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Maternal hyperphagia and hyperinsulinism characterize the second half of rat gestation. Within this period two distinct metabolic phases have been identified. Initially (day 12), fat storage is enhanced with a 2–fold greater conversion of glucose into adipose tissue triglyceride fatty acids and a diminished release of free fatty acids. Placental and fetal fuel needs are minimal at this stage. After day 12 until term, insulin effectiveness progressively deteriorates, adipose tissue fatty acid formation from glucose declines to 1/3 of control, and maternal fat stores are increasingly mobilized as free fatty acids. These events are closely synchronized with the growth of the feto—placental unit. These results indicate that maternal fat storage is promoted by increases in food intake and plasma insulin at mid—term. Despite continuation of hyperphagia and hyperinsulinism into late gestation, maternal fat storage declines because of diminished tissue responsiveness to insulin. This mechanism is viewed as an adaptation for fetal growth whereby ingested glucose is diverted away from maternal tissues to the fetus. At the same moment, previously stored lipids are mobilized to provide an alternative energy source to the mother. (Endocrinology92: 984, 1973)
Knopp et al. (Sun,) studied this question.