{'en': 'A DNA fragment opens the door to cure diabetes', 'es': 'Un fragmento de ADN abre la puerta a curar la diabetes'} Image

A DNA fragment opens the door to cure diabetes

fer's profile photo   01/08/2024 1:49 p.m.

  
fer
01/08/2024 1:49 p.m.

The ZNF808 gene has been a surprise finding for evolutionary biologists due to its incidence on the pancreas.

Type 1 diabetes, a failure of the pancreas cell cluster that produces insulin, is an incurable disease whose incidence does not stop growing in the world.Although there is effective treatment that allows patients to make a normal life by supplying artificial insulin, science is still far from understanding why the pancreatic crisis that leads to diabetes occurs.

Scientists at the University of Exeter have announced an unexpected finding, a gene that is essential for the development of the human pancreas and that is not found in most of the rest of the mammals.

Those responsible for insulin production in a healthy pancreas are the so -called beta cells.Any mammal needs them to survive.Without them, the glucose that is acquired through the consumption of food with carbohydrates cannot be processed, accumulates in the blood and generates a toxic reaction that ends with death if it is not corrected.Diabetics have suffered partial or total destruction of their beta cells for reasons that are not yet fully understood.

The new discovery, published in the "Nature Genetics" magazine has meant a paradigm shift in understanding how a pancreas develops.

An idea long assumed by evolutionary science is that the essential genes for the development of vital organs such as the heart, liver or pancreas are very stable throughout evolution and are found in many species that come from a distant common trunk.All current living animals proceed from the same evolutionary origin so that we have a common genetic ancestor.Many genes disappear with the passage from one species to another, but a few, the most important, can be distributed between beings as disparate as a fish, a lion or a human being.

However, Exeter experts, in collaboration with researchers from Helsinki and Cambridge universities, have discovered a gene (the ZNF808) that is of vital importance in the development of the pancreas and that is only present in humans and in ourclosest cousins: gorillas, chimpanzees and some monkeys.

The finding is a surprise for evolutionary biologists, equivalent to what would mean finding a new type of sun in our solar system.It is, to know, the only fundamental gene for the development of a vital organ that is not present in any non -primate animal.It is common to find exclusive genes of a species that regulate exclusive functions of that species - the gills of the fish or the size of the trunk of an elephant.But the pancreas is an organ that all vertebrates share.Why does the human pancreas have such an exclusive gene?

It is evident that, at some point in evolution, there was a genetic script turn that affected only primates.As a consequence of that jump, the ZNF808 gene appeared, a gene that is among the family of those who "turn off" certain regions of DNA.These regions, called "garbage DNA", do not have a concrete function.

But the truth is that new technologies have begun to find the meaning of those genes previously considered useless.Findings like this can help better understand the work that genes worked so far.In this case, the ZNF808 has been identified after the study of type 1 diabetes patients together with individuals who were born directly without pancreas because of a congenital disease.Through the comparison it was discovered that the gene is fundamental in the development of the baby before birth, and from there the organism activates the cataract of functions that leads to organ formation.Source: Link

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Regina
01/08/2024 7:13 p.m.

Genetic treatments will be another great revolution in medicine ... but much remains to be investigated ..

Hija de 35 años , diabética desde los 5. Glico: normalmente de 6 , pero 6,7 la última ( 6,2 marcaba el Free)
Fiasp: 4- 4- 3 Toujeo: 20

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