Metabolism depends not only on what and how we eat and what kind of lifestyle we generally lead, but also on genes. It happens that a person tries to go in for sports and eat only healthy food, but extra pounds don’t really disappear anywhere. In this case, one has to admit that the person was unlucky with some gene.
This means that he got one of the genes that control metabolism in such a variant, due to which excess fat reserves appear in the body. We talked about one of these genes just a month ago: in Nature Medicine an article was published on the gene for melanocortin receptor 4 (MC4R) – due to mutations in it, a young person by the age of 18 can accumulate as much as 17 extra pounds. Of course, you can lose weight with a bad gene or genes, but this will take a lot more effort, or even sit on some medication.
But it also happens the other way around: we know neither about healthy eating, nor about compulsory sports, and the figure remains slim. Here, too, it may be all about genes. One of these genes is described in an article published the other day in Science… The researchers analyzed the genomes of more than 640 thousand people with an eye on the sequences coding for proteins (that is, they did not take into account those DNA regions that only controlled the work of other regions, but did not code anything themselves). At the same time, they looked for genes and mutations that, in principle, affect weight, whether in the direction of increasing it or decreasing it.
One of the genes GPR75, influenced the weight very strongly. More precisely, not a gene in general, but mutations in it: the gene GPR75 we have in two copies, and if the mutation completely turned off one of the copies, the person weighed an average of 5.3 kg less, and the likelihood that he would become obese was reduced by half. GPR75 encodes a receptor on the neurons of the hypothalamus, which, as you know, regulates metabolism and eating behavior – hunger, appetite, etc. Obviously, from the receptor GPR75 depends on how the hypothalamic neurons perceive information about metabolism and what actions they can take in this regard.
Mouse experiments confirm significant role GPR75 in metabolism: mice with a disabled copy GPR75 were kept on fatty food, and despite such food, they weighed 44% less than their comrades, who have both copies GPR75 worked. (I.e GPR75 can be called a “thinness gene” only with some stretch – it becomes so when it does not work.) In addition, in mice with disabled GPR75 the cells were more sensitive to insulin and better absorbed glucose from the blood. Insensitivity of tissues to insulin leads to an increased level of sugar in the blood, and then full-fledged diabetes of the second type. It turns out that if GPR75 works half-heartedly (without one copy), then the likelihood of diabetes should be less.
People who have one of GPR75 does not work, there is a probability of one in three thousand people, so it is hardly worth abusing unhealthy food, hoping that you have the same mutation. On the other hand, those who, in spite of everything, cannot lose weight in any way, could be helped by drugs that suppress the work of the receptor. GPR75.
Source: Автономная некоммерческая организация "Редакция журнала «Наука и жизнь»" by www.nkj.ru.
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