The serum levels of the low mol wt form of somatomedin-binding protein (SMBP) were 5-fold higher in both diabetic (n = 44) and nondiabetic pregnant women (n = 14) than in nonpregnant women. No difference was found between women with type 1 diabetes and those with gestational diabetes. There was a negative correlation between maternal levels of SMBP during the last trimester and the birth weight percentile of the infants (r = -0.51). There was a 2- to 3-fold elevation of maternal insulin-like growth factor (IGF-I) levels during pregnancy in both diabetic and nondiabetic women. A positive correlation (r = 0.49) was found between maternal IGF-I levels and the birth weight percentiles of their infants. The correlation between the ratio of IGF-I to SMBP, which may reflect the IGF-I available to the placenta, to birth weight percentile was higher (r = 0.57), and the SE of estimate of weight percentile was 23%. The ratio between IGF-I and SMBP in cord blood was correlated with birth weight, although cord blood IGF-I and SMBP values were not. The IGF-II levels in cord serum were 50% higher in the infants of diabetic than in those of nondiabetic mothers. These findings raise the questions of whether maternal SMBP levels influence the amount of IGF-I available for the fetal-placental unit and whether IGF-II participates in glucose homeostasis in the fetus.
The PBGD mutation analysis was found to have full specificity and sensitivity and can be used as the sole diagnostic method in the family complex studied, representing the major AIP mutation in Sweden. The traditional diagnostic methods, used in optimal combinations, work in most cases, but they do not show high precision. However, they must be used when the specific mutation in the PBGD gene is not known.
The low molecular weight form of i nsul i n\x=req-\ like growth factor binding protein (35 kD IGFBP), determined in serum by radioimmunoassay during non-fasting conditions, was high at birth and declined with increasing age during childhood and adolescence (N = 149). Inverse correlation was found between chronological age and 35 kD IGFBP values (r = \m=-\0.61, P < 0.001) during childhood and adolescence, but no age dependency was found in adult subjects aged 20\p=n-\66 years (N = 73). The mean and 95% confidence limits of immunoreactive 35 kD IGFBP were 34 \ g=m\ g/ l and 15\p=n-\79 \g=m\g/l ,respectively, in healthy adults (N = 73) in whom the blood samples were drawn after a one\ x=req-\ night fast. The mean level of the 35 kD IGFBP in patients with acromegaly (19 \g=m\g/l, N = 23) was decreased by 50% in comparison with healthy adults, whereas a 2-fold elevation of the mean levels was found in both anorexia nervosa patients (70 \g=m\g/l , N = 13) and adult patients with GH deficiency (69 \g=m\g/l , N = 22). In patients with anorexia nervosa, the 35 kD IGFBP levels were inversely related to the body mass index (r = \m=-\0.65,P < 0.02).
Somatomedin (Sm) levels throughout pregnancy were determined in a longitudinal study of four normal women and three patients with GH deficiency by use of the RIA for Sm-A, a newly developed RIA for insulin-like growth factor 2 (IGF-2), and the placenta RRA for Sm-A. In both normal women and those with GH deficiency, there was a continuous rise of immunoreactive Sm-A throughout pregnancy. During the third trimester the levels were 2-fold elevated above the level in nonpregnant age-matched normal subjects. No change of immunoreactive IGF-2 levels was found in the normal pregnant women, whereas an increase from low to normal levels was found in GH-deficient patients during pregnancy. The placenta RRA-Sm-A did not detect the increase of Sm-A immunoactivity in the normal pregnant women, whereas the levels were normalized in GH-deficient patients. After delivery a rapid fall of Sm levels occurred in patients with GH deficiency. The calculated half-lives for immunoreactive Sm-A and IGF-2 were 27 and 52 h, respectively. The birth weights of the seven children were significantly (P less than 0.05) correlated to both the individual peak and the mean maternal value of immunoreactive Sm-A during the last trimester. The present findings indicate that the production of both IGF-1 and IGF-2 related peptides during pregnancy is independent of maternal pituitary GH production.
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