Managing Diabetes and Pregnancy

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John L. Kitzmiller

Maternal-Fetal Medicine, Good Samaritan Hospital, San Jose, Calif., USA

Introduction and Overview of Perinatal Outcome

Pregnancy produces major changes in metabolic fuels and hormones and in this way affects the management of diabetes. Basal hepatic glucose production increases significantly with advancing gestation in lean or obese controls, but increased basal insulin secretion and fetal-placental utilization of glucose result in slightly lower fasting blood glucose levels. Fat deposition is accentuated in early pregnancy, but lipolysis is enhanced later in gestation, and more glycerol and free fatty acids (FFA) are released in the postabsorptive state (distant from meals). The increased FFA may contribute to the insulin resistance on glucose utilization by skeletal muscle during pregnancy. Ketogenesis is also accentuated in the postabsorptive state during pregnancy, probably due to increased provision of substrate FFA and hormonal effects on the maternal liver cells.

Despite increased first- and second-phase insulin release after a carbohydrate load in normal pregnancy, in the fed state there is a significant reduction in net insulin-mediated glucose disposal by the third trimester. The result is somewhat higher maternal blood glucose levels in nondiabetic subjects, and marked hyperglycemia in inadequately treated pregnant diabetic women. The contra-insulin effects of gestation are related to hPL, progesterone, cortisol, and prolactin, with the defects at the postreceptor level of muscle and hepatic cells. Due to the insulin resistance and enhanced ketogenesis of pregnancy, ketoacidosis is a great danger during gestation. Markedly increased doses of insulin are usually required to control hyperglycemia after the first trimester. Glucagon is well suppressed by glucose during pregnancy, and secretory responses of glucagon to amino acids are not increased above nonpregnant levels.

Gravida

Insulin effectiveness

ÏMetabolicfuels(|) (Diet, exercise, insulin Rx)

Glucose

T Brat I amii

Branch chain amino acids

Placenta

Altered function?

Fetus

I Lipids ^

Ketones

ÏMetabolicfuels(|) (Diet, exercise, insulin Rx)

Glucose

T Brat I amii

Branch chain amino acids

I Lipids ^

Ketones

Altered function?

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