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      Fetal adaptations in insulin secretion result from high catecholamines during placental insufficiency.

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          Abstract

          Placental insufficiency and intrauterine growth restriction (IUGR) of the fetus affects approximately 8% of all pregnancies and is associated with short- and long-term disturbances in metabolism. In pregnant sheep, experimental models with a small, defective placenta that restricts delivery of nutrients and oxygen to the fetus result in IUGR. Low blood oxygen concentrations increase fetal plasma catecholamine concentrations, which lower fetal insulin concentrations. All of these observations in sheep models with placental insufficiency are consistent with cases of human IUGR. We propose that sustained high catecholamine concentrations observed in the IUGR fetus produce developmental adaptations in pancreatic β-cells that impair fetal insulin secretion. Experimental evidence supporting this hypothesis shows that chronic elevation in circulating catecholamines in IUGR fetuses persistently inhibits insulin concentrations and secretion. Elevated catecholamines also allow for maintenance of a normal fetal basal metabolic rate despite low fetal insulin and glucose concentrations while suppressing fetal growth. Importantly, a compensatory augmentation in insulin secretion occurs following inhibition or cessation of catecholamine signalling in IUGR fetuses. This finding has been replicated in normally grown sheep fetuses following a 7-day noradrenaline (norepinephrine) infusion. Together, these programmed effects will potentially create an imbalance between insulin secretion and insulin-stimulated glucose utilization in the neonate which probably explains the transient hyperinsulinism and hypoglycaemia in some IUGR infants.

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          Author and article information

          Journal
          J. Physiol. (Lond.)
          The Journal of physiology
          Wiley
          1469-7793
          0022-3751
          Aug 01 2017
          : 595
          : 15
          Affiliations
          [1 ] School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, AZ, USA.
          [2 ] Perinatal Research Center, University of Colorado School of Medicine, Aurora, CO, USA.
          Article
          10.1113/JP273324
          5538202
          28194805
          af6bcf7d-94d5-4f65-aae2-2ba3127cc0ba
          History

          intrauterine growth restriction,norepinephrine,β-cell,developmental programming,epinephrine

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