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Leukocyte alkaline phosphatase (LAP) activity was studied in 50 women at delivery and in the newborn after delivery. The foüowing findings were observed: (1) the LAP activity of newborns is lower than that of the mothers; (2) significant decrease in the LAP activity has been observed in newborns on the 4th day after delivery; (3) there are no significant differences between newborns from normal and prolonged labor; (4) immediately after delivery the LAP scores of male newborns are lower than those of females, but 4 days later these scores were reversed, and (5) 4 days after delivery, the LAP scores do correlate to the weight of the newborn.

OBJECTIVE
To test the hypothesis that insulin acts though ovarian IGF-I receptors to produce excessive amounts of androgens in polycystic ovarian syndrome (PCOS), by measuring the binding capacity of IGF-I receptors on erythrocytes and relating the findings to the degree of hyperandrogenism and hyperinsulinaemia. DESIGN
A case-control study of IGF-I receptors on erythrocytes of women with PCOS and age- and weight-matched controls. PATIENTS AND METHODS
IGF-I receptors on erythrocytes, serum levels of androgens, IGF-I, GH, basal insulin and insulin response during oral glucose tolerance test (oGTT) were measured after induced or spontaneous withdrawal bleeding in 10 women with PCOS and eight normo-ovulatory women. RESULTS
An increased number of IGF-I receptors was found on erythrocytes of patients with PCOS compared with the controls (P < 0.01), irrespective of their body mass index. Serum IGF-I levels were similar in both groups. The degree of hyperinsulinaemia, provoked by oGTT, correlated positively with basal insulin (r = 0.69; P = 0.003), but not with the number of IGF-I receptors. However, the number of IGF-I receptors correlated positively with androstenedione (r = 0.54, P = 0.0018). CONCLUSIONS
The findings in the present study that the number of IGF-I receptors and not the insulin levels correlate with serum androstenedione support the theory that the hyperandrogenism in PCOS is not a direct effect of the hyperinsulinaemia, but IGF-I mediated.

To assess whether placental DNA, glycogen, and fat are affected by diabetes mellitus and whether the changes correlate with the disturbance in maternal fuels, placentas were examined at delivery in women with normal carbohydrate metabolism, gestational diabetes mellitus, and Classes B to F diabetes and in rats rendered diabetic by the administration of streptozotocin 2 weeks before mating. Plasma glucose values during late pregnancy were higher in patients with Classes B to F diabetes than in the patients with gestational diabetes mellitus so that they were judged to have more severe metabolic disturbances; rats were also divided into groups with “mild” or “severe” diabetes on the basis of blood sugar. In rats, as in humans, diabetes tended to increase placental mass, DNA, glycogen, and lipids. However, the relative changes in glycogen and fat exceeded the alterations in mass and DNA, especially in those with more severe diabetes, so that a true increase in glycogen and fat per placental cell may have occurred. Thus, placental glycogen/DNA and placental triglycerides/DNA significantly exceeded control values in patients with Classes B to F diabetes and in rats with severe diabetes but not in women with gestational diabetes mellitus or rats with mild diabetes. Total placental triglycerides and total placental glycogen were significantly correlated (r = 0.952; p < 0.001) in rats with experimental diabetes, which suggests that these alterations in placental composition during late pregnancy may share communal dependencies.

Leukocyte alkaline phosphatase (LAP) activity was determined in 222 women during normal pregnancy, labor, and after delivery. LAP scores rise during pregnancy and reach peak values at 24 to 26weeks’ gestation. Afterward, the scores remain constant and drop a few days before delivery. Administration of estrone in the last trimester of pregnancy causes an increase in LAP activity. No significant changes were noted after progesterone administration, while hydrocortisone decreased LAP activity. The resultant LAP store during pregnancy is an expression of placental function and may serve as an indicator of placental dysfunction.