ArticleBioMed research international2014
Role of AMPK α in skeletal muscle glycometabolism regulation and adaptation in relation to sepsis.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- The expression of Eps15 homology domain 1 is negatively correlated with disease-free survival and overall survival of osteosarcoma patients.Journal of orthopaedic surgery and research · 2019Article
- Per-Arnt-Sim Kinase (PASK): An Emerging Regulator of Mammalian Glucose and Lipid Metabolism.Nutrients · 2015Review
- Increased Expression of Eps15 Homology Domain 1 is Associated with Poor Prognosis in Resected Small Cell Lung Cancer.Journal of Cancer · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
backgroundAMP-activated protein kinase (AMPK) and the translocation of glucose transporter 4 (GLUT4) protein always involve disturbance of carbohydrate metabolism.
objectiveTo determine whether the change of blood glucose in the early stage of septic rat is associated with the alteration of AMPKα protein expression and GLUT4 protein translocation expression.
methodsAnimal models of sepsis were induced by tail vein injection of LPS in Wistar rats. The dynamic values of blood glucose within 2 hours after injection of LPS were observed. AMPKα protein and GLUT4 protein translocation in different tissues (such as soleus muscle and extensor digitorum longus) were assessed by western blot.
resultsBlood glucose levels appeared to rise at 0.5 h after injection of LPS, arrived the peak value at 1 h, then fell at 1.5 h and 2 h Animals in LPS group experienced the increase of phos-AMPKα protein and GLUT4 protein translocation expression in soleus muscle and extensor digitorum longus.
conclusionThe dynamic change of blood glucose, represented in a form of initiative increase and subsequent decrease in the early stage of sepsis, may be related to glycometabolism disorder in the skeletal muscle, coming down to enhancement of GLUT4 translocation expression promoted by activation of AMPKα.
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