In DNA the switch of thinness

Molecular switch of thinness discovered in DNA: it is the Alk gene, a famous accomplice of tumors that could play a crucial role also in the regulation of fat metabolism. Already the target of numerous anti-cancer drugs, it could be targeted by new therapies against obesity. This is indicated by the study published in the journal Cell by researchers from the University of British Columbia.

"We all know those people who can eat anything while staying metabolically healthy," says study coordinator Josef Penninger. "They eat anything, they don't spend all their time in the gym, yet they don't gain weight. They are roughly 1% of the population."

To understand their secret, the researchers looked at the data contained in the Estonian Biobank, which includes clinical and genetic information relating to over 47,000 people between the ages of 20 and 44. From the comparison between lean and normal weight individuals, different variants of the Alk gene have emerged which are present only in the most slender subjects.

In light of this observation, the researchers tried to deactivate Alk in fruit flies and laboratory mice, discovering that all these animals managed to remain thin even if subjected to a high calorie diet. The mice deprived of the Alk gene, if subjected to the same feeding regime and the same physical activity as the normal weight mice, were however lighter and less fat. Considering that the Alk gene is expressed in large quantities in the brain, researchers speculate that it can regulate the metabolism of adipose tissue from there.

If these results were also confirmed by other studies, then a new scenario for anti-obesity therapies could open. "Alk inhibitors are already being used in cancer oncology, it is a gene that can be affected: that is exactly what we will try to do in the future", concludes Penninger.