainly play a key role, recent research has suggested that obesity may also have important genetic underpinnings. Earlier this year, researchers published the results from the largest ever genome-wide study on obesity, strengthening the evidence of a genetic link to the condition. The findings showed that over 100 regions of the human genome had an influence on the development of obesity, likely through regulating the brain’s perception of hunger and the distribution of fat throughout the body.
Now, researchers at the University of British Columbia (UBC) have honed in what may be the first specific gene associated with obesity. The gene, which encodes a protein called 14-3-3zeta, is found in every cell of the body. But when scientists artificially silenced the gene in mice, it resulted in 50 percent reduction in unhealthy “white fat” — a type of adipose (fat) tissue that is linked to the development of obesity, heart disease and diabetes because it stores up calories, in contrast to brown fat that burns calories to generate heat.
What’s more, the fat reduction occurred despite the mice consuming the same amount of food. In contrast, mice that were bred to have higher levels of the 14-3-3zeta protein were found to be noticeably bigger, rounder and averaged 22% more white fat when fed a high-calorie diet.
The research, published this week in Nature Communications, points to the possibility of developing new drug therapies to combat obesity through the regulation of fat production through its genetic. Scientists theorize that by suppressing the gene or blocking the protein, like they did with the mice in the study, they may be able to prevent excess fat accumulation in people who are obese or at risk of becoming so.
“People gain fat in two ways: through the multiplication of their fat cells and through the expansion of individual fat cells,” explains study author Gareth Lim, a postdoctoral fellow at UBC’s Life Sciences Institute. “This protein affects both the number of cells and how big they are, by playing a role in the growth cycle of these cells.”
Although drug therapy is currently available for obesity, its effectiveness varies greatly. But tailoring drugs to patients’ specific genetic vulnerabilities could fundamentally change our current approach to the global obesity crisis, which the World Health Organization (WHO) describes as “one of today’s most blatantly visible — yet most neglected — public health problems.”
Of course, this doesn’t mean that nutrition and exercise are any less important in the fight against obesity. But it does mean that the logic of “calories in, calories out” is a lot more complicated than often implied.