Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance that begins or is first recognized during pregnancy. The prevalence of GDM is highly variable, depending on the population studied, and reflects the underlying pattern of diabetes in the population. GDM manifests by the second half of pregnancy and disappears following delivery in most cases, but is associated with the risk of subsequent diabetes development. Normal pregnancy induces carbohydrate intolerance to favor the availability of nutrients for the fetus, which is compensated by increased insulin secretion from the maternal pancreas. Pregnancy shares similarities with adiposity in metabolism to save energy, and both conditions favor the development of insulin resistance (IR) and low-grade inflammation. A highly complicated network of modified regulatory mechanisms may primarily affect carbohydrate metabolism by promoting autoimmune reactions to pancreatic β cells and affecting insulin function. As a result, diabetes development during pregnancy is facilitated. Depending on a pregnant woman's genetic susceptibility to diabetes, autoimmune mechanisms or IR are fundamental to the development autoimmune or non-autoimmune GDM, respectively. Pregnancy may facilitate the identification of women at risk of developing diabetes later in life; autoimmune and non-autoimmune GDM may be early markers of the risk of future type 1 and type 2 diabetes, respectively. The most convenient and efficient way to discriminate GDM types is to assess pancreatic β-cell autoantibodies along with diagnosing diabetes in pregnancy.
Keywords: Autoimmune diabetes; Gestation; Islet cell autoantibodies; Pregnancy complications; Tolerance.