Study finds type-2 diabetes trigger that doesn’t involve high blood sugar

Brittany A. Roston - Jan 1, 2020, 11:35am CST
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Study finds type-2 diabetes trigger that doesn’t involve high blood sugar

Consuming too much sugar is a known risk factor for developing type-2 diabetes, but high blood glucose levels don’t tell the full story. It’s known that some people will develop insulin resistance and type-2 diabetes even if they have normal blood sugar levels, something indicating that this disease may not simply be the result of the body becoming increasing ‘deaf’ to insulin. Fat, it turns out, may play an important role in triggering this disease.

The process leading to the development of type-2 diabetes involves pancreatic cells called beta cells, which begin producing too much insulin, the hormone that keeps blood glucose levels in check. This excessive secretion was largely thought to be the result of insulin resistance due to chronically elevated blood sugar levels.

When blood sugar levels are often high, the body may start to become ‘deaf’ to the effects of insulin, requiring progressively higher quantities to keep blood sugar in check. There’s a problem with this theory, however, and it’s that beta cells are known to still produce too much insulin even if they’ve been isolated, meaning in the absence of high blood sugar levels.

Researchers with UCLA have published a new study that found that insulin resistance may not fully explain why some people develop type-2 diabetes. Fatty acids, it turns out, maybe a trigger in the early stages of this disease, causing too much insulin production regardless of blood glucose levels. Fatty acids were found to drive a phenomenon called ‘proton leak,’ which involves a protein called CypD.

Proton leak was found to promote the excessive production of insulin in pre-diabetic obese mice who had normal glucose levels. Ordinarily speaking, fatty acids can’t trigger excessive insulin production in healthy animals. In contrast, the researchers found that mice lacking the CypD gene didn’t experience excess insulin production despite being obese.

Looking at humans specifically, the study found that human pancreas cells isolated and exposed to the levels of fatty acids that would be present in obese humans caused them to over-secrete insulin. High blood glucose levels weren’t necessary for this excessive production.


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