Transplacental passage of insulin complexed to antibody.

Bauman, William A.; Yalow, Rosalyn S.

doi:10.1073/pnas.78.7.4588

Cited by 52 publications

(19 citation statements)

References 9 publications

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“…Insulin was recognised as a teratogen in chicken embryo in 1945 [27]. In the absence of specific antibodies [28], insulin is generally considered not to cross the human placenta [29] but studies do not adequately address early pregnancy. In mammals, moreover, we know that insulin is present in the maternal reproductive tract [30] and that receptors for insulin are present in the embryo as early as the morula stage [30].…”

Section: Resultsmentioning

confidence: 99%

In human gestational diabetes mellitus congenital malformations are related to pre-pregnancy body mass index and to severity of diabetes

et al. 2004

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Aims/hypothesis. This study analysed the relationship between congenital malformations (CM) and severity of gestational diabetes mellitus. Methods. A cohort of 2060 infants of mothers with gestational diabetes was studied. Universal screening and 3 rd Workshop-Conference criteria were used to diagnose gestational diabetes. The severity of diabetes was assessed on the basis of previous hyperglycaemia, blood glucose values in diagnostic OGTT, area under the glucose curve, gestational age and HbA 1 c at diagnosis, insulin requirements during pregnancy, and OGTT after delivery. Potentially confounding variables (age, pre-pregnancy BMI, smoking) were considered. The relationship of potential predictors with CM was analysed with several multivariate logistic regression analyses.Results. The rate of CM was 6% for minor and 3.8% for major malformations (1.4% heart, 0.8% renal/urinary, 0.7% skeletal, 0.3% hypospadias, 0.2% central nervous system, 0.2% cleft lip/palate, 0.1% digestive tract, 0.3% other). In the final models, forward logistic regression analysis identified pre-pregnancy BMI as the predictor of CM (area under receiver operating characteristic curve 0.616); in the backward analysis additional predictors were 1-h blood glucose in diagnostic OGTT and gestational age at diagnosis (area under receiver operating characteristic curve 0.646). Both BMI and severity of gestational diabetes were predictors of heart and minor CM, whereas BMI predicted renal/urinary CM and severity of diabetes predicted skeletal CM. Conclusions/interpretation. In these infants of mothers with gestational diabetes, severity of diabetes and pre-pregnancy BMI were predictors of CM, in accordance with the well-documented pathogenic role of BMI (in the general population) and hyperglycaemia (in diabetic pregnancy). BMI was the main predictor of more prevalent CM. [Diabetologia (2004) 47:509-514]

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Section: Resultsmentioning

confidence: 99%

In human gestational diabetes mellitus congenital malformations are related to pre-pregnancy body mass index and to severity of diabetes

et al. 2004

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“…Whereas human insulin does not cross the placenta, older investigations from pregnant diabetic women treated with animal insulin noted that placental transfer of insulin was related to the maternal level of specific insulin antibodies, which suggests a role for a complex of insulin and its antibody in transport (Bauman and Yalow, 1981;Menon et al, 1990). Secondly, correlation between the concentrations of tetanus Ag with anti-tetanus Ab found in cord blood as well as in the fetal compartment in the ex vivo model of the placenta perfused with serum containing tetanus Ag and Ab is consistent with the possibility, that the formation of an immuncomplex (IC) may be involved in the transplacental transport of the Ag (Malek et al, 1997 and1998).…”

Section: Unanswered Questionsmentioning

confidence: 99%

Receptor-mediated uptake and transport of macromolecules in the human placenta

Schneider¹,

Miller²

2010

Int. J. Dev. Biol.

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The human placenta is required to be the anchor, the conduit and the controller during pregnancy. The survival of the baby and its associated placenta is dependent upon the placenta shielding the embryo/fetus from harm, e.g., autoimmune disease -thrombophilia, antiphospholipid syndrome or infections, while simultaneously providing for the passage of critical nutrients (e.g., amino acids, vitamins) and beneficial immunoglobulins. In a number of instances, the movements of macromolecules into and through the placenta can result in the passage of the intact molecules into the fetal circulation or in the case of proteins -catabolism to amino acids which are utilized by the placenta and the fetus for continued growth and development. The transfer of two such macromolecules, immunoglobulin G (IgG) and vitamin B12 (cyanocobalamin or B12), are examined as to the unique receptor-mediated transfer capability of the human placenta, its transfer specificity as related to specific receptors and the role of endogeneous placental proteins (trancobalamins) in facilitating the recognition and transport of specifically B12. Brief comparisons will be made to other animal species and the differences in specific organ transfer capabilities. KEY WORDS: immunoglobulin IgG, transcobalamin, vitamin B12, placental transport, human Overview of macromolecule transport and catabolism by the placenta and extraembryonic membranes in different speciesThe development of the embryo and fetus is dependent upon the function of the placenta and its extraembryonic membranes in every mammalian species. Of significance is the interdependence of theses extraembryonic tissues in maintaining the conceptus and allowing for normal development.Across species, macromolecules play multiple roles in providing for this development. In particular, the transport physiologists and membrane biochemist focus on the transporters and the transcytosis that occurs for immuno-regulators and essential vitamins for normal development. Yet even the basic building blocks created by the degradation of these macromolecules provide for the growth of both fetus and placenta. The large contribution of amino acids from the metabolism of proteins, e.g., maternal albumin and other circulating proteins, provide the large Int.

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“…The underlying mechanism would be an IAfacilitated maternal insulin transfer and, as a consequence, an enhancement of fetal hyperinsulinism and related morbidity (72). Maternal insulin-IA complexes have been associated with toxemia (18,73,74), HELLP syndrome (75), hypoglycemia (18,76), respiratory distress (18), and high hematocrit in the newborn (76).…”

Section: Dras and Diabetic Pregnancymentioning

confidence: 99%