VANCOUVER -- A Vancouver-based scientist, together with a team of international researchers, says he's identified a gene mutation that may help some people stay thin.
Josef Penninger, of the University of British Columbia's Life Sciences Institute, is part of the team trying to answer the question of why some people can eat whatever they want and stay svelte.
In a study published Thursday, the team says they believe a gene called anaplastic lymphoma kinase plays some kind of role in a resistance to weight gain.
The team used data from a biobank in Estonia, UBC said in a statement about the study.
They looked at the genetic makeup and profiles of more than 47,000 people between the ages of 20 and 44. All people in the study were considered to be "healthy, thin and normal weight," UBC said.
One of the genetic variations they saw with the people in the group was a mutation of the ALK gene.
To test out the impact of the mutation, those involved in the study "deleted" the gene in flies and mice, UBC says.
They noticed those without the gene were resistant to obesity based on diet, even when consuming the same foods and keeping the same activity level as other flies and mice.
Those without ALK weighed less, and had less body fat.
The group said the deletion resulted in reduced levels of triglycerides, a type of fat found in the blood.
Triglycerides are created when a body consumes calories it doesn't need to use right away. They're then stored as fat. Read more from the Mayo Clinic on why they matter, including their impact on risk of heart disease.
UBC says the gene's role in human physiology is unclear.
"The gene is known to mutate frequently in several types of cancer, and has been identified as a driver of tumour development," UBC's statement said.
Penninger said the people the study is about make up about one per cent of the population – those who can eat whatever they want, in whatever quantity, and not gain weight, even if they don't really exercise.
"We wanted to understand why. Most researchers study obesity and the genetics of obesity. We just turned it around and studied thinness, thereby starting a new field of research," he said in the university's statement.
The study's lead author, Michael Orthofer, of Vienna, said the team's work shows ALK "acts in the brain, where it regulates metabolism by integrating and controlling energy expenditure."
The team says it will next focus on understanding how ALK balances metabolism, and how neurons regulate the brain when it comes to expressing the gene.
"It's possible that we could reduce ALK function to see if we stay skinny," Penninger said.
"ALK inhibitors are used in cancer treatments already, so we know that ALK can be targeted therapeutically."