While the underlying causes of inflammation in obesity and type 2 diabetes mellitus may not yet have been properly understood, a new research seems to have made a breakthrough by finding that the changes to mitochondria — the powerhouse of cells — drive chronic inflammation from cells exposed to certain types of fats, shattering the prevailing assumption that glucose was the culprit.
According to the study, chronic inflammation fuels many of the devastating complications of type 2 diabetes, including cardiovascular, kidney, periodontal diseases, and is thus one of the key targets for therapy development, reports The Indian Express.However the research, published in Cell Metabolism by a team led by Barbara Nikolajczyk (UK Barnstable Brown Diabetes Center, Department of Pharmacology and Nutritional Sciences) and Douglas Lauffenberger (MIT Department of Biological Engineering), didn’t 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 those immune cells from patients with type 2 diabetes would produce energy by burning glucose. “We were wrong,” Nikolajczyk said.
“We exclusively used immune cells from human subjects for all of the work,” Nikolajczyk explained, noting that humans, but not animal models of type 2 diabetes, have the specific pro-inflammatory T cell profile her team had identified in earlier research.
The team was surprised to find that glycolysis wasn’t 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.