The Thrifty gene
Blocking just one gene will help you lose weight without dieting and exercise
Anatoly Glossev, Vesti
Mice that had a single gene blocked did not gain weight, even eating very fatty foods. These experiments allow us to hope for the victory of mankind over obesity.
The discovery is described in the scientific article Regulator of Calcineurin 1 helps coordinate whole‐body metabolism and thermogenesis, published in the journal EMBO Reports by a group led by David Rotter from the University of Texas.
Man has evolved under the constant threat of starvation. Two or three hundred years ago, starvation was commonplace in almost all corners of the globe. Therefore, our body is constantly pushing us to eat something delicious (because now it is, and then it won't be!) and desperately resists our attempts to lose weight (these are rainy-day supplies, how can they be so frivolously spent?).
In conditions of an abundance of food, these "default settings" play a cruel joke on humanity. For example, in the United States, Great Britain and Australia, about two-thirds of the adult population is overweight. And this, as you know, creates a threat of a variety of diseases and rarely gives bonuses.
One of the main healthy ways to fight obesity is to force the body to burn more calories. As a rule, people resort to grueling workouts for this. But is it possible to force the body to spend more energy at rest?
It's time to remember that mammals (including humans) have two types of fat: white and brown. Everyone is familiar with white fat: it is from it that the unaesthetic folds on the body of overweight people consist. This is the "reserve warehouse" of the body: the energy deposited in the form of white fat, the body spends extremely reluctantly.
Brown fat is almost not present in an adult (but there is a lot of it in infants). The main function of this tissue is to produce heat (therefore, animals that hibernate can boast of solid reserves of brown fat). In other words, the calories deposited in the form of this tissue are quickly spent on warming the body.
As Rotter's group found out, the RCAN1 gene "prohibits" the conversion of white fat into brown. This gene was very useful in conditions of hunger, when the hard-accumulated reserves could not be used up unnecessarily for additional heat. But now he is one of the reasons for the epidemic of obesity that has engulfed humanity (how nice it is to think that it's not about hamburgers at all, but about genes!).
Blocking this gene in mice fed excessively high-calorie food helped them to quickly spend extra calories and not gain weight.
"We looked at different [high–calorie] diets with different time periods from eight weeks to six months, and in each case we saw an improvement in health in the absence of the RCAN1 gene," says co-author Damien Keating from Flinders University in Australia.
Of course, no one suggests changing a person's DNA (although there are precedents). It is possible to suppress protein synthesis, for which the "malicious" gene is responsible, and thereby actually stop the work of the latter.
"We have already developed a series of drugs targeting the protein that this gene produces, and now we are testing them to determine if they inhibit [the protein] RCAN1," Keating notes.
In the future, the authors intend to test this method of combating obesity in humans and make sure of its safety.
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