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| AuthorLois Jovanovic, MD | Section EditorsDavid M Nathan, MDMichael F Greene, MD | Deputy EditorVanessa A Barss, MD |
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Pregnancy is characterized, in part, by insulin resistance and hyperinsulinemia, thus it may predispose some women to develop diabetes during gestation. The resistance stems from placental secretion of diabetogenic hormones including growth hormone, cortisol, placental lactogen, and progesterone, as well as increased maternal adipose deposition, decreased exercise, and increased caloric intake. These and other endocrinologic and metabolic changes ensure that the fetus has an ample supply of fuel and nutrients at all times. Gestational diabetes (GDM) occurs when pancreatic function is not sufficient to overcome the insulin resistance created by changes in diabetogenic hormones during pregnancy. (See "Maternal endocrine and metabolic adaptation to pregnancy".)
Gestational diabetes is defined as any degree of impaired glucose tolerance of with onset or first recognition during pregnancy [1].
Most women with GDM have impaired glucose tolerance that begins in pregnancy, but some may have type 2 diabetes that was unrecognized prior to pregnancy. About 10 percent of women with GDM have circulating islet-cell antibodies; they may have a "latent" form of type 1 diabetes, although their risk of developing type 1 diabetes is not known [2]. Specific HLA alleles (DR3 or DR4) appear to predispose to the development of type 1 diabetes after delivery, as does the presence of islet-cell antibodies [3].
Several adverse outcomes are associated with increasing levels of glucose impairment [4-6]:
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