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University of Hyderabad identifies new enzyme, may treat Diabetic nephropathy

While it is widely known that diabetic patients suffer from kidney diseases, it was not known as to how exactly diabetes triggers the same.

Published: 14th December 2019 11:25 AM  |   Last Updated: 14th December 2019 11:25 AM   |  A+A-

Diabetes

For representational purposes

By Express News Service

HYDERABAD: In a groundbreaking study, researchers from University of Hyderabad have identified an enzyme that can be targeted by drugs to cure diabetic nephropathy — a fatal kidney disorder common among diabetic patients.

While it is widely known that diabetic patients suffer from kidney diseases, it was not known as to how exactly diabetes triggers the same.

In their study, the UoH researchers have explained how this occurs — including the role of the enzyme known as gamma-secretase — and opens up the possibility of developing a drug that can inhibit this enzyme and prevent kidney diseases among diabetic patients.

The production of growth hormone in human beings declines with age, but in diabetic patients the hormone gets produced in excess due to a variety of factors, including lack of insulin production.

The team of UoH researchers headed by Anil K Pasupulati, Assistant Professor at the Department of Biochemistry, have reported that excess growth hormone in diabetic patients activates the Notch1 signalling channel in podocytes, a type of cells in the kidney that play an instrumental role in ultrafilteration of blood. As the Notch1 signalling channel gets activated, it causes a decline in the number of podocytes, affecting the functioning of kidney which is manifested in proteinuria (presence of proteins in the urine).

The researchers report that activation of Notch1 signalling pathway also results in glomerular fibrosis, another reason behind kidney disorder among diabetic patients. Speaking to Express, Pasupulati said, “We are now working on how exactly gamma-secretase gets activated due to the presence of  excess growth hormones.”



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