By: Brenda Neugent
According to the results of a recent study, the onset of type 2 diabetes may be more closely related to inflammation than previous research has suggested.
Inflammation–the body’s attempt to heal itself in response to harmful substances or irritants–has been linked to type 2 diabetes and obesity for decades.
Researchers recently learned that those with type 2 diabetes have elevated levels of cytokines, a protein released in response to inflammation, especially inside fat tissue. This latest study, from the Department of Diabetes Complication Biology at Novo Nordisk in Malov, Denmark, expands on that research.
The study found that in mice, during the early stages of diabetes, a certain type of immune cell–the pathogen-fighting macrophage cell, which specializes in the removal of damaged cells from the body–invades the pancreas in response to the disease. The cells then flood the area with cytokines, which are linked to the loss of insulin-producing cells in the pancreas.
When the pancreas is no longer able to produce insulin, or the insulin amounts are compromised, diabetes symptoms worsen.
The research in part explains why diabetes symptoms grow more severe–and what particular actions contribute to the disease, opening the door to improved treatment options.
“The study may provide novel insights allowing development of tailor-made anti-inflammatory based therapies reducing the burden of type 2 patients,” said Alexander Rosendahl, Ph.D., a researcher involved in the study, in a press release. “These novel treatments may prove to complement existing therapies such as insulin and GLP-1 analogs.”
The study followed mice from a young age, and compared healthy mice with both early and more advanced cases of type 2 diabetes, focusing on the levels of macrophages in both. The diabetic mice had significantly more inflammation-related changes compared to the healthy mice.
“The more researchers learn about obesity and type 2 diabetes, the more it appears that inflammation plays a critical role in the progression and severity of these conditions,” said John Wherry, Ph.D., deputy editor of the Journal of Leukocyte Biology, where the research appeared. “This study sheds light on how a key inflammatory cell is connected to disease and what might go wrong when someone has type 2 diabetes. The knowledge gained from such studies offers hope that new immune-based therapies could be developed to mitigate the severity of such diseases.”
The new research appeared in the January 2014 issue of the Journal of Leukocyte Biology.