Insulin-dependent Diabetic Mothers Research Articles

Attenuated glucose production rate in newborn infants of insulin-dependent diabetic mothers.

Hypoglycemia frequently develops in infants of diabetic mothers in the immediate postnatal period.1 , 2 Even in the presence of strict metabolic control during pregnancy, a greater decrease of bloo...

Neontal hypoglycaemia in infants of insulin-dependent diabetic mothers.

Neonatal hypoglycaemia (blood glucose smaller than 20 mg/100 ml) occurred in the first 6 hours of life in 25 of 34 infants born to diabetic mothers receiving insulin. Despite severe hypoglycaemia (blood glucose smaller than 10 mg/100 ml) in 17, clinical features of hypoglycaemia were absent in all but 2. Hypoglycaemia was not related either to the level of plasma insulin in cord blood, determined as nonextracted immunoreactive insulin, or to the degree of control of maternal blood glucose during pregnancy. The frequent occurrence of severe neonatal hypoglycaemia in the infants born to diabetic mothers receiving insulin appears to be due rather to failure to maintain basal glucose homoeostasis after birth than to hyperinsulinism.

Placental barrier to human insulin-I125 in insulin-dependent diabetic mothers.

Although the normal human placenta is impermeable to insulin, the effect of anti-insulin antibodies on this placental barrier in insulin-dependent diabetic mothers is not known. The placental transfer of human insulin-I125 was examined in 4 normal and 4 insulin-dependent diabetic mothers. Human insulin-I125 was infused at a constant rate for 60–90 min prior to delivery and immuno-precipitable insulin-I125 was measured in the maternal and umbilical venous plasma at delivery. In diabetic patients, insulin-I125 was separated from circulating endogenous anti-insulin antibodiesby acid alcohol extraction prior to immunoprecipita-tion. In normal mothers insulin-I125 radioactivitywas 683 ±110 cpm/ml (mean ± sem) in the maternal vein and 6 ± 2 cpm/ml in the umbilical vein. In three diabetic mothers with high plasma insulin binding capacities between 2580–8400 μU/ml, the umbilical venous insulin-I125 was 10 ± 10 cpm/ml when the maternal plasma insulin-I125 was maintained at 1388 ± 356 cpm/ml even though the antibodies were present in the fetal plasma. In another diabetic subject with low anti-insulin anti-bodies, no placental transfer of insulin-I125 was demonstrated. Thus in both normal and diabetic subjects, placental transfer of insulin-I125 is negligible and the presence of anti-insulin antibodies does not induce insulin transfer.

Insulin Response to Arginine in Normal Newborn Infants and Infants of Diabetic Mothers

The effect of maternal diabetes during pregnancy on insulin release of the newborn infant was examined employing arginine infusion as stimulus. At age two hours, eight normal newborn infants, six of gestationally diabetic mothers (IGDM) and four of insulin-dependent diabetic mothers (IDM) were infused with arginine hyd-rochloride 0.5 gm. per kilogram body weight for thirty minutes. Eight additional normal newborn infants were infused with isotonic saline. A small but definite rise in plasma IRI was observed in the normal newborns receiving arginine; however, the infants of gestationally diabetic mothers responded with an enhanced blood glucose and plasma insulin rise compared with the normal newborns. It seemed that intermittent or sustained hyperglycemia in utero may have potentiated the neonatal insulin response to arginine.

INCREASED GLYCOGEN CONTENT IN SUBCUTANEOUS ADIPOSE TISSUE FROM NEWBORN OFFSPRING OF DIABETIC MOTHERS: DYNAMICS AND ULTRASTRUCTURE

Glycogen content of adipose tissue in the human neonate falls rapidly in the first hours of life. Since little or no glucose-6-phosphatase is found in fat tissue (rats), presumably glycogen is utilized only in situ, both to support energy metabolism (ATP generation) and to furnish alpha-glycerophosphate for reesterification of fatty acids. Previous investigations showed increased lipolysis (glycerol release) in adipose tissue from offspring of diabetic mothers. In this study glycogen content (mg/gm w.w.) was measured in adipose tissue samples from the subcutaneous fat pad of the buttocks in 30 infants of insulin dependent diabetic mothers (IDM) and in 34 infants of gestational diabetic mothers (IGDM) obtained during the first five days of life. Comparisons were made with 86 infants from normal gestations. Glycogen content was significantly increased in fat tissue from both IDM and IGDM. The rapid rate of decrease seen in normal infants was not observed regardless of whether these infants were infused with glucose or not. Electron microscopic studies suggested a characteristic ultrastructure of adipose tissue glycogen deposits when increased amounts of glycogen are present. These results are consistent with the hyperinsulinism of IDM and IGDM.

THE PLACENTAL BARRIER TO HUMAN INSULIN-I-125 IN INSULIN DEPENDENT DIABETIC MOTHERS

Although the normal human placenta is impermeable to insulin, the effect of anti-insulin antibodies upon the placental barrier to insulin has not been defined. The placental transfer of human insulin-I125 was examined in normal (n=4) and insulin-dependent diabetic mothers (n=4) by infusing human insulin-I125 at a constant rate for 60-90 min. prior to delivery and measuring immuno-precipitable insulin-I125 radioactivity in the maternal and umbilical venous plasma at delivery. In normal mothers plasma insulin-I125 radioactivity was 683±110 cpm/ml (Mean±SEM) in the maternal vein and 6±2 cpm/ml in the umbilical vein. In three diabetic mothers with high plasma insulin binding capacity (1850-8400 μU/ml) the umbilical venous insulin-I125 was 10±10 cpm/ml when the maternal plasma insulin-I125 was maintained at 1388±356 cpm/ml, even though the antibodies were present in the fetal plasma. In another insulin-dependent diabetic mother with negligible anti-insulin antibodies, no placental transfer of human insulin-I125 was demonstrated. Thus, in both normal and diabetic mothers, placental transfer of human insulin-I125 is negligible and the presence of maternal anti-insulin antibodies does not induce insulin transfer.

Transient neonatal diabetes: Delayed maturation of the pancreatic beta cell

1. McCann, M. L., and Likly, B. F.: The role of epinephrine prophylactic therapy in infants of diabetic mothers, Atlantic City, N. J., 1967, Society for Pediatric Research. 2. Porte, D., Jr., Graber, A. L., Kuzuya, T., and Williams, R. H. : The effect of epinephrine on immunoreactive insulin leveIs in man, J. Clin. Invest. 45: 228, 1966. 3. Chen, C. H., Adam, P. A. J., Laskowski, D. E., McCann, M. L., and Schwartz, R.: The plasma free fatty acid composition and blood glucose of normal and diabetic pregnant women and of their newborns, Pediatrics 36: 843, 1965. 4. Light, I. J., Sutherland, J. M., Loggie, J. M., and Gaffney, T. E.: Impaired epinephrine release in hypoglycemic infants of diabetic mothers, N. Engl. J. Med. 277: 394, 1967. 5. Stern, L., Ramos, A., and Leduc, J.: Urinary catecholamine excretion in infants of diabetic mothers, Pediatrics 42: 598, 1968. 6. McCann, M. L.: Prevention of RDS and decreased mortality in infants of insulin dependent diabetic mothers (IDM) treated with epinephrine, Atlantic City, N. J., 1971, Society for Pediatric Research. 7. Cornblath, M., and Schwartz, R.: Disorders of carbohydrate metabolism in infancy, Philadelphia, 1966, W. B. Saunders Company, p. 57. 8. Huggett, A. St. G., and Nixon, D. A.: The use of glucose oxidase, peroxidase and odianisldine in determination of blood and urinary glucose, Lancet 2: 368, 1957. 9. Hohorst, H. J.: L-(+)-lactate determination with lactic dehydrogenase and DPN, in Bergmeyer, H. V., editor: Methods of enzymatic analysis, New York, 1963, Academic Press, Inc., p. 266. 10. Stevens, J. F.: Biochemical changes in the blood of the newborn, J. Med. Lab. Technol. 22: 47, 1965.

INFANTS OF DIABETIC MOTHERS: ATTENUATED GLUCOSE UPTAKE WITHOUT HYPERINSULINEMIA DURING CONTINUOUS GLUCOSE INFUSION

Blood glucose, plasma insulin, and free fatty acid interrelationships were examined in newborn infants during and after continuous hourly glucose infusions at rates varying from 4 to 24 mg/kg/minute. Normal newborn infants disposed of glucose efficiently until glucose was infused at rates greater than 6 mg/kg/minute. Plasma insulin levels rose gradually during glucose infusion. When large loads of glucose infusion were initiated (12 mg/kg/minute), however, there was a delay in plasma insulin rise. At the slow rates of glucose infusion, the infants of gestational or insulin-dependent diabetic mothers disposed of the exogenous glucose more slowly than the normal newborns. Plasma insulin levels in the infants of gestational diabetic mothers were similar to those in the normal infants. These observations suggest that, with comparable glucose stimulus by continuous infusion, the infants of diabetic mothers do not have excessive insulin output.

Prevention of hypoglucosemia by fructose in infants of diabetic mothers.

HYPOGLUCOSEMIA occurs consistently in infants of insulin-dependent diabetic mothers during the initial hours of life.1 2 3 4 Previous studies have not clearly related symptomatology to the level of blood glucose.5 6 7 Furthermore, the effect of hypoglucosemia on mortality, morbidity and ultimate mental development is not well defined. The following observations suggest that subtle as well as overt symptoms regularly occur in the initial hours of life in association with hypoglucosemia. Fructose administration was found to alleviate symptoms and to alter the course of blood glucose. Methods In addition to the methods and material previously described4 7 infants received fructose directly into the umbilical . . .