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GDM is similar to type 2 diabetes, as it is associated with insulin resistance and insen-sitivity. The exact mechanism responsible for the development of GDM is not fully understood; however, pancreatic beta-cell dysfunction may be responsible. As hormonal levels continue to rise in the second and third trimesters, beta-cells are unable to produce or secrete sufficient insulin for glucose regulation. Fasting blood glucose levels are elevated as insulin deficiency and resistance increase. Delayed insulin response, insulin resistance, and placental hormonal antagonism are responsible for postprandial glucose excursions. Human placental lactogen and cortisol block insulin receptors, which creates a deficiency in circulating insulin production, and results in increased glucose intolerance. In normal pregnancy, the beta-cells compensate by increasing insulin secretion; in GDM the decreased insulin response will result in elevated glycemic levels [57].

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