Abstract: Gestational Diabetes Mellitus is carbohydrate intolerance resulting in hyperglycemia of variable severity with onset or first recognition during pregnancy. The predominant pathogenic factor in GDM could be inadequate insulin secretion. It has been convincingly demonstrated that GDM occurs as
a result of combination of insulin resistance and decreased insulin secretion. Pregnancy is associated with profound hormonal changes that have a direct effect on carbohydrate tolerance. In early pregnancy, both
progesterone and estrogen levels rise, but their action on insulin is counterbalanced, as progesterone causes insulin resistance and estrogen is protective. In the second trimester, HPL, cortisol and prolactin levels
all rise, causing decreased phosphorylation of IRS-1 and profound insulin resistance. In most subjects, pancreatic insulin secretion rise to meet this need, but in those with underlying beta-cell defects, hyperglycemia ensues. In women with GDM, the insulin resistance of pregnancy is exaggerated, especially if fasting hyperglycemia is present,
and is related to additional defective tyrosine phosphorylation of the insulin receptor beta-subunit. Keywords: insulin resistance, gestational
diabetes, human hormones