Gestational diabetes and obesity are the common metabolic abnormalities occurring during pregnancy. Decreased maternal pregravid insulin sensitivity (insulin resistance) coupled with an inadequate insulin response are the pathophysiological mechanisms underlying the development of gestational diabetes. Insulin-regulated carbohydrate, lipid and protein metabolism are all affected to a variable degree. Decreased maternal insulin sensitivity in women with gestational diabetes may increase nutrient availability to the fetus, possibly accounting for an increased risk of fetal overgrowth and adiposity. Epidemiological studies from Europe show an increased risk of the insulin resistance syndrome in adults who were low birth weight at delivery. However, in the United States over the past 20 y there has been a significant 33% increase in the incidence of type 2 diabetes, which has been associated with a parallel increase in obesity. All age groups have been affected but the most dramatic increases have occurred in adolescents. The relationship between decreased maternal insulin sensitivity and fetal overgrowth particularly in obese women and women with gestational diabetes may help explain the increased incidence of adolescent obesity and related glucose intolerance in the offspring of these women. In this review, we address 1) the pathophysiology of gestational diabetes, 2) the changes in maternal insulin sensitivity during pregnancy that effect maternal accretion of adipose tissue and energy expenditure, 3) the influence of maternal metabolic environment on fetal growth, 4) the life-long effect of being born at either extreme of the birth weight continuum and 5) micronutrients and decreased insulin sensitivity during pregnancy.