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      Diabetes in pregnancy: a new decade of challenges ahead

      review-article
      1 , 2 , , 3 , 4 , 5 , the Diabetic Pregnancy Study Group
      Diabetologia
      Springer Berlin Heidelberg
      Fetus, Gestational diabetes mellitus, Obesity, Placenta, Pregnancy, Review, Type 1 diabetes, Type 2 diabetes

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          Abstract

          Every 10 years, the Diabetic Pregnancy Study Group, a study group of the EASD, conducts an audit meeting to review the achievements of the preceding decade and to set the directions for research and clinical practice improvements for the next decade. The most recent meeting focused on the following areas: improving pregnancy outcomes for women with pregestational type 1 diabetes and type 2 diabetes; the influence of obesity and gestational diabetes on pregnancy outcomes; the determinants and assessment of fetal growth and development; and public health issues, including consideration of transgenerational consequences and economic burden. The audit meeting also considered the likely impact of ‘omics’ on research within the field and the potential of these technologies to enable precision-medicine approaches to management. Through sharing of the findings and ideas of audit meeting participants, the DPSG hopes to promote networking, research and advances in clinical care, to improve outcomes for all women and their offspring affected by diabetes and obesity in pregnancy.

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          Most cited references56

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          Diagnostic criteria and classification of hyperglycaemia first detected in pregnancy: a World Health Organization Guideline.

          (2014)
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            Serotonin Regulates Pancreatic β-Cell Mass during Pregnancy

            During pregnancy, the energy requirements of the fetus impose changes in maternal metabolism. Increasing insulin resistance in the mother maintains nutrient flow to the growing fetus, while prolactin and placental lactogen counterbalance this resistance and prevent maternal hyperglycemia by driving expansion of the maternal population of insulin-producing β-cells1–3. However, the exact mechanisms by which the lactogenic hormones drive β-cell expansion remain uncertain. Here we show that serotonin acts downstream of lactogen signaling to drive β-cell proliferation. Serotonin synthetic enzyme Tph1 and serotonin production increased sharply in β-cells during pregnancy or after treatment with lactogens in vitro. Inhibition of serotonin synthesis by dietary tryptophan restriction or Tph inhibition blocked β-cell expansion and induced glucose intolerance in pregnant mice without affecting insulin sensitivity. Expression of the Gαq-linked serotonin receptor Htr2b in maternal islets increased during pregnancy and normalized just prior to parturition, while expression of the Gαi-linked receptor Htr1d increased at the end of pregnancy and postpartum. Blocking Htr2b signaling in pregnant mice also blocked β-cell expansion and caused glucose intolerance. These studies reveal an integrated signaling pathway linking β-cell mass to anticipated insulin need during pregnancy. Modulators of this pathway, including medications and diet, may affect the risk of gestational diabetes4.
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              Perinatal mortality and congenital anomalies in babies of women with type 1 or type 2 diabetes in England, Wales, and Northern Ireland: population based study.

              To provide perinatal mortality and congenital anomaly rates for babies born to women with type 1 or type 2 diabetes in England, Wales, and Northern Ireland. National population based pregnancy cohort. 231 maternity units in England, Wales, and Northern Ireland. 2359 pregnancies to women with type 1 or type 2 diabetes who delivered between 1 March 2002 and 28 February 2003. Stillbirth rates; perinatal and neonatal mortality; prevalence of congenital anomalies. Of 2359 women with diabetes, 652 had type 2 diabetes and 1707 had type 1 diabetes. Women with type 2 diabetes were more likely to come from a Black, Asian, or other ethnic minority group (type 2, 48.8%; type 1, 9.1%) and from a deprived area (type 2, 46.3% in most deprived fifth; type 1, 22.8%). Perinatal mortality in babies of women with diabetes was 31.8/1000 births. Perinatal mortality was comparable in babies of women with type 1 (31.7/1000 births) and type 2 diabetes (32.3/1000) and was nearly four times higher than that in the general maternity population. 141 major congenital anomalies were confirmed in 109 offspring. The prevalence of major congenital anomaly was 46/1000 births in women with diabetes (48/1000 births for type 1 diabetes; 43/1000 for type 2 diabetes), more than double that expected. This increase was driven by anomalies of the nervous system, notably neural tube defects (4.2-fold), and congenital heart disease (3.4-fold). Anomalies in 71/109 (65%) offspring were diagnosed antenatally. Congenital heart disease was diagnosed antenatally in 23/42 (54.8%) offspring; anomalies other than congenital heart disease were diagnosed antenatally in 48/67 (71.6%) offspring. Perinatal mortality and prevalence of congenital anomalies are high in the babies of women with type 1 or type 2 diabetes. The rates do not seem to differ between the two types of diabetes.
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                Author and article information

                Contributors
                ute.schaefer-graf@sjk.de
                Journal
                Diabetologia
                Diabetologia
                Diabetologia
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                0012-186X
                1432-0428
                22 January 2018
                22 January 2018
                2018
                : 61
                : 5
                : 1012-1021
                Affiliations
                [1 ]Berlin Center for Diabetes in Pregnancy, Department of Obstetrics and Gynecology, St Joseph’s Hospital, Wüsthoffstraße 15, 12101 Berlin, Germany
                [2 ]Department of Obstetrics, Charité, Humboldt University, Berlin, Germany
                [3 ]GRID grid.7841.a, Department of Clinical and Molecular Medicine, Sant’Andrea Hospital, Faculty of Medicine and Psychology, , Sapienza University, ; Rome, Italy
                [4 ]ISNI 0000 0000 9984 5644, GRID grid.413314.0, Department of Endocrinology, , The Canberra Hospital, ; Garran, ACT Australia
                [5 ]ISNI 0000 0001 2180 7477, GRID grid.1001.0, Australian National University Medical School and John Curtin School of Medical Research, , Australian National University, ; Acton, ACT Australia
                Article
                4545
                10.1007/s00125-018-4545-y
                6448995
                29356835
                929a8713-39ff-44f2-860d-b9705be99d4c
                © The Author(s) 2018

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 16 August 2017
                : 21 November 2017
                Categories
                Review
                Custom metadata
                © Springer-Verlag GmbH Germany, part of Springer Nature 2018

                Endocrinology & Diabetes
                fetus,gestational diabetes mellitus,obesity,placenta,pregnancy,review,type 1 diabetes,type 2 diabetes

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