In addition to high blood sugar, study finds another possible trigger for type 2 diabetes

According tomedia reports, excessive sugar consumption is a known risk factor for type 2 diabetes, but high blood sugar does not tell the whole story. Insulin resistance and type 2 diabetes are known to occur even if some people’s blood sugar levels are normal, suggesting that the disease may not be just the result of an increase in the body’s “deaf ear” to insulin. It turns out that fat may play an important role in causing the disease.

In addition to high blood sugar, study finds another possible trigger for type 2 diabetes

The process that causes type 2 diabetes to develop involves pancreatic cells called beta cells, which begin to produce too much insulin, a hormone that controls blood sugar levels. It is widely believed that this oversecretion is due to insulin resistance caused by a long-term rise in blood sugar levels. When blood sugar levels are usually high, insulin may not work effectively and a gradual increase in amounts is required to control blood sugar. However, the problem with this theory is that it is well known that even if beta cells have been isolated, too much insulin is produced, which means that there is no high blood sugar level.

Researchers at the University of California, Los Angeles, have published a new study that finds that insulin resistance may not fully explain why some people develop type 2 diabetes. Fatty acids have been shown to be an early trigger for the disease, which can lead to excess insulin production regardless of blood sugar levels. Fatty acids have been found to cause a phenomenon called proton leakage, which involves a protein called CypD.

In addition to high blood sugar, study finds another possible trigger for type 2 diabetes

The researchers found that “proton leakage” contributed to excess insulin production in prediabeted obese mice with normal glucose levels. In general, fatty acids do not trigger the production of too much insulin in healthy animals. By contrast, the researchers found that mice that lacked the CypD gene do not produce too much insulin even if they were obese.

Looking at humans, the study found that human pancreatic cells are isolated and exposed to levels of fatty acids present in obese humans, causing them to over-secrete insulin. High blood sugar levels are not required for this overproduction.

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