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T2DM

Changes to mitochondria drive chronic inflammation linked to T2DM

Researchers at the University of Kentucky have reported that changes to mitochondria drive chronic inflammation from cells exposed to certain types of fats, shattering the prevailing assumption that glucose was the culprit

The underlying causes of inflammation in obesity and type 2 diabetes mellitus (T2DM) are multifactorial and complex, which has hampered efforts to develop treatments to prevent complications from a disease that is the third leading cause of death in the US. Researchers at the University of Kentucky have reported that changes to mitochondria drive chronic inflammation from cells exposed to certain types of fats, shattering the prevailing assumption that glucose was the culprit.

The study, ‘Fatty Acid Metabolites Combine with Reduced β Oxidation to Activate Th17 Inflammation in Human Type 2 Diabetes’, published in Cell Metabolism, was led by Barbara Nikolajczyk (UK Barnstable Brown Diabetes Center, Department of Pharmacology and Nutritional Sciences) and Douglas Lauffenberger (MIT Department of Biological Engineering).

Nikolajczyk and Lauffenberger did not set out to disprove the glucose-inflammation causation theory. Based on the importance of glycolysis - a 10-reaction sequence that produces energy - in other types of inflammation, the team hypothesised that immune cells from patients with type 2 diabetes would produce energy by burning glucose.

"We were wrong," said Nikolajczyk. "We exclusively used immune cells from human subjects for all of the work.” The team was surprised to find that glycolysis was not driving chronic inflammation. Instead, a combination of defects in mitochondria and elevated fat derivatives were responsible.

Nikolajczyk said she sees applications for this research in both basic and clinical sciences. She hopes to precisely define pro-inflammatory lipid types and explore associations between circulating and/or tissue-associated lipids and insulin resistance, one key feature of Type 2 diabetes. She is also interested in contributing to the development of new analytical approaches, spearheaded by Lauffenburger's team, that leverage ongoing lipid-related findings into a new understanding of pathology in type 2 diabetes.

"Aggressive blood glucose control to lower the risk of diabetic complications has been the goal for most people with Type 2 Diabetes for decades," added Nikolajczyk. "Our data provide an explanation for why people with tight glucose control can nonetheless have disease progression."

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