Pregnancy has a diabetogenic effect on maternal carbohydrate metabolism, characterized by reduced tissue response to insulin, hyperinsulinemia, and hyperglycemia. Insulin resistance isprimarily due to the action of human placental lactogen (hPL), which increases the resistance of peripheral tissues to the effects of insulin. The hormone hPL is secreted in proportion to placental mass, resulting in increased insulin resistance as pregnancy progresses. Progesterone and estrogen may also contribute to insulin resistance. Hepatic glycogen synthesis and storage is increased, and gluconeo-genesis is inhibited.
The net effect of these changes is that the maternal response to a glucose load is blunted, producing postprandial hyper-glycemia Additionally, the fetoplacental unit serves as a constant drain on maternal glucose levels. Glucose is the primary fuel for the placenta and fetus and, thus, delivery of glucose from the mother to the fetus occurs by facilitated diffusion. As a result, maternal hypoglycemia develops during periods of fasting.
Pregnancy causes an increase in circulating concentrations of all lipids, lipoproteins, and apolipoproteins. During early preg-nancy, fat storage in central tissues predominates. Later in pregnancy, lipolysis predominates, possibly triggered by maternal fasting hypoglycemia. In the absence of glucose, increased plasma concentrations of free fatty acids, triglyc-erides, and cholesterol provide energy for the mother; this has been characterized as accelerated starvation. Following delivery, the concentrations of all lipids return to nonpregnancy levels, a process accelerated by breast-feeding.
Pregnancy is characterized by the intake and utilization of approximately 1 kg of protein above the normal non-pregnant state. At term, 50% of the additional protein is utilized by the fetus and placenta, and the remainder is shared by the uterus, breasts, maternal hemoglobin, and plasma proteins.