Disease relevance of LOC449474

• Further analysis of the PRKAG3 signaling pathway may provide insights into muscle physiology as well as the pathogenesis of noninsulin-dependent diabetes mellitus in humans, a metabolic disorder associated with impaired glycogen synthesis [1].
• Anoxia resulted in degradation of the labeled glycogen within 6 min and appearance of 13C label in lactic acid [2].
• In contrast, the rate of labeled glycogen mobilization during ischemia in GIK-treated hearts was one third the rate observed in control hearts [3].
• In brain-dead pigs given saline, liver glycogen decreased from 45 +/- 11 mmol/g DNA (mean +/- SEM) to 7 +/- 3 mmol/ g DNA after 6 hours [4].
• A novel domain in AMP-activated protein kinase causes glycogen storage bodies similar to those seen in hereditary cardiac arrhythmias [5].

Psychiatry related information on LOC449474

• Metabolic changes such as the lack of complete metabolic pathways for the synthesis of numerous compounds (e.g., glycogen, biotin, NAD, and choline) are consistent with adaptation of brucellae to an intracellular life-style [6].
• Agonistic behavior, neuroendocrine and plasma metabolite changes, and muscle glycogen content were studied in 16 fed and 16 24 h-fasted domestic Large White pigs (100 +/- 5 kg) submitted to dyadic encounters (30 min) in a novel environment [7].
• The present results provide indirect evidences suggesting a major influence of fighting-induced physical activity on muscle glycogen depletion in response to aggressive interactions in pigs [8].

High impact information on LOC449474

• A high proportion of purebred Hampshire pigs carries the dominant RN- mutation, which causes high glycogen content in skeletal muscle [1].
• Although tissue depolarization with high K+ resulted in a substantial reduction of endogenous glycogen, exogenous glucose remained the sole precursor of aerobic lactate production [9].
• Once free within the polymorphonuclear leukocyte cytoplasm, the rickettsiae were preferentially localized in the glycogen-packed areas which are devoid of lysosomes and other cytoplasmic organelles [10].
• Ultrastructural changes consisted of a partial loss of myofibrils and an increase in mitochondria and glycogen deposition [11].
• Myocardial ATP and creatine phosphate concentrations were identical in both groups, although glycogen was lower in the ischemic hearts [12].

Chemical compound and disease context of LOC449474

• Effects of brain death and glucose infusion on hepatic glycogen and blood hormones in the pig [4].
• Hepatic glycogen content, arterial gluconeogenic precursor concentrations as well as the glycaemic response (delta 0.60 mmol/l) to alanine infusion (23 mumol x kg body weight-1.min-1) were all unaffected by hyperthyroidism [13].
• During ischemia, PSP decreased to 23.3 +/- 2.7 mm Hg, EDP increased to 12.3 +/- 0.7 mm Hg, myocardial glycogen decreased to 181.5 +/- 30.3 mumol/gdry, and lactate (approximately 154 mumol/gwet) and glycerol (approximately 930 nmol/gwet) were released [14].
• This study examines myocardial purine nucleotides, glycogen (MG), lactate, creatine phosphate (CP) and the subsequent tolerance to ischemia in hearts exposed to varying levels of hypoxia (2 h) [15].
• When compared to responses in oxygenated hearts, hypoxia reduced the isoproterenol-produced increase in myocardial cyclic AMP content, cyclic AMP-dependent protein kinase activity and contractility but enhanced the increase in glycogen phosphorylase alpha formation [16].

Biological context of LOC449474

• In this work, the role of glycogen phosphorylase in this unusual functional compartmentalization of of vascular energy metabolism was investigated [17].
• Hippocampal glycogen and glucose concentrations promptly decreased during repeated glucose deprivation, indicating that glycogenolysis does not fuel synaptic adaptation to repeated hypoglycemia [18].
• Results on the pH activity profiles and the requirements of Ca2+ for phosphorylation suggest that this phosphoprotein may correspond to glycogen phosphorylase [19].
• We recently reported the partial purification of a cAMP-independent and Ca2+-calmodulin-independent glycogen synthase kinase from porcine renal cortex (Schlender, K. K., Beebe, S. J., and Reimann, E. M. (1981) Cold Spring Harbor Conf. Cell Proliferation, 389-400) [20].
• A dominant missense mutation (R225Q) in pig PRKAG3, encoding the muscle-specific gamma3 isoform, causes a marked increase in glycogen content [21].

Anatomical context of LOC449474

• Transmural biopsies from the anterior myocardium were taken for the measurement of ATP, creatine phosphate, and glycogen [22].
• The role of cyclic adenosine 3', 5'-monophosphate and calcium in the regulation of contractility and glycogen phosphorylase activity in guinea pig papillary muscle [23].
• Glycogen content, 7 days after reperfusion, was higher in the treatment group than in the controls: 70.25 per cent vs. 21.66 per cent positive hepatocytes (score 3 vs. score 1) [24].
• In all species of experimental animal, intracytoplasmic aggregations of granular material, believed to be glycogen, were seen frequently in macrophages and PMN which had phagocytosed L. pneumophila [25].
• The volume fraction of glycogen in type II cells was 51% for hypophysectomized fetuses and 12% for control fetuses, while lamellar body volume fraction was 8% in hypophysectomized fetuses and 23% in control fetuses [26].

Associations of LOC449474 with chemical compounds

• Intracellular metabolites, primarily glycogen and glutamate, were labeled with 13C by addition of [1-13C]glucose to the perfusate during a normoxic, preischemic period [3].
• Both the I (independent of glucose 6-phosphate) and D (dependent on glucose 6-phosphate) forms of glycogen synthase (UDP-glucose:glycogen alpha-4-glucosyltransferase EG 2.4.1.11) have been partially purified from pig brain and the kinetic constants of the enzymes have been examined [27].
• Glycogen synthase I was converted to glycogen synthase D by the cyclic AMP-dependent protein kinase [28].
• A parallelism was observed between the total amount of glycogen in the sensitized lung and the total amount of histamine released from the lung by antigen-antibody reactions [29].
• 1. During conversion of [6-3H,U-14C]glucose to glycogen in liver, loss of 6-3H can occur either by cycling via pyruvate (between glycolysis and gluconeogenesis) or by other mechanisms [30].

Other interactions of LOC449474

• Marker polymorphisms in the porcine genes for muscle glycogen synthase (GYS1) and muscle glycogen phosphorylase (PYGM) [31].
• Phosphatidylinositol (PI) 3-kinase plays an important role in various insulin-stimulated biological responses including glucose transport, glycogen synthesis, and protein synthesis [32].
• Crude porcine pancreatic alpha-amylase was purified using a glycogen precipitation method [33].

Analytical, diagnostic and therapeutic context of LOC449474

• During intravenous infusion of D-[1-13C]glucose and insulin, the time course of myocardial glycogen synthesis was followed serially for up to 4 hr [2].
• Tissue glycogen levels were slow to recover in early reflow and at end reperfusion were still significantly depressed from aerobic levels [34].
• Concentrations of glycogen and creatine phosphate did not differ from the control group; ATP was 76% of controls [35].
• The purified glycogen synthase was substantially similar to rabbit skeletal muscle enzyme with respect to Mr (gel electrophoresis and gel filtration), pH dependence, aggregation properties, temperature dependence, and kinetic constants for substrates and activators [28].
• Effect of intraportal glucose infusion on hepatic glycogen content and degradation, and outcome of liver transplantation [36].

References