Insulin resistance is a consequence of excess fat originating from an imbalance of energy intake and expenditure. Unwanted fat deposition in various non-adipose organs leads to the synthesis of sphingolipids, which interfere with the signaling and secretion of insulin. Over the last couple of decades, a sphingolipid species, ceramide, has been found to be a deleterious lipid associated with the development of type 2 diabetes, which is indicated by the person's resistance to insulin. This study investigates the role of two genes, TSPAN and ACSM5, which are involved in lipid metabolism. We speculate that these two genes may also be involved in ceramide synthesis. To better understand their biological properties, this study assesses the expression pattern of sphingolipid metabolizing proteins in various in-vitro disease models upon overexpressing the gene of interest. This research has a clinical translational value by regulating the metabolism of sphingolipids and thereby aiding in the treatment of type 2 diabetes and other metabolic diseases by regulating ceramide synthesis.