Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glycogen Storage Disease Type I (GSD-I) is a metabolic disorder characterized by deficiency of glucose-6-phosphatase resulting in ineffective glycogen metabolism to glucose. These patients frequently have hyperlipidemia, among many other metabolic derangements. There is no consensus regarding the risk of developing atherosclerosis. We report an adult male with GSD-I who presented with cerebral infarction and a history of prior ischemic stroke and multiple coronary stent placements. We suggest that patients with GSD-I do have an increased risk of atherosclerosis and its complications and predict that these complications will be seen more frequently since patients with GSD-I are living longer as a result of better treatment.
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PMID:Ischemic stroke in an adult with glycogen storage disease type I. 2069 97

Hyperglycemia is common after acute stroke. In the acute phase of stroke (within 24h), rats with permanent cerebral ischemia developed higher fasting blood glucose and insulin levels in association with up-regulation of hepatic gluconeogenic gene expression, including phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, and fructose-1,6-bisphosphatase. In addition, hepatic gluconeogenesis-associated positive regulators, such as FoxO1, CAATT/enhancer-binding proteins (C/EBPs), and cAMP responsive element-binding protein (CREB), were up-regulated. For insulin signaling transduction, phosphorylation of insulin receptor (IR), insulin receptor substrate-1 (IRS1) at the tyrosine residue, Akt, and AMP-activated protein kinase (AMPK), were attenuated in the liver, while negative regulators of insulin action, including phosphorylation of p38, c-Jun N-terminal kinase (JNK), and insulin receptor substrate-1 (IRS1) at the serine residue, were increased. In addition, the brains of rats with stroke exhibited a reduction in phosphorylation of IRS1 at the tyrosine residue and Akt. Circulating cortisol, glucagon, C-reactive protein (CRP), monocyte chemoattractant protein 1 (MCP-1), and resistin levels were elevated, but adiponectin was reduced. Our data suggest that cerebral ischemic insults might modify intracellular and extracellular environments, favoring hepatic gluconeogenesis and the consequences of hyperglycemia.
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PMID:Hyperglycemia is associated with enhanced gluconeogenesis in a rat model of permanent cerebral ischemia. 2327 76