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Question #47646
The Question
In a patient suffering from severe insulin deficiency (Diabetes Mellitus), the body shifts to fat metabolism, leading to the production of harmful ketone bodies. Which of the following best explains the metabolic bottleneck in the amphibolic pathway that triggers this ketogenesis?
Options
- A.
Depletion of oxaloacetic acid for gluconeogenesis prevents the entry of excess acetyl-CoA into the TCA cycle.
- B.
Excess acetyl-CoA allosterically inhibits the conversion of fatty acids to pyruvic acid in the mitochondrial matrix.
- C.
Glucagon-induced inhibition of the electron transport chain causes an accumulation of NADH, halting the Krebs cycle.
- D.
The inability of glucose to enter cells directly forces the conversion of pyruvic acid into ketone bodies.
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
Acetyl_CoA|Citric_Acid_Cycle|Insulin_vs_Glucagon_Effects
Why This Question Is Tricky
Common Mistakes
Conceptual Pivot: Students often memorize the isolated fact from Chemical Coordination that 'insulin deficiency causes ketone body formation' but fail to integrate it with the 'Amphibolic Pathway' from Respiration.
The trap lies in understanding the exact biochemical bottleneck: Acetyl-CoA cannot enter the Krebs cycle without Oxaloacetate, which is being diverted for gluconeogenesis.
Quick Facts About This Question
Question Information
| Subject | Biology |
| Chapter | Respiration in Plants - Class 11 |
| Concept | Amphibolic Pathway |
| Difficulty | 8 |
| Cognitive Load | 5 |
| Target Solve Time | 120 sec |
| Access | Free |