In the catabolic phase of pregnancy, what mechanism ensures fetal glucose supply?

Prepare for the NCC Credential in Inpatient Antepartum Nursing. Study with flashcards and multiple choice questions, each question has hints and explanations. Get ready for your exam!

Multiple Choice

In the catabolic phase of pregnancy, what mechanism ensures fetal glucose supply?

Explanation:
In late pregnancy, the body shifts to ensure the fetus has a steady glucose supply. This happens because placental hormones induce insulin resistance in the mother, reducing how effectively maternal tissues use insulin. As insulin sensitivity decreases by a substantial amount (often described as a 50–70% drop), maternal blood glucose remains elevated enough to cross the placenta through glucose transporters, delivering glucose to the growing fetus. This mechanism is why glucose transfer to the fetus is maintained during the catabolic phase. If glucose uptake by the mother increased due to higher insulin sensitivity, glucose would be drawn into maternal tissues rather than passed to the fetus, which would not meet the fetal needs. Blocking placental glucose transport would stop fetal glucose supply, and fetal glucose metabolism ceasing would be incompatible with fetal growth.

In late pregnancy, the body shifts to ensure the fetus has a steady glucose supply. This happens because placental hormones induce insulin resistance in the mother, reducing how effectively maternal tissues use insulin. As insulin sensitivity decreases by a substantial amount (often described as a 50–70% drop), maternal blood glucose remains elevated enough to cross the placenta through glucose transporters, delivering glucose to the growing fetus. This mechanism is why glucose transfer to the fetus is maintained during the catabolic phase.

If glucose uptake by the mother increased due to higher insulin sensitivity, glucose would be drawn into maternal tissues rather than passed to the fetus, which would not meet the fetal needs. Blocking placental glucose transport would stop fetal glucose supply, and fetal glucose metabolism ceasing would be incompatible with fetal growth.

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