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Maternal Diabetes and Fetal Programming Toward Neurological Diseases: Beyond Neural Tube Defects

TLDR
The state of the art on this topic is explored to help establish the way forward in the study of fetal programming under hyperglycemia and its impact on neurological and psychiatric disorders.
Abstract
The purpose of this review was to search for experimental or clinical evidence on the effect of hyperglycemia in fetal programming to neurological diseases, excluding evident neural tube defects. The lack of timely diagnosis and the inadequate control of diabetes during pregnancy have been related with postnatal obesity, low intellectual and verbal coefficients, language and motor deficits, attention deficit with hyperactivity, problems in psychosocial development, and an increased predisposition to autism and schizophrenia. It has been proposed that several childhood or adulthood diseases have their origin during fetal development through a phenomenon called fetal programming. However, not all the relationships between the outcomes mentioned above and diabetes during gestation are clear, well-studied, or have been related to fetal programming. To understand this relationship, it is imperative to understand how developmental processes take place in health, in order to understand how the functional cytoarchitecture of the central nervous system takes place; to identify changes prompted by hyperglycemia, and to correlate them with the above postnatal impaired functions. Although changes in the establishment of patterns during central nervous system fetal development are related to a wide variety of neurological pathologies, the mechanism by which several maternal conditions promote fetal alterations that contribute to impaired neural development with postnatal consequences are not clear. Animal models have been extremely useful in studying the effect of maternal pathologies on embryo and fetal development, since obtaining central nervous system tissue in humans with normal appearance during fetal development is an important limitation. This review explores the state of the art on this topic, to help establish the way forward in the study of fetal programming under hyperglycemia and its impact on neurological and psychiatric disorders.

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Standards of Medical Care in Diabetes

TL;DR: These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care.
Journal Article

Global Gene Expression Analysis of Cranial Neural Tubes in Embryos of Diabetic Mice

TL;DR: Altered expression of a variety of genes involved in brain development is associated with cranial neural tube dysmorphogenesis that may subsequently contribute to intellectual impairment of the offspring of a diabetic mother.
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Pregestational diabetes in pregnancy: Complications, management, surveillance, and mechanisms of disease—A review

TL;DR: There is an increasing understanding of the mechanisms by which congenital anomalies and disorders of fetal growth occur, involving epigenetic modifications, changes in gene expression in critical developmental pathways, and oxidative stress, which may lead to pathways for improved care for these high risk pregnancies.
Journal ArticleDOI

Stem cell fate determination through protein O-GlcNAcylation.

TL;DR: Evidence demonstrating how stem cells couple metabolic inputs to gene regulatory pathways through O-GlcNAc-mediated epigenetic/transcriptional regulatory mechanisms to govern self-renewal and lineage-specific differentiation programs is reviewed.
References
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Standards of Medical Care in Diabetes

TL;DR: These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care.
Journal ArticleDOI

Central nervous system control of food intake

TL;DR: A model is described that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of food intake and the means by which obesity can arise from inherited or acquired defects in their function.
Journal ArticleDOI

Coexpression of Agrp and NPY in fasting-activated hypothalamic neurons

TL;DR: These findings suggest that hypothalamic NPY/Agrp neurons constitute a unique cell type that is activated by fasting to stimulate food intake via a simultaneous increase of NPY and decrease of melanocortin.
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Obstetric Complications and Schizophrenia: Historical and Meta-Analytic Review

TL;DR: Current methods of investigating the relationship between obstetric complications and schizophrenia are reaching the limit of their usefulness, and a combination of disciplines and approaches will be needed to elucidate the mechanisms underlying these small but important associations.
Journal ArticleDOI

Histamine in the Nervous System

TL;DR: Mutual interactions with other transmitter systems form a network that links basic homeostatic and higher brain functions, including sleep-wake regulation, circadian and feeding rhythms, immunity, learning, and memory in health and disease.
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Trending Questions (1)
How does hyperglycemia during pregnancy affect the developing embryo's neural tube closure and brain development?

Hyperglycemia during pregnancy can impact neural tube closure and brain development, leading to neurological diseases beyond neural tube defects in the offspring.