Final answer:
In a glucose receptor knockout mouse, glucose would not be transported efficiently into cells due to the lack of glucose receptors, causing high glucose levels in the bloodstream and low levels within cells, similar to the effects observed in insulin resistance and type 2 diabetes.
Step-by-step explanation:
If a glucose receptor knockout mouse was injected with glucose directly into the bloodstream, the expected outcome would be that glucose levels in the blood would be elevated. Since the mouse lacks functional glucose receptors, glucose transport into the cells would be impaired.
In normal physiology, glucose is transported into cells via glucose transport proteins, particularly GLUT4, which is mobilized to the cell membrane in response to insulin signaling. Without the glucose receptors, insulin cannot promote the uptake of glucose into the cells, leading to hyperglycemia, or high blood sugar levels. Within the cells, glucose levels would remain low due to the absence of glucose uptake.
Moreover, since glucose is the body's primary source of energy, and is converted into ATP through glycolysis, the mouse's cells would likely be energy-depleted. Long-term effects could mimic those seen in type 2 diabetes, where persistent high blood glucose levels are common due to insulin resistance. The controlling blood glucose mechanisms would be ineffective due to the cells' inability to respond to insulin.