In a recent study published in the journal, EBioMedicine, researchers showed that patients who suffer from diabetic nephropathy (DN) experience mitochondrial DNA changes prior to the onset of symptoms. Evidence points to a disruption in mitochondrial bioenergetics as a factor in the development and progression of the disease.
Diabetic nephropathy is a progressive kidney disease that arises as a complication of diabetes. DN affects >100 million people worldwide and is the leading cause of kidney failure.
In this current study, researchers determined that hyperglycemia has a detrimental effect on mitochondria. This was determined using the Bioenergetic Health Index (BHI), which gauges mitochondria function by measuring energy production. It is thought that as the BHI declines it acts as a biomarker of the patient’s overall ability to provide sufficient energy to fight disease.
Mitochondrial dysfunction can affect the function of cells throughout the body resulting in a variety of diseases. Similarly, diabetes can cause an increased risk of other complications that affect major organs, including the eyes (retinopathy), heart (diabetic cardiomyopathy), blood vessels (peripheral vascular disease) and brain (dementia). This multi-organ impact of diabetes complications resembles mitochondrial genetic disease and suggests a systemic dysfunction in the body.
Therapeutic strategies that promote the removal of damaged mitochondria from the cell and restore mitochondrial function may hold the key to treating DN before the progression of the disease.