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Question #45443
The Question
A transgenic mouse model is engineered with a targeted mutation that renders insulin receptors completely non-functional across all tissues. The mouse exhibits severe hyperglycemia. Surprisingly, despite the high blood glucose and administration of high doses of exogenous insulin, blood glucagon levels remain paradoxically elevated. Which of the following best explains this persistent hyperglucagonemia?
Options
- A.
Insulin normally exerts a paracrine inhibitory effect on pancreatic alpha-cells, which is abolished due to the receptor mutation.
- B.
The lack of insulin-mediated glucose uptake via GLUT-4 in alpha-cells creates intracellular hypoglycemia, triggering glucagon release.
- C.
Exogenous insulin competitively binds to glucagon receptors on hepatocytes, initiating a compensatory positive feedback loop.
- D.
Severe systemic hyperglycemia directly stimulates alpha-cells to secrete glucagon to promote renal reabsorption of glucose.
Check Your Answer
Correct Answer
Step-by-Step Solution
Explanation
How the Examiner Thinks
Regulatory_Failure
Understand how NOT, EXCEPT, and logical constraints are used to manipulate exam results.
Concepts Behind This Question
Insulin|Glucagon|Transgenic Animal Purpose
Why This Question Is Tricky
Common Mistakes
Conceptual Pivot: Students often memorize the simplified NCERT fact that 'high blood glucose inhibits glucagon secretion' without understanding the micro-level mechanism.
The trap lies in failing to recognize that this inhibition is heavily dependent on the local (paracrine) action of insulin on alpha-cells.
Option B serves as a strong distractor by exploiting the misconception that all cells require insulin (via GLUT-4) for glucose uptake.
Quick Facts About This Question
Question Information
| Subject | Biology |
| Chapter | Chemical Coordination and Integration - Class 11 |
| Concept | Insulin vs Glucagon Effects |
| Difficulty | 8 |
| Cognitive Load | 5 |
| Target Solve Time | 120 sec |
| Access | Free |