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UoH scientists unravel cellular and molecular basis for obesity-related Proteinuria

Research led by scientists, Dr. Anil Kumar Pasupulati of Department of Biochemistry at UoH, and Dr. G Bhanuprakash Reddy, Scientist G with NIN, investigated the pathobiology of obesity-induced kidney ailments.

Published Date – 16 May 2024, 06:53 PM


UoH scientists unravel cellular and molecular basis for obesity-related Proteinuria

Dr. G Bhanuprakash Reddy (L), Dr. Anil Kumar Pasupulati.

Hyderabad: A study carried out by University of Hyderabad (UoH) scientists has unraveled the cellular and molecular basis for obesity related proteinuria, a kidney ailment.

Research led by scientists, Dr. Anil Kumar Pasupulati of Department of Biochemistry at UoH, and Dr. G Bhanuprakash Reddy, Scientist G with NIN, investigated the pathobiology of obesity-induced kidney ailments.


The scientists unraveled the cellular and molecular basis for obesity-related proteinuria using the Wistar NIN-Obese rat model and a high-fat (40 per cent) fed mice model.

They found that both models of obesity have severe proteinuria, elevated protein in urine.

Developmental Origins Of Obesity Kidney Disease

Developmental Origins Of Obesity Kidney Disease

Upon investigation, they found that podocytes, crucial cells in the nephron (the functional unit of the kidney), are injured, i.e., they showed cellular distortions. Further, they found that the WT1 (Wilms Tumor1) transcription factor gets up-regulated in podocytes from obese rats and high-fat-fed mice.

Interestingly, WT1 is essential in kidney development in the embryonic stages, and in adults, its expression is minimal and confined only to podocytes. The scientists observed reactivation of WT1 in obese rodent models, which is concurrent with increased mobility of otherwise static podocytes. They believe that reactivation of the embryologically active transcription factor, WT1, could be the basis for observed podocyte damage and proteinuria in obese-rodent models.

Big-data analysis from patients with chronic kidney disease revealed elevated WT1 expression in podocytes and their precursors.

Currently, both groups are intensively investigating means to curtail WT1 in obese settings to prevent obesity-induced podocyte injury and, in turn, to control proteinuria. The study was recently published in the International Journal of Obesity, a Nature Press Journal.

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