Abstract
Gestational diabetes mellitus is caused primarily by peripheral insulin resistance and by a relative lack of the hormone. The gestational diabetic’s insulin production can cover her basal insulin requirement — as evident in the often normal fasting blood glucose level-but insulin secretion after carbohydrate intake (bolus production) is delayed and decreased. The resulting pulsatile hyperglycemia causes an oversupply of glucose to the fetus, which eventually reacts to even slight glucose elevations by overproducing insulin. As a result of the maternofetal concentration gradient, even more glucose is metabolized by the fetus. Because of this syphoning (the extent of which is not known), the fetal glucose turnover can no longer be estimated by the maternal blood glucose level. Hyperstimulation of the fetal pancreas, fetal hyperinsulinism, and biochemical fetopathy (see p. 18 f.) can occur even at seemingly normal maternal blood glucose values.
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© 1988 Springer-Verlag/Wien
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Hofmann, H.M.H., Weiss, P.A.M., Kainer, F. (1988). Insulin Treatment of Gestational Diabetes. The Basal Bolus Concept. In: Weiss, P.A.M., Coustan, D.R. (eds) Gestational Diabetes. Springer, Vienna. https://doi.org/10.1007/978-3-7091-8925-2_13
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DOI: https://doi.org/10.1007/978-3-7091-8925-2_13
Publisher Name: Springer, Vienna
Print ISBN: 978-3-7091-8927-6
Online ISBN: 978-3-7091-8925-2
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