Final answer:
A genetic change causing a disrupted cellular response to insulin signaling in an individual without diabetes, similar to type 2 diabetes, would likely affect the insulin receptors or glucose transporters, leading to insulin resistance and hyperglycemia.
Step-by-step explanation:
Insulin Signaling Disruption and Type 2 Diabetes
A genetic change in an individual without diabetes that could result in a disrupted cellular response to insulin signaling, similar to that seen in individuals with type 2 diabetes, would likely involve the insulin receptors or the glucose transporters within cells. Since insulin resistance is a hallmark of type 2 diabetes, a mutation that leads to defective insulin receptors on the cell membrane, or that impairs the ability of glucose transporters to respond to insulin, would mimic the effects of this condition. Such changes would prevent cells from taking up glucose efficiently, leading to elevated levels of glucose in the blood, which is symptomatic of type 2 diabetes.
Considering the mechanism of insulin resistance in type 2 diabetes, the genetic change most likely to cause a similar phenotype would be one that disrupts the function or expression of the insulin receptor or the glucose transporter proteins. These disruptions can result in target cell resistance to insulin, preventing the normal uptake of glucose into cells and leading to hyperglycemia (high blood sugar levels).