The natural tendency of normal pregnancy hormones is to sustain elevated postprandial blood glucose levels to provide nourishment to the fetus. Table 3 outlines the sequential rise of these hormones. The first of these hormones, human chorionic gonadotropin (hCG), does not, itself, possess diabetogenic properties. It does, however, maintain the corpus luteum, which produces progesterone, a hormone with powerful anti-insulin properties. Estradiol has weaker diabetogenic traits. Its full effect is difficult to determine because it is released almost simultaneously with the very potent progesterone. The major diabetogenic hormones of the placenta are hCS, previously referred to as human placental lactogen (hPL), and progesterone. Also, serum maternal cortisol levels (both bound and free) are increased. At the elevated levels seen during gestation, prolactin also has a diabetogenic effect (36).
In addition to the increasing anti-insulin hormones of pregnancy, there is also increased degradation of insulin in pregnancy caused by placental enzymes comparable to liver insulinases. The placenta also has membrane-associated insulin-degrading activity (37). Concomitant with the hormonally induced insulin resistance and increased insulin degradation, the rate of disposal of insulin slows. The normal pancreas can adapt to these factors by increasing the insulin secretory capacity up to fourfold. If the pancreas fails to respond adequately to these alterations, gestational diabetes develops.
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