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Background: Diabetes is an important disease that affects fetal development during pregnancy and causes metabolic disorders in newborns. Changes in serum glucose, ketone bodies, and somatomedin-C inhibitors in the diabetic pregnancies are responsible for the development of metabolic syndromes. The frequency of maternal hyperglycemia has reduced with careful monitoring during pregnancy of diabetic mothers. Nevertheless, morbidity in offspring of mothers with gestational diabetes mellitus (GDM) continues to be significant. We aimed to investigate the cardiac function of infants of mothers with GDM by echocardiographic (ECHO) Doppler and tissue Doppler methods and to evaluate their demographic features, somatomedin-C level and the relations them with each other. Methods: ECHO findings, laboratory data of newborns applied to our clinic between January and December 2016, and demographics of GDM mothers were examined. In the study, 108 neonates born to GDM mothers, and 100 healthy neonates (controls) were enrolled at postpartum 48th hour. Serum somatomedin-C levels were measured and detailed clinical and ECHO examination were performed. Isovolumetric relaxation (IVRT), isovolumetric contraction (IVCT), Myocardial Performance Index (MPI=ei Index) as an index that include both systolic and diastolic time intervals in expressing global systolic and diastolic ventricular functions [MPI: (IVRT + IVCT) / systolic ejection time] were calculated using both ventricular function M-mode, pulsed-wave and tissue Doppler ECHO methods. In addition, pulmonary arterial pressure (PAP) and tricuspid and mitral valves annular plan systolic excursion motions (TAPSE, MAPSE) were measured. Anamnesis and laboratory studies (fasting blood glucose [GHG] and glycosylated hemoglobin c [HbA1c]) measurements of all mothers were performed. Results: In the study group, 49 (45.4%) of infants were females and 59 were males (54.6%), the incidence of macrosomia was 4 (3.7%) in the study group and 2 (2.0%) in the control group. In comparison between the maternal groups, GDM mothers had significantly higher levels of fasting blood glucose (FBG) and HbA1c (p<0.0001). There was no significant difference in birth weight and somatomedin-C levels in neonates between two groups, but head circumference and height values were significantly higher in infants born to GDM mothers (p<0.05). In the echocardiographic examinations, small muscular ventricular septal defects were detected in 3 infants (2.77%) in study group, and 1 infant (1.0%) in control group. The M mode review revealed that diastolic end-interventricular septum thickness was significantly higher in IDMs group (p<0.001). In the evaluation of right ventricular function, MPI values were significantly higher in the infants of GDM group than control group (p<0.05). Also, IVCT, a diastolic function indicator, was significantly longer in the study group (p<0.05). There was a statistically insignificant decrease in TAPSE values in infants of GDM group (p>0.05). In evaluation of left ventricular function between groups, MPI and IVRT values were significantly higher in infants of GDM group (p<0.05), whereas MAPSE values were significantly decreased in the study group (p<0.05). Conclusion: Although infants of mothers with GDM were clinically normal in our study, we determined significant differences in diastolic parameters in addition to subclinical findings of ventricular septal thickness. We emphasize that cardiac involvement requires early diagnosis and neonatal approach even though complications in infants born to GDM mothers usually recover spontaneously. As expected, these infants are prone to various hyperglycemic adverse outcomes. Therefore, recognizing and treating hyperglycemia in time should be an important target for prevention of metabolic problems and deaths in severe cases. [ABSTRACT FROM AUTHOR]

We report on a Japanese girl with short stature, malar hypoplasia, up-slanting palpebral fissures, blue sclerae and thin, stiff and slightly brownish hair. Short stature started in utero and her psychomotor development was normal. Menarche appeared at 13 years 8 months. Height at 14 years 5 months was 132 cm (-4.6 SD). Her growth hormone (GH) sleep pattern and responses to insulin, L-dopa, arginine, propranolol-glucagon and growth hormone-releasing hormone were normal. Plasma insulin-like growth factor I (IGF-I) was high (2170-4860 units/l) and increased from 4860 to 7080 units/l 20 h after biosynthetic GH injection. Gel infiltration patterns of the free and protein-bound IGF-I in plasma from the patient were not different from the controls; IGF-I fraction of the high and low molecular weight binding protein and the non-protein bound fraction were 75.5%, 15.8% and 8.7%, respectively. IGF-I from the patient showed normal bioactivities when determined by [35S]sulphate and [3H]thymidine uptake into cultured rat chondrocytes, and by [3H]thymidine and [3H]alpha-aminoisobutyric acid uptake into the patient's skin fibroblasts. IGF-I binding to cultured skin fibroblasts from the patient was comparable to that of controls. These results suggest that tissue specific defects of IGF-I receptors may be the cause of increased IGF-I levels in the patient. [ABSTRACT FROM AUTHOR]

In the present study we evaluated somatomedin-C (Sm-C) plasma levels in diabetic patients, with and without retinopathy. One hundred and thirty four diabetic patients (65 type I and 69 type II) and 90 controls, strictly matched for age and sex, were enrolled in the study. Ophthalmoscopy and fluorescein angiography allowed to distinguish: 49 patients without retinopathy, 45 patients with background retinopathy, and 40 with proliferative retinopathy. Growth hormone (GH) and Sm-C plasma levels were measured using a pool of 20-24 blood samples over 24h. Sm-C levels in type I (0.62±0.11 U/ml) and type II (0.56±0.09 U/ml) patients were significantly decreased (p<0.01) when compared to controls (0.89±0.30 U/ml). The mean daily secretion of GH was significantly (p<0.01) greater in diabetic patients (7.8±2.6 ng/ml) than in controls (4.1±1.5 ng/ml), but no correlation was found between Sm-C and GH (r=0.15; p=n.s.). Our findings did not show any correlation between Sm-C plasma levels and either the existence of retinopathy, regardless of the degree of microvascular damage, or duration of the disease, or degree of metabolic control, as evaluated by HbA. [ABSTRACT FROM AUTHOR]

Streptozotocin-induced diabetes causes a decrease in growth hormone and prolactin receptors in the livers of female rats, and in the serum concentration of somatomedin-C/insulin-like growth factor-1, concomitantly with an increase in the serum testosterone levels. In this study, a possible role for adrenal androgens in the loss of receptors was examined. Rats were adrenalectomised bilaterally 3 days after the induction of diabetes with streptozotocin (100 mg/kg intravenously), and livers were removed 3 days later. Adrenalectomy had no effect on binding of ovine prolactin or bovine growth hormone to liver microsomal membranes from non-diabetic rats, but in diabetic rats it entirely abolished the 56% decrease in prolactin binding and significantly reversed the 66% decrease in growth hormone binding and the parallel fall in serum levels of somatomedin-C/insulin-like growth factor-I ( p<0.05). Adrenalectomy also prevented the diabetes-induced rise in serum testosterone. Daily injection of testosterone to normal and diabetic rats for 12 days significantly reduced both prolactin and growth hormone binding ( p<0.001), with the effect of diabetes being additive upon the testosterone effect. Implantation of testosterone-filled silastic capsules at the time of adrenalectomy (i. e. for 3 days) did not prevent the adrenalectomy-induced restoration of both growth hormone and prolactin receptors. The resulting high serum testosterone level did not reduce binding to growth hormone receptors in control rats over the 3 day period, and caused no further decrease in diabetic rats. However, binding to prolactin receptors was reduced by 47% in control animals with no further loss in diabetic animals ( p<0.001). Adrenalectomy prevented the loss of prolactin receptors in both testosterone-treated and diabetic rats. These results indicate that, whether or not the rise in testosterone of adrenal origin contributes to the receptor loss in diabetes, the effect also depends on another factor of adrenal origin. [ABSTRACT FROM AUTHOR]

The growth response during short-term growth hormone (GH) treatment was evaluated in eight prepubertal non-GH-deficient (non-GHD) children and compared with six prepubertal GH-deficient (GHD) patients. Standard doses of GH can improve growth rate in GHD and in some non-GHD patients. In neither group the growth response can be predicted by the acute increase in Thymidine Activity or Somatomedin-C levels. A diagnostic trial of GH treatment may be the only certain method of selecting the short non-GHD patients who may benefit from long-term GH therapy. [ABSTRACT FROM AUTHOR]

The effect of growth hormone-releasing factor (GRF) 1-44 on growth hormone and somatostatin release in plasma has been studied in 20 obese children. Twenty age and sex-matched children with normal weight served as controls. Mean peak growth hormone response in obese children after 1 microgram/kg body wt. GRF 1-44 was significantly lower than in controls (23.7 +/- 3.6 ng/ml vs. 41.1 +/- 3.0 ng/ml; P less than 0.01), as were mean integrated growth hormone response areas (1544 +/- 272 ng X ml-1 X 2 h vs. 2476 +/- 283 ng X ml-1 X 2 h; P less than 0.01). Mean plasma levels of somatostatin-like immunoreactivity did not change after GRF in both groups. Mean somatomedin-C levels in obese children were significantly higher compared to controls (1.6 +/- 0.4 U/ml vs. 0.86 +/- 0.4 U/ml; P less than 0.01). Somatomedin-C levels were not related to the integrated growth hormone responses. In conclusion there is no relation between somatomedin-C levels and the reduced growth hormone-releasing effect of GRF in obese children. GRF does not alter peripheral somatostatin-like immunoreactivity levels either in normal or obese children. [ABSTRACT FROM AUTHOR]

The effect of thyroid hormone on plasma somatomedin-C (SmC) level and on SmC release from perfused rat liver was investigated. Plasma SmC levels and liver tissue SmC were significantly increased in thyroxine-treated rats. Physiological doses of triiodothyronine increased SmC release and SmC concentration in the perfused rat liver. These results indicate that thyroid hormone directly enhances the synthesis and release of SmC in the rat. [ABSTRACT FROM AUTHOR]

This study was undertaken to assess the nature of somatomedin-C (SM-C) in baboon (Papio cynocephalus) blood and to compare various methods for estimating SM-C concentrations. Parallel dose-response curves were obtained with normal baboon serum, normal human serum, and purified SM-C. Recovery of purified SM-C added to baboon serum over a wide dosage range (n = 17) was 111 ± 12%, with slightly better recovery at higher potencies. Chromatography of normal baboon serum on Sephadex G-200 at neutral pH produced a profile similar to that observed in the human, as did samples chromatographed on Sephadex G-50 in acid. Although the SM-C content in acid chromatographed plasma was approximately 2.5 times higher than in native unprocessed plasma, there was excellent correlation between the values (r = 0.9143, p < 0.0001). The SM-C in baboon plasma which had been preincubated with glycine HCl was approximately twice that of unprocessed plasma, but the correlation between the two methods was excellent (r = 0.9593, p < 0.0001). The correlation between values obtained after simple acid-ethanol extraction and those observed in unextracted plasma were also significant (r = 0.7689, p < 0.0001). Following a series of four injections of human growth hormone (hGH) to a normal baboon, plasma SM-C rose approximately sevenfold above the initial concentration and returned to basal levels five days after the final injection. These studies show that although the radioimmunoassay (RIA) for SM-C in unprocessed baboon plasma does not measure all of the SM-C present, it provides a reliable index of the total SM-C concentration and reflects GH status in the baboon., (Copyright © 1983 Wiley‐Liss, Inc., A Wiley Company.)