Diabetogenic forces of normal pregnancy increase insulin requirements10

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The fetal demise associated with pregnancy complicated by Type 1 diabetes seems to arise from glucose extremes. Elevated maternal plasma glucose levels should always be avoided, because of the association of maternal hyperglycemia with subsequent congenital malformation and spontaneous abortions.2,5 To achieve normoglycemia, a clear understanding of 'normal' carbohydrate metabolism in pregnancy is paramount.

Thus, the amount of insulin required to treat Type 1 diabetic women throughout pregnancy needs to be sufficient to compensate for (1) increasing caloric needs; (2) increasing adiposity; (3) decreasing exercise; and (4) increasing anti-insulin or diabetogenic hormones of pregnancy. The major diabetogenic hormones of the placenta are human chorionic somatomam-motropin (hCS), previously referred to as human placental lactogen (hPL), estrogen and progesterone. Also, serum maternal cortisol levels (both bound and free) are increased. In addition, at the elevated levels seen during gestation, prolactin has a diabetogenic effect.10 The strongest insulin antagonist of pregnancy is hCS. This placental hormone appears in increasing concentrations beginning at 10 weeks of gestation. By 20 weeks of gestation, plasma hCS levels are increased 300-fold, and by term the turnover rate is 1000 mg/dL. The mechanism of action whereby hCS raises plasma glucose levels is unclear, but probably originates from its growth hormone-like properties. hCS also promotes free fatty acid (FFA) production by stimulating lipolysis, which promotes peripheral resistance to insulin.

Placental progesterone rises 10-fold above nonpregnant levels and is associated with an insulin increase in normal healthy pregnant women by 2- to 4-fold.

Most of the marked rise of serum cortisol during pregnancy can be attributed to the increase of cortisol-binding globulin induced by estrogen. However, free cortisol levels are also increased. This increase potentiates the diurnal fluctuations of cortisol with the highest levels occurring in the early morning hours.

The rising estrogen levels also trigger the rise in pituitary prolactin early in pregnancy. Prolactin's structure is similar to a growth hormone and at concentrations reached by the second trimester (>200 ng/mL) prolactin can affect glucose metabolism. Although there are no studies that have examined prolactin alone as an insulin antagonist, there is indirect evidence that suppressing prolactin in gestational diabetic women with large doses of pyridoxine improves glucose tolerance.

In addition to the increasing anti-insulin hormones of pregnancy, there is also increased degradation of insulin in pregnancy caused by placental enzymes comparable to liver insulinases.

The placenta also has membrane-associated insulin-degrading activity. Concomitant with the hormonally induced insulin resistance and increased insulin degradation, the rate of disposal of insulin slows. The normal pancreas can adapt to these factors by increasing the insulin secretory capacity. If the pancreas fails to respond adequately to these alterations, then gestational diabetes mellitus (GDM) results. In a woman with Type 1 diabetes, her insulin requirement will rise progressively. Failure to increase her insulin doses appropriately will result in increasing hyperglycemia.10

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Responses

  • ruby
    How wheat have the strongest diabetogenic effect?
    2 years ago
  • erik
    What hormone reverse the diabetogenic effect of pregnancy?
    1 year ago

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