Some people never get fat. Why?

For example, biologists found out, two years ago, that high-calorie food disrupts the normal functioning of the gene that controls the activity of cells in the saturation center in the brain of mice. A year ago, scientists discovered that fat people have an unusually high sensitivity to the taste of food, and consider sweet food

Comparison of the DNA of the thinnest and fattest people has helped biologists identify a dozen mutations in various genes that protect people from the development of obesity in all circumstances. The findings of scientists published in the journal PLoS Genetics.

In the past few years, scientists are finding more and more signs that obesity and metabolic problems associated with it, are developing not only due to the presence of problems with the strength of will , but also for genetic reasons or due to the fact that eating such foods changes the work of the brain.

For example, biologists found out, two years ago, that high-calorie food disrupts the normal functioning of the gene that controls the activity of cells in the saturation center in the brain of mice. A year ago, scientists discovered that fat people have an unusually high sensitivity to the taste of food, and consider sweet food more delicious than other people, due to changes in their taste buds and other regions of the brain.

Faruki and his colleagues conducted one of the most extensive tests of this hypothesis, collecting and decoding DNA samples from about two thousand extremely thin British people, a similar number of extremely fat people and about ten thousand volunteers with “normal” weight.

Analyzing and comparing their genomes, scientists were guided by extremely simple considerations. If this genes do have the greatest effect on the development of obesity, then the differences in the sets of small mutations in these sections of DNA will particularly strongly influence the chances of gaining excess weight or remaining thin.
Accordingly, the thinnest and fattest people will have the maximum number of “useful” and “harmful” variations in such genes, which will allow them to be distinguished and prove that they exist simply by comparing a large number of genomes.

In total, the British geneticists were able to isolate thirteen small mutations that particularly influenced whether a person would remain thin after going on the wrong diet or refusing to play sports. Ten of them, as Faruki notes, in the past were associated with the development of obesity.
Interestingly, all these mutations and the genes associated with them influenced the gaining of excess weight and the maintenance of thinness in quite different ways. For example, mutations in FTO, the well-known “obesity gene”, contributed much more to gaining fat mass than maintaining low weight. Other sites, in particular, the CADM2 gene associated with the work of brain receptors, behaved exactly the opposite way.

It is not clear how exactly all these genes are thin and obese. As scientists hope, observing the families of the thinnest people who took part in these experiments, and analyzing their DNA, will help them understand what these mutations are changing.

This website uses cookies.