Question

In one experiment, you have 2 mice of different strains, the first has no mutation or wild type (WT) and the second is a conditional knockout (KO) of the insulin receptor specifically in skeletal muscle. After an overnight fast, both are fed a glucose solution. One hour later, in both mice blood glucose levels have peaked suggesting that the glucose has been processed through the portal vein and into general circulation. Two hours later, blood glucose levels in the WT mouse have decreased and are back to baseline levels. However, blood glucose levels in the KO mouse remain high. At this 2 hour point, why does blood glucose levels remain high in the KO mouse? BRIEFLY describe the mechanism for this and any specific mediator/protein responsible for this mechanism.

Answer 1

In the second mice, the blood glucose level will remain high. Because insulin receptor encoding gene is knocked out in in this mice. That's why insulin receptor is not found functional in second mice. The insulin protein is synthesized in the second mice in wild type manner but it cannot bind to the insulin receptor. That's why the signalling event will not be preceded by the insulin receptor in the cell. It will not uptake glucose in the cell and there is not found any glycogenesis process in the cell. The glycogenesis leads to formation of glycogen from the glucose. That's why the Glucose level remain High in second mice.