ReviewThe Journal of endocrinology2017
The impact of IUGR on pancreatic islet development and β-cell function.
Review in The Journal of endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
57 citing papers in PubMed, 80 citations in OpenAlex.
- The Potential Physiologic Mechanisms by Which Early-Life Nutrition May Influence Type 2 Diabetes Pathophysiology in Humans.Annual review of nutrition · 2026Review
- Maternal dietary citrulline supplementation increases fetal growth and programs pancreatic development in the lambs.Amino acids · 2026Article
- Combined association of birth weight and current overweight/obesity with cardiometabolic risk factor clustering in Chinese children and adolescents: a cross-sectional study.Frontiers in endocrinology · 2026Article
- Fetal Pancreas in Growth Restriction: A Prenatal Window Into Metabolic and Genetic Risk.Prenatal diagnosis · 2025Article
- Fetal programming of early-onset type 2 diabetes: a Swedish nationwide cohort and sibling analysis.European journal of epidemiology · 2025Article
- Mechanisms of LncRNA FTX in Regulating Islet Function of Pregnant Mice Born With Low-Protein Diet-Induced Intrauterine Growth Retardation.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Long-term health in individuals born preterm or with low birth weight: A cohort study.Pediatric research · 2025Article
- IGF-1 LR3 does not promote growth in late-gestation growth-restricted fetal sheep.American journal of physiology. Endocrinology and metabolism · 2025Article
- Molecular regulators of defective placental and cardiovascular development in fetal growth restriction.Clinical science (London, England : 1979) · 2024Review
- IGF-1 infusion increases growth in fetal sheep when euinsulinemia is maintained.The Journal of endocrinology · 2024Article
- Potential pathogenetic role of a novel ABCC8 missense variant on both transient neonatal diabetes mellitus and fetal growth restriction: a case report.Molecular biology reports · 2024Article
- Fetal Hypoglycemia Induced by PlacentalInternational journal of molecular sciences · 2024Article
- Paternal DDT exposure induces sex-specific programming of fetal growth, placenta development and offspring's health phenotypes in a mouse model.Scientific reports · 2024Article
- Metabolic and fecal microbial changes in adult fetal growth restricted mice.Pediatric research · 2024Article
- Calorie restriction during gestation impacts maternal and offspring fecal microbiome in mice.Frontiers in endocrinology · 2024Article
- Article
- RISING STARS: Mechanistic insights into maternal-fetal cross talk and islet beta-cell development.The Journal of endocrinology · 2023Review
- Review
- Maternal-fetal cross-talk via the placenta: influence on offspring development and metabolism.Development (Cambridge, England) · 2023Review
- A Low Dose of Ouabain Alters the Metabolic Profile of Adult Rats Experiencing Intrauterine Growth Restriction in a Sex-Specific Manner.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Placental insufficiency is a primary cause of intrauterine growth restriction (IUGR). IUGR increases the risk of developing type 2 diabetes mellitus (T2DM) throughout life, which indicates that insults from placental insufficiency impair β-cell development during the perinatal period because β-cells have a central role in the regulation of glucose tolerance. The severely IUGR fetal pancreas is characterized by smaller islets, less β-cells, and lower insulin secretion. Because of the important associations among impaired islet growth, β-cell dysfunction, impaired fetal growth, and the propensity for T2DM, significant progress has been made in understanding the pathophysiology of IUGR and programing events in the fetal endocrine pancreas. Animal models of IUGR replicate many of the observations in severe cases of human IUGR and allow us to refine our understanding of the pathophysiology of developmental and functional defects in islet from IUGR fetuses. Almost all models demonstrate a phenotype of progressive loss of β-cell mass and impaired β-cell function. This review will first provide evidence of impaired human islet development and β-cell function associated with IUGR and the impact on glucose homeostasis including the development of glucose intolerance and diabetes in adulthood. We then discuss evidence for the mechanisms regulating β-cell mass and insulin secretion in the IUGR fetus, including the role of hypoxia, catecholamines, nutrients, growth factors, and pancreatic vascularity. We focus on recent evidence from experimental interventions in established models of IUGR to understand better the pathophysiological mechanisms linking placental insufficiency with impaired islet development and β-cell function.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.