Podocytes demonstrate a strong reliance on insulin to function properly, according to a study published in Cell Metabolism (2010;12:329-340). Mice hosting podocytes with no insulin receptors developed significant albuminuria as well as histologic features of diabetic nephropathy, even though the mice were neither diabetic nor normoglycemic.
The study showed that insulin rapidly and directly signals to the podocyte in the glomerulus, is able to remodel the actin cytoskeleton of this cell, and is crucial in maintaining the integrity of the glomerular filtration barrier. When podocyte insulin signaling is lost, glomerular changes characteristic of the features of diabetic nephropathy develop.
The results suggest that insulin resistance of the podocyte could be an important trigger for many of the pathological processes seen in diabetic nephropathy.