14
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Maternal diet during pregnancy and adaptive changes in the maternal and fetal pancreas have implications for future metabolic health

      review-article
      1 , 2 , , 3
      Frontiers in Endocrinology
      Frontiers Media S.A.
      nutrition, pregnancy, fetus, pancreas, insulin, programming

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Fetal and neonatal development is a critical period for the establishment of the future metabolic health and disease risk of an individual. Both maternal undernutrition and overnutrition can result in abnormal fetal organ development resulting in inappropriate birth size, child and adult obesity, and increased risk of Type 2 diabetes and cardiovascular diseases. Inappropriate adaptive changes to the maternal pancreas, placental function, and the development of the fetal pancreas in response to nutritional stress during pregnancy are major contributors to a risk trajectory in the offspring. This interconnected maternal-placental-fetal metabolic axis is driven by endocrine signals in response to the availability of nutritional metabolites and can result in cellular stress and premature aging in fetal tissues and the inappropriate expression of key genes involved in metabolic control as a result of long-lasting epigenetic changes. Such changes result is insufficient pancreatic beta-cell mass and function, reduced insulin sensitivity in target tissues such as liver and white adipose and altered development of hypothalamic satiety centres and in basal glucocorticoid levels. Whilst interventions in the obese mother such as dieting and increased exercise, or treatment with insulin or metformin in mothers who develop gestational diabetes, can improve metabolic control and reduce the risk of a large-for-gestational age infant, their effectiveness in changing the adverse metabolic trajectory in the child is as yet unclear.

          Related collections

          Most cited references201

          • Record: found
          • Abstract: found
          • Article: not found

          Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth

          Two follow-up studies were carried out to determine whether lower birthweight is related to the occurrence of syndrome X-Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia. The first study included 407 men born in Hertfordshire, England between 1920 and 1930 whose weights at birth and at 1 year of age had been recorded by health visitors. The second study included 266 men and women born in Preston, UK, between 1935 and 1943 whose size at birth had been measured in detail. The prevalence of syndrome X fell progressively in both men and women, from those who had the lowest to those who had the highest birthweights. Of 64-year-old men whose birthweights were 2.95 kg (6.5 pounds) or less, 22% had syndrome X. Their risk of developing syndrome X was more than 10 times greater than that of men whose birthweights were more than 4.31 kg (9.5 pounds). The association between syndrome X and low birthweight was independent of duration of gestation and of possible confounding variables including cigarette smoking, alcohol consumption and social class currently or at birth. In addition to low birthweight, subjects with syndrome X had small head circumference and low ponderal index at birth, and low weight and below-average dental eruption at 1 year of age. It is concluded that Type 2 diabetes and hypertension have a common origin in sub-optimal development in utero, and that syndrome X should perhaps be re-named "the small-baby syndrome".
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            WEIGHT IN INFANCY AND DEATH FROM ISCHAEMIC HEART DISEASE

              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Maternal body mass index and the risk of fetal death, stillbirth, and infant death: a systematic review and meta-analysis.

              Evidence suggests that maternal obesity increases the risk of fetal death, stillbirth, and infant death; however, the optimal body mass index (BMI) for prevention is not known. To conduct a systematic review and meta-analysis of cohort studies of maternal BMI and risk of fetal death, stillbirth, and infant death. The PubMed and Embase databases were searched from inception to January 23, 2014. Cohort studies reporting adjusted relative risk (RR) estimates for fetal death, stillbirth, or infant death by at least 3 categories of maternal BMI were included. Data were extracted by 1 reviewer and checked by the remaining reviewers for accuracy. Summary RRs were estimated using a random-effects model. Fetal death, stillbirth, and neonatal, perinatal, and infant death. Thirty eight studies (44 publications) with more than 10,147 fetal deaths, more than 16,274 stillbirths, more than 4311 perinatal deaths, 11,294 neonatal deaths, and 4983 infant deaths were included. The summary RR per 5-unit increase in maternal BMI for fetal death was 1.21 (95% CI, 1.09-1.35; I2 = 77.6%; n = 7 studies); for stillbirth, 1.24 (95% CI, 1.18-1.30; I2 = 80%; n = 18 studies); for perinatal death, 1.16 (95% CI, 1.00-1.35; I2 = 93.7%; n = 11 studies); for neonatal death, 1.15 (95% CI, 1.07-1.23; I2 = 78.5%; n = 12 studies); and for infant death, 1.18 (95% CI, 1.09-1.28; I2 = 79%; n = 4 studies). The test for nonlinearity was significant in all analyses but was most pronounced for fetal death. For women with a BMI of 20 (reference standard for all outcomes), 25, and 30, absolute risks per 10,000 pregnancies for fetal death were 76, 82 (95% CI, 76-88), and 102 (95% CI, 93-112); for stillbirth, 40, 48 (95% CI, 46-51), and 59 (95% CI, 55-63); for perinatal death, 66, 73 (95% CI, 67-81), and 86 (95% CI, 76-98); for neonatal death, 20, 21 (95% CI, 19-23), and 24 (95% CI, 22-27); and for infant death, 33, 37 (95% CI, 34-39), and 43 (95% CI, 40-47), respectively. Even modest increases in maternal BMI were associated with increased risk of fetal death, stillbirth, and neonatal, perinatal, and infant death. Weight management guidelines for women who plan pregnancies should take these findings into consideration to reduce the burden of fetal death, stillbirth, and infant death.
                Bookmark

                Author and article information

                Contributors
                URI : https://loop.frontiersin.org/people/1481481Role: Role: Role:
                Role: Role:
                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrinol.
                Frontiers in Endocrinology
                Frontiers Media S.A.
                1664-2392
                23 September 2024
                2024
                : 15
                : 1456629
                Affiliations
                [1] 1 Lawson Health Research Institute, St. Joseph’s Health Care , London, ON, Canada
                [2] 2 Departments of Medicine, Physiology and Pharmacology, Western University , London, ON, Canada
                [3] 3 Oxford Centre for Diabetes, Endocrinology, and Metabolism, Wellcome Centre for Human Genetics, University of Oxford , Oxford, United Kingdom
                Author notes

                Edited by: Lawrence Merle Nelson, Mary Elizabeth Conover Foundation, Inc., United States

                Reviewed by: Chellakkan Selvanesan Blesson, Baylor College of Medicine, United States

                Sumiko Morimoto, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico

                *Correspondence: David J. Hill, david.hill@ 123456lawsonresearch.com
                Article
                10.3389/fendo.2024.1456629
                11456468
                39377073
                55209426-5d39-4210-9726-7044ad52ab11
                Copyright © 2024 Hill and Hill

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 28 June 2024
                : 28 August 2024
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 201, Pages: 15, Words: 8153
                Funding
                The author(s) declare financial support was received for the research, authorship, and/or publication of this article. For cited studies that were carried out by the authors, thanks are extended to the Lawson Foundation for financial support in the form of an endowed research chair to DJH. TGH was the recipient of a Novo Nordisk-Oxford Postdoctoral Fellowship.
                Categories
                Endocrinology
                Review
                Custom metadata
                Developmental Endocrinology

                Endocrinology & Diabetes
                nutrition,pregnancy,fetus,pancreas,insulin,programming
                Endocrinology & Diabetes
                nutrition, pregnancy, fetus, pancreas, insulin, programming

                Comments

                Comment on this article