Changes within the podocyte slit diaphragm, actin cytoskeleton, and tubulin cytoskeleton structures lead to varying forms of Nephrotic syndrome, a renal disease that affects the filtration function in every 16 of 100,000 individuals, a third of those being children. Using Drosophila melanogaster nephrocytes, podocyte-equivalent cells, I elucidated the roles of individual actin and tubulin genes, examining how they work together to form the sophisticated structures in the nephrocytes. I further investigate how the cytoskeleton crosslinking protein GAS2L1 (Pickled eggs, Pigs) affects nephrocyte structure and function. Diabetes can also affect these podocyte structural components, resulting in diabetic nephropathy. I examined the environmental factor via high sugar diets and genetic manipulation of the insulin metabolic pathway to model diabetes, revealing the slit diaphragm and cytoskeleton structural defects in diabetic nephropathy. Furthermore, I show metformin, an antidiabetic drug, can be used to rescue nephrocyte function and structure using slit diaphragm, actin cytoskeleton, tubulin cytoskeleton, and mitochondria markers. This study provides essential insight to understand the filtration structure and sets up a platform to test new anti-diabetic medications using the nephrocyte model. The outlined markers can then be used to understand the medication’s mechanisms of action, allowing the clinical trial process to be streamlined through the reduction of time and resources necessary by utilizing Drosophila nephrocytes as the initial screening model.