Inflammation may be behind diabetic nephropathy in individuals with type 2 diabetes
Changes that control inflammatory responses within the kidneys may be the root cause of severe nephropathy stemming from type 2 diabetes, according to a team of researchers from the University of Louisville.
Type 2 diabetes is the leading cause of nephropathy and kidney failure, but the process that underlies the progression of the disease has been poorly understood. Experts knew that loss of kidney function was associated with long-term uncontrolled blood sugar levels, but the exact reason for this connection was unknown.
Studying the progression of nephropathy can be difficult due to the short life expectancy of individuals who suffer from the condition. Additionally, their treatment schedule can make nephropathy patients a difficult population to examine.
However, the current study was the first to examine changes in all kidney-related genes in mice as they progressed from moderate to severe nephropathy. The results, which were published in the journal Experimental Nephropathy
, indicated that some gene expression differences in mice bred to experience diabetic nephropathy increased by a factor of 10, compared to normal mice.
Additionally, the study revealed that genes involved in inflammatory responses changed the most, indicating that their functions are likely at the heart of the progression of diabetic nephropathy.
While the findings pointed in the direction of inflammatory genes, they still do not indicate the exact process through which DNA cause nephropathy. Furthermore, the findings stopped short of suggesting any theoretical treatment approach.
"In future studies, we can use this mouse model to explore whether inflammation causes disease progression or if the progression of the disease causes further inflammation," said Paul Epstein, PhD, the lead author of the study on type 2 diabetes complications. "If it turns out that inflammation is causal, the next step would be to test the effectiveness of anti-inflammatory drugs."