US research finds new trigger for Type-2 diabetes in fatty acids
New research from the University of California, Los Angeles (UCLA), sheds light on a possible trigger for the overproduction of insulin in type-2 diabetes: another, separate molecular pathway stimulated by fatty acids appears to boost insulin production, instead of high glucose levels. Glucose – from eating too much sugary/fatty foods – was thought to cause insulin production in pancreatic beta cells; but, even beta cells isolated in a lab can over-secrete insulin, without glucose playing a part. This latest discovery could eventually lead to new types of pre-diabetes/diabetes treatment, by manipulating factors other than glucose.
In tests on obese, pre-diabetic mice, high levels of fatty acids would see a protein called Cyclophilin-D (CypD) “leaking” protons into the mitochondria of beta cells which triggered a boost of insulin. However, the insulin levels of mice engineered without the gene that codes for CypD remained acceptable. No glucose was present throughout the experiment.
The researchers also tested human pancreatic cells isolated in the lab to see whether the same mechanism could be occurring in humans. When exposed to high levels of fatty acids – as found in obese people with type-2 diabetes – the cells began to produce more insulin. Again, there was no glucose present.
Type-2 diabetes typically develops due to poor lifestyle choices, such as a bad diet. It involves a vicious cycle of insulin – where beta cells can produce too much insulin, causing the body to become resistant to it; which in turn causes the beta cells to produce even more to compensate.
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