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Delaying Diabetes Through Signal Pathway

Apart from obesity and lack of exercise as the main factors that pull the trigger on diabetes, researchers from the Institute of Cell Biology of ETH Zurich suggest the possibility that some diabetics may actually have an abnormality in signal pathway and deactivating it may delay the illness for many years.

Wilhelm Krek, one of the researchers, explained that cells are fueled with energy called adenosine triphosphate (ATP) in order to function. In a diabetes-free person, the beta cells of the pancreas are the ones responsible for insulin production once food is ingested. Sugar is broken down in the mitochondria of the beta cells to produce ATP And ATP as the cell energy would trigger insulin secretion.

Insulin has the ability to regulate and normalize the blood sugar and according to Krek some cases of diabetes may have been triggered by an abnormality in this signal pathway. However, a study on mice revealed that though there is an equal amount of ATP produced, insulin levels vary when the pVHL changes. pVHL and HIF1a genes have a significant role in cell energy supply.

Such finding suggests that ATP production in the mitochondria activates even more factors that are crucial in the release of insulin.

Another significant observation is the increase in the volume of beta cells for obese mice. It was recorded that the newly formed beta cells normally have worse blood supply at first. This is attributed to oxygen deficiency. This leads to another hypothesis that oxygen deficiency activates the suppressed HIF1a gene to keep the oxygen-starved cells alive.

The transition from a regulated, effective secretion of insulin to a physically increased but less efficient glucose-stimulated insulin secretion could possibly ignite type 2 diabetes. The illness develops when all the beta cells gradually die off through permanent overloading.

“The study shows that pVHL and HIF1a play an important part in insulin secretion and ATP production,” Krek said. “If we are to inactivate the HIF1a signal pathway in the beta cells of diabetes patients, it might be possible to delay the outbreak of the illness perhaps for many years.”

Deactivated HIF1a in mice showed that their insulin secretion was stimulated solely by the ATP formed in the mitochondria and functioned with no problems. In the end, the researchers recommended that further studies should be undertaken in order to formulate a cure for diabetes using this premise.

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