4 Feb 2020

Figuring out why diabetes affects the kidneys

L-R: Professors Karin Jandeleit-Dahm,
Mark Cooper and Dr Jakob Oestergaard
Dr Jakob Oestergaard is a Danish physician, who is currently visiting Central Clinical School's Department of Diabetes for one year from Aarhus University Hospital in Denmark to pursue his interest in diabetes research and clinical treatment.

In particular, he’s interested in the mechanisms which lead to diabetic nephropathy and other complications from diabetes. This represents a major health issue, as type 2 diabetes is on the increase, now affecting almost 10% of the world’s population. Up to 40% of these patients will develop diabetic kidney disease.

Dr Oestergaard has been doing research for fifteen years on diabetic kidney disease, and it seems perhaps inevitable that he would have crossed paths with two of the world’s leading diabetic kidney disease researchers, Professors Mark Cooper and Karin Jandeleit-Dahm, both in Monash University’s Department of Diabetes. He is now visiting Monash University to work closely with them during 2020, as both clinician and researcher.

Dr Oestergaard said that his own particular line of interest stemmed from his discovery that the innate immune system contributes to diabetic kidney disease.

“The innate immune system is primed to recognise - and attack – patterns of carbohydrate structures which are common on pathogenic microorganisms. These particular structures are rare on healthy human cells and extracellular matrix, but might arise in subjects with diabetes because of their elevated glucose concentration.

“Pattern recognition molecules from the innate immune system seem to recognise self-cells or extracellular matrix in diabetes, which then could cause an attack to take place on the body’s own cells. Activating these immune components causes inflammation, and may also stimulate cell proliferation.”

While at Monash University, Dr Oestergaard will be investigating other drivers of inflammation in diabetic kidney disease. “There is a complicated cross-talk of multiple mechanisms that are involved in diabetic kidney disease. More of these pathways are connected and cause inflammation. We are currently interested in inflammation that is induced via activation of what is called an ‘inflammasome’.

Professor Mark Cooper (right) examines a patient in clinic with
Dr Jakob Oestergaard observing.
"We’re working on a mouse model of diabetic kidney disease and aim to block inflammasome activation. We want to dampen down the body’s pro-inflammatory response and investigate the impact of this on the development of diabetic kidney disease."

Dr Oestergaard will be following Professors Cooper and Jandeleit-Dahm in clinic as part of his specialist training as an endocrinologist, in addition to joint submission of scientific work to the American Diabetes Association, taking place in June this year.

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