Mitochondria, not glucose, could be driving inflammation in type 2 diabetes

Jack Woodfield
Wed, 21 Aug 2019
Mitochondria, not glucose, could be driving inflammation in type 2 diabetes
A breakthrough discovery has cast doubt on previous assumptions that glucose is the main driving force behind chronic inflammation within type 2 diabetes.

University of Kentucky researchers carried out a study to test whether glucose is the cause of chronic inflammation - previously it has been assumed that raised blood glucose levels is the cause.

Their investigations indicate that an interaction between certain lipids (blood fats) and mitochondria (the powerhouse of cells in the body) appeared to be the problem.

Blood glucose control is still important for managing type 2 diabetes, but the researchers state it may not be the key factor in the development of problems related to inflammation such as heart and kidney disease.

Originally the researchers had set out to prove another theory: that immune cells from people with type 2 diabetes would produce energy by burning glucose.

"We were wrong," said Barbara Nikolajczyk, from the UK Barnstable Brown Diabetes Center, Department of Pharmacology and Nutritional Sciences, who co-led the study.

The researchers found instead that energy from glucose was not driving chronic inflammation, but rather it was a combination of defects in mitochondria and an increase in fat derivatives that were responsible.

"Our data provide an explanation for why people with tight glucose control can nonetheless have disease progression."

Nikolajczyk and colleagues now plan to precisely identify which types of fatty derivatives are linked with inflammation and to investigate associations between lipids and insulin resistance.

The findings have been published in the Cell Metabolism journal.
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