However, the same gene is also associated with a wide spectrum of renal or kidney manifestations that eventually lead to end-stage kidney failure among individuals.
Published Date – 5 June 2024, 11:20 PM
Representational Image
Hyderabad: If you are obese, then invariably you carry the risk of chronic kidney disease leading to kidney failure.
A group of researchers from Hyderabad in a study have indicated that a WT1 gene, which is linked to making protein necessary for development of kidneys and gonads, is also a major reason why obese people stand a risk of renal or kidney failure.
It is a known fact that WT1 (Wilms’ tumor 1) plays a vital role in the development of kidneys at an embryonic stage.
However, the same gene is also associated with a wide spectrum of renal or kidney manifestations that eventually lead to end-stage kidney failure among individuals.
The research group from Hyderabad-based National Institute of Nutrition (NIN) and University of Hyderabad (UoH) in the study said, “Our study discovered elevated expression of WT1 in the pathogenesis of obesity- related glomerulopathy and kidney dysfunction.”
However, the precise mechanism of WT1 induction and its involvement needs further investigation, the study, published in International Journal of Obesity, Nature Press Journal (March, 2024), said.
Essentially, the researchers employed two obese rodent models with high-fat content (40 per cent) and unravelled the cellular and molecular basis for obesity-related kidney ailment (glomerulopathy).
The team found “Elevated expression of WT1 in podocytes (highly specialized cells in kidneys) in obesity settings. The role of WT1 in kidney disease was confirmed by expressing WT1 in HEK293 cells.
The researchers, including senior NIN scientist Dr G Bhanuprakash Reddy and Dr P Anil Kumar from UoH, said, “This study indicated the novel role of WT1 in the pathogenesis of obesity- related chronic kidney diseases.
Big-data analysis from patients with CKD revealed elevated WT1 expression on podocytes and their precursors.”
