During pregnancy, the fetus receives nutrients from across the placenta, including glucose, amino acids, and fatty acids via either active transport or facilitated diffusion. In the first trimester, maternal glycogen storage and endogenous glucose production increase. Pregnancy hormones (human placental lactogen and cortisol), estrogen, progesterone, and the constant fetal demand of glucose lower fasting maternal blood glucose levels [15, 16]. The maternal appetite is stimulated resulting in consumption of additional calories. Fasting and postprandial glucose levels rise in response to the extra glucose required for fetal growth. Elevated hormonal levels increase insulin resistance and the beta-cells produce and secrete additional insulin as glucose is transported across the placenta. Insulin resistance peaks by the latter part of the third trimester, which is characterized by a three-fold increase in insulin production and secretion. After delivery, insulin production returns to prepregnancy levels.
Other hormones thought to affect insulin resistance include leptin, insulin-like growth factors, relaxin, and adiponectin [17-19]. Maternal insulin does not cross the placental barrier unless bound to insulin immunoglobulins. Fat is deposited and stored primarily in early pregnancy, then mobilized in the third trimester as fetal energy demands increase. Free fatty acids have been shown to contribute to insulin resistance in late pregnancy .
Insulin is necessary for carbohydrate, fat, and protein metabolism. In type 1 diabetes, blood glucose levels remain elevated as insulin deficiency and the rise in free fatty acids lead to the formation of ketones and beta-hydroxybutyrate. The risk of diabetic ketoacidosis increases in the absence or lack of insulin. Women in optimal glycemic control may experience increased insulin sensitivity and decreased insulin requirements in the first trimester. During the second and third trimesters, elevated hormonal levels increase insulin resistance and additional insulin is necessary to maintain normal maternal glyc-emic levels and decrease fetal complications.
Type 2 diabetes is associated with impaired insulin secretion, insulin insensitivity, and pancreatic beta-cell dysfunction. Women with type 2 diabetes tend to be older, heavier, and have higher insulin resistance than women with type 1 diabetes. The fetal pancreas is stimulated to secrete additional insulin in the presence of excessive glucose. Higher fetal insulin levels may result in macrosomic growth. Exogenous insulin may be necessary to maintain normoglycemia as insulin deficiency and insulin resistance increase.
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