Krebs (citric acid) cycle entry step Before most 2-carbon fragments derived from carbohydrates, fats, or proteins can enter the Krebs citric acid cycle, they must be converted into which common intermediate?

Introduction / Context:
The Krebs (citric acid) cycle is a central hub of metabolism. Diverse fuels—glucose, fatty acids, and amino acids—are funneled into a common 2-carbon carrier before condensation with oxaloacetate. Recognizing this “gateway” molecule is essential for integrating catabolic pathways.

Given Data / Assumptions:

• Glycolysis yields pyruvate from glucose.
• Beta-oxidation yields acetyl units from fatty acids.
• Certain amino acids are catabolized to acetyl units or TCA intermediates.

Concept / Approach:
Pyruvate is decarboxylated and activated by the pyruvate dehydrogenase complex to form acetyl-CoA (a 2-carbon thioester) plus CO₂ and NADH. Acetyl-CoA then condenses with oxaloacetate to form citrate, initiating the cycle. NADH and FADH₂ are electron carriers generated by prior steps; they are not substrates entering the cycle.

Step-by-Step Solution:
Trace glucose → pyruvate via glycolysis.Convert pyruvate → acetyl-CoA by oxidative decarboxylation.Feed acetyl-CoA into the Krebs cycle by combining with oxaloacetate to form citrate.Therefore, the required common intermediate is acetyl-CoA.

Verification / Alternative check:
Fatty acid beta-oxidation and ketogenic amino acid breakdown also produce acetyl-CoA, converging on the same entry route into the TCA cycle, confirming its central role.

Why Other Options Are Wrong:

• Citrate/oxaloacetate: cycle intermediates, not the universal entry product.
• NADH/FADH₂: electron carriers, not carbon fragments entering the cycle.
• Pyruvate: must first be converted to acetyl-CoA in aerobic metabolism.

Common Pitfalls:
Confusing pyruvate with acetyl-CoA; overlooking the regulatory role of the pyruvate dehydrogenase complex in controlling carbohydrate flux into the TCA cycle.

Final Answer:
Acetyl-CoA.