Why would a thiamin deficiency result in lactic acidosis?

Why would a thiamin deficiency result in lactic acidosis?

• A. It impairs glycolysis, leading to lactate buildup
• B. It prevents glycolysis by blocking glyceraldehyde-3-phosphate dehydrogenase
• C. It blocks conversion of pyruvate to acetyl-CoA, causing pyruvate to convert to lactate
• D. It increases hepatic glucose production

Answer: (C)

Thiamin serves as a cofactor for the pyruvate dehydrogenase complex, the enzyme that converts pyruvate into acetyl-CoA to feed the Krebs cycle. When thiamin is deficient, PDH activity falls, so pyruvate accumulates. With limited ability to oxidize pyruvate in the mitochondria, the excess pyruvate is diverted to lactate production via lactate dehydrogenase, leading to an buildup of lactate and a drop in pH—lactic acidosis. The glycolytic steps themselves don’t rely on thiamin in the same way, so glycolysis isn’t directly blocked by thiamin deficiency. The result is lactate accumulation from the impaired conversion of pyruvate to acetyl-CoA, not from increased hepatic glucose production.

Thiamin serves as a cofactor for the pyruvate dehydrogenase complex, the enzyme that converts pyruvate into acetyl-CoA to feed the Krebs cycle. When thiamin is deficient, PDH activity falls, so pyruvate accumulates. With limited ability to oxidize pyruvate in the mitochondria, the excess pyruvate is diverted to lactate production via lactate dehydrogenase, leading to an buildup of lactate and a drop in pH—lactic acidosis. The glycolytic steps themselves don’t rely on thiamin in the same way, so glycolysis isn’t directly blocked by thiamin deficiency. The result is lactate accumulation from the impaired conversion of pyruvate to acetyl-CoA, not from increased hepatic glucose production.