glycogen and Pre-Eclampsia

The metabolic syndrome that occurs in preeclampsia reflects the complex interactions between immunological alterations and the systemic inflammation that have been shown to take place during this complication of human pregnancy. Inositol phosphoglycans play a definite role in the insulin resistance in preeclampsia with a higher production and urinary excretion of this molecule before and during preeclampsia. Recent researches suggest that the feto-placental glucose metabolism in the first and early second trimester is mainly linked to the nonoxidative pathway of glycogen catabolism supporting the pivotal role of the inositol phosphoglycan P-type. In this article we present the results of a case-control study carried out in the first trimester to evaluate the potential of urinary P-IPG release as a early marker of the disease. A single mid-stream sample of maternal urine was collected at 11 weeks of gestation for this single centre retrospective study. Twenty-seven patients out of 331 women recruited (8.1%) went on to develop preeclampsia but no sample attained positivity. Further details about the development of the metabolic syndrome during preeclampsia were retrieved also from other studies to implement our knowledge about the pathophysiology of this syndrome and to identify biochemical aspects that could help in clinical practice.

Topics: Female; Fetus; Glucose; Glycogen; Humans; Inflammation; Inositol Phosphates; Metabolic Syndrome; Placenta; Polysaccharides; Pre-Eclampsia; Pregnancy; Pregnancy Trimester, First; Pregnancy Trimester, Third

Topics: Animals; Birth Weight; Blood Glucose; Carbohydrate Metabolism; Cardiomegaly; Female; Fetus; Glucose; Glycogen; Haplorhini; Humans; Hydrocortisone; Hypoglycemia; Infant, Newborn; Infant, Newborn, Diseases; Insulin; Lipids; Liver; Polycythemia; Pre-Eclampsia; Pregnancy; Prognosis; Rabbits; Sex Factors; Time Factors

Preeclampsia remains a clinical challenge due to its poorly understood pathogenesis. A prevailing notion is that increased placental production of soluble fms-like tyrosine kinase-1 (sFlt-1) causes the maternal syndrome by inhibiting proangiogenic placental growth factor (PlGF) and VEGF. However, the significance of PlGF suppression in preeclampsia is uncertain. To test whether preeclampsia results from the imbalance of angiogenic factors reflected by an abnormal sFlt-1/PlGF ratio, we studied PlGF KO (Pgf-/-) mice and noted that the mice did not develop signs or sequelae of preeclampsia despite a marked elevation in circulating sFLT-1. Notably, PlGF KO mice had morphologically distinct placentas, showing an accumulation of junctional zone glycogen. We next considered the role of placental PlGF in an established model of preeclampsia (pregnant catechol-O-methyltransferase-deficient [COMT-deficient] mice) by generating mice with deletions in both the Pgf and Comt genes. Deletion of placental PlGF in the context of COMT loss resulted in a reduction in maternal blood pressure and increased placental glycogen, indicating that loss of PlGF might be protective against the development of preeclampsia. These results identify a role for PlGF in placental development and support a complex model for the pathogenesis of preeclampsia beyond an angiogenic factor imbalance.

Topics: Animals; Blood Pressure; Disease Models, Animal; Female; Glycogen; Mice; Mice, Knockout; Models, Biological; Placenta; Placenta Growth Factor; Pre-Eclampsia; Pregnancy; Vascular Endothelial Growth Factor Receptor-1

The human placenta is a difficult tissue to work with using proteomic technology since it contains large amounts of lipids and glycogen. Both lipids and glycogen are known to interfere with the first step in the two-dimensional polyacrylamide gel electrophoresis (2D-PAGE), the isoelectric focusing. In order to gain the best possible protein separation on 2D-PAGE, an optimized sample preparation protocol for placental proteins was developed. Two different buffers, urea/CHAPS and Hepes, were used for solubilization in combination with six different precipitation methods. The removal of glycogen from the samples by centrifugation was crucial for the final proteome maps. Solubilization with urea/CHAPS in combination with dichloromethane/methanol or acidified acetone proved to be the best precipitation procedures. When applied to clinical placenta samples apolipoprotein A1 was found to be accumulated in the preeclamptic placenta, where it may either have a nutritional effect or act as a modifier of signal transduction.

Topics: Adult; Apolipoprotein A-I; Chemical Precipitation; Cholic Acids; Electrophoresis, Gel, Two-Dimensional; Electrophoresis, Polyacrylamide Gel; Female; Glycogen; HEPES; Humans; Immunohistochemistry; Lipids; Middle Aged; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Proteins; Proteome; Proteomics; Reproducibility of Results; Solubility; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; Urea

Measurements have been made of the urinary content of inositol phosphoglycans IPG P-type and IPG A-type, putative insulin second messengers, in preeclampsia, in type I insulin-treated diabetic pregnant women and their matched control subjects, and nonpregnant women of child-bearing age. The content of IPG P-type and IPG A-type was also measured in the placenta from preeclamptic patients and from normal pregnancies. Pregnancy was associated with an increase, approximately twofold, in urinary output of IPG-P-type relative to nonpregnant controls (P<0.01). The 24-h output of IPG P-type in urine in preeclamptic women was significantly higher (2- to 3-fold) than in pregnant control subjects matched for age, parity, and stage of gestation (P<0.02). In contrast, insulin-dependent diabetic pregnant women did not show any significant change in urinary output of IPG P-type or IPG A-type relative to pregnant control subjects. Evidence for a possible relationship and correlation between the urinary excretion of IPG P-type and markers of preeclampsia, including proteinuria (r = 0.720, P<0.01), plasma aspartate transaminase (r = 0.658, P<0.05), and platelet counts (r = 0.613, P<0.05) is presented. A high yield of IPG P-type was extracted from human placenta, in preeclampsia some 3-fold higher (P = 0.03) than the normal value, whereas no IPG A-type (with lipogenic-stimulating activity) was found. Low concentrations of placental IPG A-type were detected relative to IPG P-type using assay systems dependent upon the effect of this mediator on cAMP-dependent protein kinase or on a proliferation assay using thymidine incorporation into DNA of EGFR T17 fibroblasts. It is postulated that the high urinary excretion IPG P-type in preeclampsia reflects high placental levels and relates to the accumulation of glycogen in the placenta. The paracrine effects of placental IPG P-type (stimulation off other endocrine glands and/or endothelial cells) could contribute to the pathogenesis of the maternal syndrome. A possible theoretical link between elevated placental IPG P-type and apoptosis is proposed.

Topics: Adult; Animals; Biomarkers; Cell Line; Cyclic AMP-Dependent Protein Kinases; Diabetes Mellitus, Type 1; Enzyme Activation; Female; Fibroblasts; Gestational Age; Glycogen; Glycogen Synthase; Humans; Inositol Phosphates; Male; Placenta; Polysaccharides; Pre-Eclampsia; Pregnancy; Pregnancy in Diabetics; Rats; Rats, Wistar; Signal Transduction

Pre-eclampsia is a placental disorder, but until now, biochemical details of dysfunction have been lacking. During an analysis of the oligosaccharide content of syncytiotrophoblast microvesicles purified from the placental chorionic villi of 10 primigravid women with proteinuric pre-eclampsia, we found an excess of glycogen breakdown products. Further investigation revealed a 10-fold increase in glycogen content (223 +/- 117 micrograms glycogen/mg protein), when compared with controls matched for gestational age at delivery (23 +/- 18 micrograms glycogen/mg protein) (P < 0.01). This was confirmed by examination of electron micrographs of chorionic villous tissue stained for glycogen. The increase in glycogen content was associated with 16 times more glycogen synthase (1,323 +/- 1,013 relative to 83 +/- 96 pmol glucose/mg protein per min) (P < 0.001), and a threefold increase in glycogen phosphorylase activity (2,280 +/- 1,360 relative to 700 +/- 540 pmol glucose/mg protein per min; P < 0.05). Similar changes in glycogen metabolism were found in trophoblast microvesicles derived from hydatidiform moles. Glycogen accumulation in villous syncytiotrophoblast may be a metabolic marker of immaturity of this cell which is unable to divide. The implications of these findings with regard to the pathogenesis of pre-eclampsia are discussed.

Topics: Adult; Chorion; Diabetes Mellitus; Female; Glucose; Glycogen; Glycogen Synthase; Glycoproteins; Humans; Hydatidiform Mole; Oligosaccharides; Phosphorylases; Placenta; Polysaccharides; Pre-Eclampsia; Pregnancy; Trophoblasts

Succinate dehydrogenase, phospholipid and glycogen activities were measured by cytochemical methods in puerperae with massive blood loss in the presence of gestosis in order to investigate platelet metabolism and the possible approaches to metabolic correction. A significant depression of platelet intracellular metabolism was revealed in these puerperae. Metabolic correction agents (acetyl salicylic acid, essential, alpha-tocopherol, retinol) were added to routine intensive therapy. The treatment was conducive to normalization of the metabolic processes and rapid recovery of puerperae with massive blood loss developing in the presence of gestosis.

Topics: Aspirin; Blood Platelets; Drug Combinations; Female; Glycogen; Humans; Lipid Peroxidation; Phospholipids; Postpartum Hemorrhage; Pre-Eclampsia; Pregnancy; Succinate Dehydrogenase; Vitamin A; Vitamin E

We estimated in vitro degradation and consumption of glycogen by placental tissue derived from pregnancies complicated by gestosis and anemia. Placental tissue was incubated in suitable medium. Glycogen concentration either before or after incubation was assayed. Glycogen consumption was expressed as micromoles of glucose per 1 g of wet tissue, the percentage of glycogen consumption has been shown in tables. It is concluded that in advanced gestosis and severe anemia of pregnancy the consumption of native glycogen is increased, consequently it may lead to metabolic insufficiency of human placenta.

Topics: Anemia; Female; Glycogen; Humans; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Hematologic

Pathways of human placental glycogen degradation either in normal or gestotic pregnancy were examined. Determinations of glycogen phosphorylase served as an index of glycogen cleavage in the phosphorylitic pathway. The activity of hydrolytic route was measured by estimating placental glucoamylase. Samples of placental tissue were obtained after delivery (between the 36th and the 40th week of pregnancy). In placentas derived from gestotic cases elevated activity of phosphorylase A, the decrease in phosphorylase B activity and the rise in glucoamylase were found. It suggests that gestosis may evoke certain impairment of placental glycogen metabolism deteriorating chiefly the glycogen degradation as it may be observed in hypoxic experiments.

Topics: Female; Glycogen; Humans; Phosphorylase a; Phosphorylase b; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Trimester, Third; Reference Values

The quantity and distribution of glycogen has been studied in 86 placentae from the last trimester of pregnancy and 8 of 8 to 16 weeks gestational age. In the first trimester glycogen concentrations were high, between 4-5 to 6-5 mg/g of blood-free tissue, but from about 12 weeks to term the concentrations were within a narrow range around 1-5 mg/g. The level did not deviate appreciably from normal in a range of clinical conditions: diabetes, intrauterine growth retardation, pre-eclampsia or acute fetal distress, and was unaffected by the length of labour and whether or not the mother had been given an infusion of dextrose. Nor was it affected by a wide range of glucose concentrations in the maternal and fetal plasma and in the placental tissue itself or by insulin concentrations in either circulation. After the first few weeks of pregnancy glycogen in the placenta was shown to be restricted to the vicinity of major fetal blood vessels. Here it may be presumed to act as an energy reserve for vasomotor activity. All the evidence suggests that any importance placental glycogen may have is likely to be local, in relation to the placental vessels; a more general role, as an emergency energy source for the fetus, seems unlikely.

Topics: Birth Weight; Cesarean Section; Female; Glucose; Glycogen; Humans; Infant, Newborn; Infant, Premature; Insulin; Labor, Obstetric; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy in Diabetics; Pregnancy Trimester, First; Pregnancy Trimester, Third

Topics: Erythrocyte Count; Erythropoiesis; Female; Glycogen; Humans; Infant, Newborn; Leukocytes; Maternal-Fetal Exchange; Peroxidases; Pre-Eclampsia; Pregnancy; Pregnancy Trimester, Third

Topics: Adult; Blood Glucose; Carbohydrate Metabolism; Female; Glucose; Glycogen; Humans; Infant, Newborn; Lactates; Maternal-Fetal Exchange; Placenta; Pre-Eclampsia; Pregnancy; Pyruvates

Topics: Animals; Chorionic Gonadotropin; Female; Fibrin; Glycogen; Glycoproteins; Glycosaminoglycans; Humans; Hydatidiform Mole; Kidney; Obstetric Labor Complications; Placenta; Pre-Eclampsia; Pregnancy; Rats; Staining and Labeling

Topics: Female; Fetal Diseases; Glucose; Glycogen; Growth Disorders; Growth Hormone; Humans; Hypoglycemia; Infant Nutritional Physiological Phenomena; Infant, Newborn; Infant, Newborn, Diseases; Jaundice, Neonatal; Male; Placenta Diseases; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Prognosis; Respiratory Distress Syndrome, Newborn

Topics: Eclampsia; Female; Glycogen; Glycosaminoglycans; Histocytochemistry; Humans; Placenta; Pre-Eclampsia; Pregnancy

Topics: Birth Weight; Female; Fetal Diseases; Gestational Age; Glycogen; Humans; Infant, Newborn; Organ Size; Placenta; Pre-Eclampsia; Pregnancy

Topics: Female; Gestational Age; Glucosyltransferases; Glycogen; Histocytochemistry; Humans; Male; Maternal-Fetal Exchange; Microscopy, Electron; Phosphoric Monoester Hydrolases; Placenta; Pre-Eclampsia; Pregnancy; Trophoblasts

Topics: Adult; DNA; Female; Glycogen; Glycosaminoglycans; Histocytochemistry; Humans; Lipid Metabolism; Methods; Placenta; Pre-Eclampsia; Pregnancy; RNA

Topics: Abortion, Spontaneous; Adult; Amino Acids; Citric Acid Cycle; Contraception; DNA; Fatty Acids; Female; Fetus; Fructose; Gestational Age; Glucose; Glycogen; Humans; Lactates; Maternal-Fetal Exchange; Placenta; Pre-Eclampsia; Pregnancy; Pyruvates; RNA

Topics: Carbohydrate Metabolism; Female; Glycogen; Humans; Leukocytes; Pre-Eclampsia; Pregnancy; Puerperal Disorders

Topics: Female; Glycogen; Glycogenolysis; Humans; Placenta; Pre-Eclampsia; Pregnancy

Topics: Bacterial Infections; Carbohydrate Metabolism; Carbohydrates; Female; Glycogen; Humans; Physical Therapy Modalities; Pre-Eclampsia; Pregnancy; Sepsis