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Hereditary obesity is not always determined by genes

17.03.2016

It is known that metabolic disorders that can lead to obesity and diabetes often develop due to genetic mutations: a damaged gene ceases to properly monitor metabolism, and because of this, problems begin with the absorption of glucose, with insulin, with adipose tissue and etc.

Such a gene, once having arisen, can pass from generation to generation for quite a long time, so that all members of the genus in any line, maternal or male, will have to carefully monitor the waist and blood sugar levels.

However, genes never work on/off, they always have some range of activity. In other words, a gene can work weakly, not very weakly, moderately strongly, etc. How a gene is set to work depends on mutations, but also on external and internal factors - that is, roughly speaking, on our lifestyle with ecology and the activity of other genes. So, if we return to obesity, then it is not always associated with a genetic "curse" - improper nutrition may well change the metabolism for the worse without any mutations.

Living organisms have a lot of molecular ways to tune the activity of genes, and many of these mechanisms do not function for long - after working for some time in some force majeure circumstances, the gene returns to its normal state. However, it also happens that changes in genetic activity persist for life, and even, moreover, are transmitted to the next generation. At the same time, we emphasize that the gene itself does not change, its DNA does not change, no mutations occur, just regulatory molecules do not let go of their grip.

Such cases are called epigenetic regulation, and, as the studies of Johannes Beckers and his colleagues from the Munich Center show. Helmholtz on the study of environment and health, obesity can be transmitted from generation to generation precisely with the help of epigenetics. That is, the consequences of an unhealthy lifestyle of parents can pass on to their descendants, despite the fact that the actual genes of both will be quite normal, without mutant changes.

The researchers kept genetically identical male and female mice on three different diets for six weeks: high-fat, regular, and low-fat. As expected, the fat-fed animals became obese and had the first signs of type XNUMX diabetes. Then germ cells were taken from all mice for in vitro fertilization. The procedure itself was carried out in all possible combinations: a spermatozoon from a “fat” male was brought together with an egg from a female who was on a normal diet, then a spermatozoon from the same male was brought together with an egg from a female who was on a low-fat diet, etc. The embryos were implanted in healthy females, and then, when the mice were born, they were fed normal food for nine weeks, without fatty distortions, and then they were still transferred to fatty foods.

Fatty foods added weight to everyone, but the amount of excess weight clearly depended on what the parents ate. So, for example, females born from a "fat" male and female were 20% fatter than the offspring of normal mice (that is, those who were fed normal food).

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