glycogen and Anemia

Hepatic glucose production (HGP) normally begins just prior to birth. Prolonged fetal hypoglycemia, intrauterine growth restriction, and acute hypoxemia produce an early activation of fetal HGP. To test the hypothesis that prolonged hypoxemia increases factors which regulate HGP, studies were performed in fetuses that were bled to anemic conditions (anemic: n = 11) for 8.9 ± 0.4 days and compared with control fetuses (n = 7). Fetal arterial hematocrit and oxygen content were 32% and 50% lower, respectively, in anemic vs. controls (P < 0.005). Arterial plasma glucose was 15% higher in the anemic group (P < 0.05). Hepatic mRNA expression of phosphonenolpyruvate carboxykinase (PCK1) was twofold higher in the anemic group (P < 0.05). Arterial plasma glucagon concentrations were 70% higher in anemic fetuses compared with controls (P < 0.05), and they were positively associated with hepatic PCK1 mRNA expression (P < 0.05). Arterial plasma cortisol concentrations increased 90% in the anemic fetuses (P < 0.05), but fetal cortisol concentrations were not correlated with hepatic PCK1 mRNA expression. Hepatic glycogen content was 30% lower in anemic vs. control fetuses (P < 0.05) and was inversely correlated with fetal arterial plasma glucagon concentrations. In isolated primary fetal sheep hepatocytes, incubation in low oxygen (3%) increased PCK1 mRNA threefold compared with incubation in normal oxygen (21%). Together, these results demonstrate that glucagon and PCK1 may potentiate fetal HGP during chronic fetal anemic hypoxemia.

Topics: Anemia; Animals; Female; Fetal Hypoxia; Fetus; Glucagon; Glucose-6-Phosphatase; Glycogen; Hepatocytes; Hydrocortisone; Hypoxia; Liver; Organ Size; Phosphoenolpyruvate Carboxykinase (GTP); Pregnancy; RNA, Messenger; Sheep; Umbilical Cord

Anaemia is a common health problem in the developing world. This condition is characterized by a reduction in erythrocyte density, primarily from malnutrition and/or infectious diseases such as malaria. As red blood cells are the primary source of protein for haematophagous mosquitoes, any reduction could impede the ability of mosquito vectors to transmit malaria by influencing their fitness or that of the parasites they transmit. The aim of this study was to determine the impact of differences in the density of red blood cells in human blood on malaria vector (Anopheles gambiae sensu stricto) fitness. The hypotheses tested are that mosquito vector energetic reserves and fitness are negatively influenced by reductions in the red cell density of host human blood meals commensurate with those expected from severe anaemia.. Mosquitoes (An. gambiae s.s.) were offered blood meals of different packed cell volume (PCV) of human blood consistent with those arising from severe anaemia (15%) and normal PCV (50%). Associations between mosquito energetic reserves (lipid, glucose and glycogen) and fitness measures (reproduction and survival) and blood meal PCV were investigated.. The amount of protein that malaria vectors acquired from blood feeding (indexed by haematin excretion) was significantly reduced at low blood PCV. However, mosquitoes feeding on blood of low PCV had the same oviposition rates as those feeding on blood of normal PCV, and showed an increase in egg production of around 15%. The long-term survival of An. gambiae s.s was reduced after feeding on low PCV blood, but PCV had no significant impact on the proportion of mosquitoes surviving through the minimal period required to develop and transmit malaria parasites (estimated as 14 days post-blood feeding). The impact of blood PCV on the energetic reserves of mosquitoes was relatively minor.. These results suggest that feeding on human hosts whose PCV has been depleted due to severe anaemia does not significantly reduce the fitness or transmission potential of malaria vectors, and indicates that mosquitoes may be able exploit resources for reproduction more efficiently from blood of low rather than normal PCV.

Topics: Anemia; Animals; Anopheles; Erythrocytes; Feeding Behavior; Glucose; Glycogen; Lipids; Sexual Behavior, Animal; Survival Analysis

The present study describes light and electron microscopic changes in the liver of Atlantic salmon during the development of infectious salmon anemia (ISA). Atlantic salmon postsmolts weighing 80-100 g were infected by intraperitoneal injections, and liver samples were collected sequentially between day 0 and day 25 post infection (p.i.), with time intervals of 3-4 days. At each collection time, livers from five infected fish and two control fish were examined. Changes involving the perisinusoidal macrophages were observed by transmission electron microscopy, from day 4 p.i. Large vacuoles, containing a fine-granular material with low electron density, accumulated in the cytoplasm. These changes persisted and became more severe throughout the investigation, leading to a considerable increase in the size of the cells. At day 14 p.i., degenerative features of the sinusoidal endothelium were observed. By day 18 p.i., areas of the liver were devoid of a sinusoidal endothelial lining, bringing hepatocytes in direct contact with blood cells. At this stage, the sinusoids were moderately congested. From day 21 p.i., heavy sinusoidal congestion, peliosis hepatis, and degeneration of the hepatocytes were observed. No virus was observed in any of the inhabitant cell types of the liver. Gross and light microscopic changes were first recorded at day 18 p.i., as was a significant decrease in the hematocrit values. By day 25 p.i., characteristic multifocal, confluent, hemorrhagic necroses were present. Results of the present investigation suggest that the liver lesions observed with ISA are not the result of the development of an anemia alone or caused by direct viral damage to hepatocytes. Hepatocellular degeneration succeeded changes in the perisinusoidal macrophages and degeneration of the sinusoidal endothelium. These changes may have impeded the sinusoidal blood flow and hence caused an ischemic hepatocellular necrosis.

Topics: Anemia; Animals; Communicable Diseases; Endothelium; Fish Diseases; Glycogen; Hematocrit; Injections, Intraperitoneal; Liver; Liver Diseases; Microscopy, Electron; Salmon; Tissue Fixation

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

Topics: Adolescent; Adult; Aged; Anemia; Diagnosis, Differential; Female; Glycogen; Guinea-Bissau; Humans; Lymphocytes; Male; Middle Aged; Neutrophils; RNA; Tropical Climate

Topics: Anemia; Blood Platelet Disorders; Blood Platelets; Glycogen; Hematologic Diseases; Humans; Myeloproliferative Disorders

Topics: Anemia; Animals; Dogs; Electron Transport Complex IV; Glycogen; Hemorrhage; Histocytochemistry; Neutrophils; Peroxidases; RNA

Topics: Anemia; Animals; Bile Ducts; Cell Division; Edema; Endoplasmic Reticulum; Female; Glycogen; Graft vs Host Reaction; Hepatic Veins; Histocompatibility; Infarction; Liver; Liver Transplantation; Methods; Mitochondrial Swelling; Necrosis; Phlebitis; Plasma Cells; Rats; Transplantation Immunology; Transplantation, Homologous

Topics: Anemia; Bone Marrow Diseases; Glycogen; Histocytochemistry; Humans; Megakaryocytes; Methods; Myeloproliferative Disorders; Periodic Acid; Staining and Labeling

Topics: Anemia; Animals; Bloodletting; Capillaries; Coronary Vessels; Endoplasmic Reticulum; Erythrocyte Count; Glycogen; Hemoglobins; Lipids; Male; Microscopy, Electron; Mitochondria, Muscle; Myocardium; Myofibrils; Rats; Ribosomes

Topics: Aminosalicylic Acids; Anemia; Animals; Brain Chemistry; Brain Stem; Glycogen; Male; Medulla Oblongata; Mesencephalon; Neurons; Nissl Bodies; Oxidoreductases; Pons; Rabbits; Staining and Labeling; Vagus Nerve

Topics: Anemia; Anemia, Hypochromic; Blood Chemical Analysis; Erythrocytes; Glycogen; Hematologic Diseases; Humans; Leukemia, Erythroblastic, Acute; Thalassemia

Topics: Alkaline Phosphatase; Anemia; Anemia, Macrocytic; Anemia, Myelophthisic; Anemia, Pernicious; Clinical Enzyme Tests; Coloring Agents; Glycogen; Hematologic Diseases; Hematology; Histocytochemistry; Leukemia; Periodic Acid; Polycythemia Vera; Staining and Labeling

Topics: Anemia; Erythrocytes; Glycogen; Humans; Iron

Topics: Anemia; Animals; Ducks; Glycogen; Humans; Leukemia; Leukocytes; Polycythemia