Why is obesity re-adapting adipocytes work – Digital AIM



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Emerging disease has become an important problem in public health, and also at risk in diseases such as type 2 diabetes, cardiovascular disease and some of the diseases; cancer.

This study carried out in humans has shown the importance of changing epigenetic symptoms due to obesity. (Picture: Pixabay)

Although it is traditionally considered that it is due to an imbalance between income and energy spending that left the storage of cars, it has now recognized that the – evolution between environmental and genetic causes (known as epigenetics) in development.

Researchers at the Center for the Behavioral Research of the Psychiatric Disease Network and Metabolic Associated Diseases (Ciberdem), from the group by Joan Vendrell and Sonia Fernández-Veledo at the Pere Virgili Sanitary Research Institute (IISPV) ( Catalonia, Spain), just given One other step in knowledge of the processes that promote these interactions.

Experts have identified a new device where obesity causes epigenetic disclosure of adipocyte adverse cells that are acute; prove that the new carcass cells are not being created.

Previous studies of the same group have already shown that adipocyte measures that cause cells in obese patients do not work properly. However, so far, the molecular foundations of these changes have not been identified.

"There is an anti-functional rod of cells that adds adipocyte into a complex object of obesity subjects and there is evidence that there is a link between obesity and loss of cell cells without ", the definition of Sonia Fernández Veledo, the last nominee of the study that is" ending being published in the International Journal of Obesity.

An appropriate number of adipocyte precursors is essential in the proper expansion of advanced handsets, lipid management and the prevention of lipotoxicity in the face of a constant positive energy balance (that is, when all the catches are not caught to burn). .

"We believe that a better understanding of the biology of this set of advanced gaming can contribute to the development of new strategies designed to address obesity or increase of meat healthy healthy ", a & # 39; add to the expert.

In order to do this, this new work was investigated cellular cell cells (pre-used) and adult adipocytes of a thin and fattened patient.

"Our work shows that obesity produces important epigenetic changes in DNA of the advanced cells, which mislead the new adipocytes that are created, "said Joan Vendrell, chief of the Ciberdem group at IISPV.

"Obesity that impacts on the cell cells that adds adipocyte is a dynamic call of methylation DNA in selected areas that cause a white medicine misuse and a metabolic sprayer in obesity, "he said.

One of the most modified genera is the TBX15 transcription factor, which is involved in adipogenesis, fat distribution and browning & # 39; (Transformation of white white to brown, the ones that are healthy and essential for their body).

The study showed that TBX15 is one of the genera with the greatest epigenetic changes in the pre-cell cells, which means that it is transmitted into these cells. "TBX15 shows a strong loss of epigenetic marks with a corresponding increase in genealogy and profitability levels," they are. explained.

The work has identified that TBX15 is a regulator of mitochondrial damage in adipocytes obes, organelle is fundamental in the metabolic control of cells dependent on cellular spirit. "The increase of TBX15 in a working patient's aircraft causes change to the mitochondrial network, making changes in shape and number," which researchers added.

This new research carried out in humans has shown the importance of changing epigenetic markers due to obesity in the future adipocytes capabilities, supporting the theory of bad treatment in advance as a major event in this disease.

"Nowadays, we are investigating whether this epigenetic detection can be reintroduced, that is, if the weight of stress can be back on the epigenetic changes that caused by obesity, "said Joan Vendrell.

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