Another cause of obesity
Scientists have uncovered an unusual link between obesity and body temperature
Disorders in the genes that control body temperature and its response to cold may be one of the main causes of obesity, scientists have found out, who published an article in the Journal of Neuroscience.
"Despite the fact that the body temperature in mice and humans is different, the genes and receptors responsible for recognizing cold and reacting to it are arranged approximately the same in humans and rodents. For this reason, we can say that changes in the structure of the TRPM8 gene can play a very serious role in the development of obesity, which we did not suspect before," Alfonso Reimundez from the Spanish University of Santiago de Compostela and his colleagues write (in a press release New link between obesity and body temperature – VM).
According to WHO, there has been a global obesity epidemic in the world since the 1980s. Last year, every third inhabitant of the planet (about 1.9 billion people) suffered from extra pounds, about 15 percent had severe forms of pathology. At the same time, almost half of diseases, such as cardiovascular diseases, diabetes and cancer, are associated with obesity.
In recent years, scientists have been increasingly talking about the connection between obesity and chronic inflammatory processes. The appearance of extra pounds leads to the development of foci of inflammation, and this, in turn, leads to even greater weight gain. Moreover, biologists have recently found out that substances that suppress inflammation, for example, capsaicin (the main component of the burning taste of pepper) – they turned out to be very effective medications for excess weight.
Reimundez and his colleagues found another link between obesity and body temperature. To do this, they observed the behavior of mice in which the TRPM8 gene, responsible for the reaction to cold, was damaged.
Scientists were interested in whether the behavior of rodents would change when this DNA section was removed. They assumed that mice that had lost the ability to feel low and high temperatures would spend more energy in the cold and overheat in the heat.
In fact, the removal of TRPM8 practically did not affect the ability of mice to maintain body temperature – on average, it differed from the norm by only 0.7 degrees, and this did not threaten the rodents in any way.
On the other hand, damage to the gene had a strange effect on the appetite of mice and on how their bodies used fat reserves when the temperature dropped. With the onset of cold weather, rodents developed unusual insomnia, which they constantly tried to jam, which led to rapid weight gain and the development of obesity.
As it turned out, the mice's body did not use fat reserves for warming up, but in fact only those nutrients that got into the blood after the next trip to the feeder.
Interestingly, such obesity did not develop immediately, but only at about the 24th week of rodent life (in humans, this corresponds to late adolescence). According to the researchers, the disease can develop similarly in people with similar mutations in TRPM8.
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