glycogen has been researched along with Fetal-Death* in 18 studies
2 review(s) available for glycogen and Fetal-Death
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Prenatal development as a predisposing factor for perinatal losses in pigs.
The pig industry is confronted with substantial losses due to piglet mortality. With 3-8% stillbirths and generally > 10% preweaning mortality, approximately one fifth of all fetuses formed fully at the end of gestation die before weaning. Most of these losses occur in the perinatal period. Overall prenatal development (birth weight) and specific prenatal developmental and maturational processes in late gestation are predisposing factors for perinatal losses. Birth weight and variation in birth weight remain important risk factors for perinatal mortality. Genetic selection against piglet mortality will not necessarily increase birth weight but will affect body composition and proportional organ development. Many maturational processes that occur in late gestation in preparation for extrauterine life, for example specific biochemical changes in the gastrointestinal tract, are influenced by glucocorticosteroids and are, therefore, dependent on maturation of the pituitary-adrenal system. The carbohydrate metabolism of perinatal piglets is related closely to viability in the perinatal period. The prenatal deposition of carbohydrate reserves (glycogen) and prenatal effects on perinatal glucogenic capacity, glucose homeostasis, carbohydrate metabolism and thermostability are reviewed. Topics: Animal Nutritional Physiological Phenomena; Animals; Animals, Newborn; Birth Weight; Carbohydrate Metabolism; Female; Fetal Death; Genotype; Glucose; Glycogen; Homeostasis; Mortality; Pituitary-Adrenal System; Swine; Thyroid Gland; Weaning | 2001 |
[Pathological anatomy and pathogenesis of diabetic embryofetopathies].
Topics: Congenital Abnormalities; Embryo, Mammalian; Female; Fetal Death; Fetal Diseases; Fetus; Glycogen; Humans; Hypoglycemia; Infant, Newborn; Infant, Newborn, Diseases; Insulin; Maternal-Fetal Exchange; Placenta Diseases; Pregnancy; Pregnancy in Diabetics | 1975 |
16 other study(ies) available for glycogen and Fetal-Death
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Deficiency of the BiP cochaperone ERdj4 causes constitutive endoplasmic reticulum stress and metabolic defects.
Endoplasmic reticulum-localized DnaJ 4 (ERdj4) is an immunoglobulin-binding protein (BiP) cochaperone and component of the endoplasmic reticulum-associated degradation (ERAD) pathway that functions to remove unfolded/misfolded substrates from the ER lumen under conditions of ER stress. To elucidate the function of ERdj4 in vivo, we disrupted the ERdj4 locus using gene trap (GT) mutagenesis, leading to hypomorphic expression of ERdj4 in mice homozygous for the trapped allele (ERdj4(GT/GT)). Approximately half of ERdj4(GT/GT) mice died perinatally associated with fetal growth restriction, reduced hepatic glycogen stores, and hypoglycemia. Surviving adult mice exhibited evidence of constitutive ER stress in multiple cells/tissues, including fibroblasts, lung, kidney, salivary gland, and pancreas. Elevated ER stress in pancreatic β cells of ERdj4(GT/GT) mice was associated with β cell loss, hypoinsulinemia, and glucose intolerance. Collectively these results suggest an important role for ERdj4 in maintaining ER homeostasis during normal fetal growth and postnatal adaptation to metabolic stress. Topics: Animals; Blood Glucose; Crosses, Genetic; Endoplasmic Reticulum Chaperone BiP; Endoplasmic Reticulum Stress; Female; Fetal Death; Fetal Growth Retardation; Fetus; Gene Expression Regulation, Developmental; Genes, Essential; Genetic Loci; Glucose Intolerance; Glycogen; Heat-Shock Proteins; Homozygote; Hypoglycemia; Insulin; Insulin-Secreting Cells; Liver; Male; Membrane Glycoproteins; Mice; Mice, Inbred C57BL; Mice, Transgenic; Mutagenesis; Signal Transduction | 2014 |
Fetal growth restriction in hypothyroidism is associated with changes in proliferative activity, apoptosis and vascularisation of the placenta.
The objective of this study was to evaluate fetal weight, histomorphometric changes and proliferative activity, apoptosis and angiogenesis of the placenta in rats with hypothyroidism. Thirty-six adult female rats were divided into two groups with 18 animals each: control and hypothyroidism. Hypothyroidism was induced by daily administration of propylthiouracil (1 mg/animal). The administration began five days before becoming pregnant and the animals were sacrificed at 14 or 19 days of gestation. The control group received a placebo. The number and weight of fetuses and the rate of fetal death was determined, as well as the morphometric characteristics, the immunohistochemical expression of cell division control protein 47 (CDC)-47 and vascular endothelial growth factor (VEGF) and the number of apoptotic cells in the placental disk. The data were analysed by Mann-Whitney U test. Hypothyroidism reduced the weight of fetuses and of the uterus and placenta (P<0.05), altered the thickness of the placental labyrinth and spongiotrophoblast (P<0.05), increased the population of glycogen cells in the spongiotrophoblast (P<0.05), interfered with the vascular development of the placental labyrinth and decreased VEGF expression (P<0.05), reduced the expression of CDC-47 and cellularity and increased the apoptotic rate in the placental disk (P<0.05). We conclude that hypothyroidism affects fetal weight by altering the proliferative activity, apoptosis and vascularisation of the placenta. Topics: Adenosine Triphosphatases; Animals; Apoptosis; Biomarkers; Cell Proliferation; Disease Models, Animal; DNA-Binding Proteins; Down-Regulation; Female; Fetal Death; Fetal Growth Retardation; Fetal Weight; Gestational Age; Glycogen; Hypothyroidism; Immunohistochemistry; Minichromosome Maintenance Complex Component 7; Neovascularization, Physiologic; Placenta; Pregnancy; Propylthiouracil; Rats; Trophoblasts; Vascular Endothelial Growth Factor A | 2012 |
Increased glycogen content and glucose transporter 3 mRNA level in the placenta of Holtzman rats after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.
Exposure to a low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produces a variety of toxic manifestations, including fetal death. In order to evaluate the effects of low-dose TCDD on placental function in this study, pregnant Holtzman rats were given a single oral dose of 800 or 1600 ng TCDD/kg body wt or an equivalent volume of vehicle (control) on gestation day (GD) 15 and the results were observed on GD16 and GD20. The number of fetal deaths increased in the animals exposed to TCDD. Although fetal and placental weight did not differ significantly between the control group and the TCDD groups, histological differences from the control rats were clearly observed in the junctional zone (JZ) of the placentas of the TCDD-exposed rats. In the control placenta, glycogen cells occupied the majority of the JZ on GD16, but then decreased in number and almost disappeared by GD20, whereas on GD20 the placenta of the TCDD-exposed rats exhibited a larger area occupied by the glycogen cells and cysts filled with eosinophilic material surrounded by glycogen cells in the JZ than that of the control group. Glycogen assay revealed that the glycogen content of the placentas from the TCDD-exposed rats was higher than in the control rats. Semiquantitative RT-PCR analysis was performed to assess the expression of glucose transporter 1 (GLUT1) and GLUT3, the two major placental glucose transporter isoforms. On GD20 the level of expression of GLUT1 mRNA in the placentas was not different between the control and TCDD groups, whereas the level of expression of GLUT3 mRNA approximately doubled in both the 800 and 1600 ng/kg TCDD groups. GLUT3 mRNA expression was restricted to the labyrinth zone of placenta, where zone-specific expression of mRNA arylhydrocarbon receptor and induction of cytochrome P450 1A1 mRNA by TCDD were observed, and none was detected in the JZ. These results, including the increase of glycogen content and GLUT3 mRNA level in TCDD-exposed placentas, provide the first evidence of alteration of glucose kinetics in the placenta by TCDD. Topics: Animals; Dose-Response Relationship, Drug; Environmental Pollutants; Female; Fetal Death; Gas Chromatography-Mass Spectrometry; Glycogen; Male; Monosaccharide Transport Proteins; Placenta; Polychlorinated Dibenzodioxins; Pregnancy; Rats; Rats, Sprague-Dawley; RNA, Messenger | 2002 |
Targeted disruption of the low-affinity leukemia inhibitory factor receptor gene causes placental, skeletal, neural and metabolic defects and results in perinatal death.
The low-affinity receptor for leukemia inhibitory factor (LIFR) interacts with gp130 to induce an intracellular signal cascade. The LIFR-gp130 heterodimer is implicated in the function of diverse systems. Normal placentation is disrupted in LIFR mutant animals, which leads to poor intrauterine nutrition but allows fetuses to continue to term. Fetal bone volume is reduced greater than three-fold and the number of osteoclasts is increased six-fold, resulting in severe osteopenia of perinatal bone. Astrocyte numbers are reduced in the spinal cord and brain stem. Late gestation fetal livers contain relatively high stores of glycogen, indicating a metabolic disorder. Hematologic and primordial germ cell compartments appear normal. Pleiotropic defects in the mutant animals preclude survival beyond the day of birth. Topics: Animals; Astrocytes; Base Sequence; Blotting, Southern; Bone Development; Cell Count; DNA Primers; Embryonic and Fetal Development; Fetal Death; Gene Deletion; Glycogen; Growth Inhibitors; Hematopoiesis; Interleukin-6; Leukemia Inhibitory Factor; Leukemia Inhibitory Factor Receptor alpha Subunit; Liver; Lymphokines; Mice; Mice, Transgenic; Molecular Sequence Data; Mutagenesis, Insertional; Nervous System; Osteoclasts; Placenta; Polymerase Chain Reaction; Receptors, Cytokine; Receptors, OSM-LIF; Stem Cells | 1995 |
Anti-implantation role for substance P and neurotensin in rat.
Substance P (SP) and neurotensin (NT), two structurally related peptides with contrasting biological actions, have been shown to have some role in peripheral reproductive processes. Intrauterine microinjection of SP or NT on day 4 or 5 of pregnancy in the rat significantly reduced the number of viable fetuses, weight and glycogen content of the uterus. The number of viable fetuses, uterine weight or glycogen content were not modified when SP/NT was microinjected on day 8, 9, 10 or on day 14, 15 and 16. The results indicate that the peptides possibly exert a direct local alteration in uterine vascular permeability causing failure in implantation. Topics: Animals; Embryo Implantation; Female; Fetal Death; Glycogen; Neurotensin; Organ Size; Pregnancy; Rats; Substance P; Time Factors; Uterus | 1992 |
[Morphology of the rat placenta in experimental, hormone-induced, prolonged pregnancy. II. Plancenta in intrauterine macerated dead rat fetuses].
In course of overdue pregnancy in rats, produced by application of synthetic gestagens the intrauterine death rate rises, when the gestation time is more than 23 days. Placentas of 47 macereted fetus rats we have investigated. The pathologic-anatomical picture of the placenta characterized by collaps and following regression of the peripheral fetal blood system. Furthermore, there are narrowing processes in great fetal vessels. In the maternal sinus occurs fibrin. The labyrinth of the placenta inclines by production of collagen fibers to a homogenous structure. The trophoblastic epithel is less differentiated. These findings in rat placentas we have compared with those in human placentas in cases of fetal maceration. The worth of these changes for differentiation of intravital against postmortal regressive processes is evident. Topics: Animals; Epithelial Cells; Female; Fetal Death; Fibrin; Gestational Age; Glycogen; Placenta; Pregnancy; Pregnancy, Prolonged; Rats; Thrombosis; Trophoblasts | 1975 |
Cycloalkanones. 4. Antifertility activity.
Topics: Androstenedione; Animals; Carbon Radioisotopes; Contraceptives, Oral, Synthetic; Cyclic AMP; Cycloparaffins; Deoxyribonucleases; DNA; DNA-Directed RNA Polymerases; Female; Fertility; Fetal Death; Follicle Stimulating Hormone; Glycogen; Ketones; Lipids; Liver; Liver Glycogen; Luteinizing Hormone; Male; Mice; Pituitary Gland; Pregnancy; Protein Biosynthesis; Proteins; Rats; RNA; Testosterone; Tyrosine; Uterus | 1974 |
The effect of the polyethylene IUD on rat embryogenesis.
Topics: Animals; Cell Differentiation; DNA Replication; Embryo Implantation; Embryology; Female; Fetal Death; Glycogen; Intrauterine Devices; Photomicrography; Polyethylenes; Pregnancy; Rats; Thymidine; Tritium; Uterus | 1972 |
Fine structural changes in the rabbit placenta induced by cortisone.
Topics: Animals; Cell Nucleus; Cortisone; Female; Fetal Death; Fetus; Glycogen; Injections, Intramuscular; Maternal-Fetal Exchange; Microscopy, Electron; Mitosis; Placenta; Pregnancy; Pregnancy, Animal; Rabbits; Trophoblasts | 1972 |
A morphological and histochemical study of thalidomide-induced upper limb malformations in rabbit fetuses.
Topics: Abnormalities, Drug-Induced; Alkaline Phosphatase; Animals; Bone and Bones; Calcium; Cartilage; Embryonic and Fetal Development; Female; Fetal Death; Forelimb; Gestational Age; Glycogen; Glycosaminoglycans; Limb Deformities, Congenital; Ossification, Heterotopic; Pregnancy; Rabbits; Thalidomide; Thumb | 1971 |
Salicylate-induced foetal damage late in pregnancy. An experimental study in mice.
Topics: Abnormalities, Drug-Induced; Animals; Animals, Newborn; Aspirin; Carbon Isotopes; Coumarins; Female; Fetal Death; Fetus; Gestational Age; Glycogen; Hemorrhage; Injections, Intramuscular; Liver; Maternal-Fetal Exchange; NADP; Obstetric Labor, Premature; Pentobarbital; Pregnancy; Prothrombin; Rats; Time Factors | 1971 |
[Effect of tetracycline on embryogenesis in albino rats].
Topics: Abnormalities, Drug-Induced; Alkaline Phosphatase; Animals; Ascorbic Acid; Body Weight; Corpus Luteum; Depression, Chemical; Embryo, Mammalian; Female; Fertility; Fetal Death; Gestational Age; Glycogen; Histocytochemistry; Nucleic Acids; Organ Size; Placenta; Placenta Diseases; Pregnancy; Rats; Tetracycline | 1971 |
[Effects of parathion on quail embryo development and certain of its organs in vivo and in vitro].
Topics: Abnormalities, Drug-Induced; Abnormalities, Multiple; Animals; Birds; Dwarfism; Embryo, Nonmammalian; Female; Fetal Death; Glycogen; Gonads; Infertility; Jaw Abnormalities; Kidney; Leg; Lordosis; Male; Parathion; Pregnancy | 1969 |
Role of hyperkalaemia in experimental fetal asphyxia.
Topics: Animals; Asphyxia Neonatorum; Carbohydrates; Female; Fetal Death; Glycogen; Heart Arrest; Humans; Hyperkalemia; Hypoxia; Infant, Newborn; Myocardium; Pregnancy; Rabbits | 1968 |
CARBOHYDRATE RESERVES IN THE NEWBORN INFANT.
Topics: Carbohydrate Metabolism; Fetal Death; Fetus; Glycogen; Heart; Humans; Infant Mortality; Infant, Newborn; Liver Glycogen; Muscles; Respiratory Insufficiency | 1964 |
ENVIRONMENTAL AND AGING EFFECTS OF POSTMATURITY ON FETAL DEVELOPMENT AND CARBOHYDRATE METABOLISM.
Topics: Animals; Animals, Newborn; Birth Weight; Brain; Carbohydrate Metabolism; Carbon Isotopes; Female; Fetal Death; Fetal Development; Glycogen; Glycolysis; Histocytochemistry; Hypoxia; Liver; Metabolism; Myocardium; Pregnancy; Pregnancy, Prolonged; Pyruvates; Rabbits; Research | 1964 |