Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/89456
Type: Artigo de periódico
Title: Hypothalamic Ampk Activation Blocks Lipopolysaccharide Inhibition Of Glucose Production In Mice Liver
Author: Santos G.A.
Moura R.F.
Vitorino D.C.
Roman E.A.F.R.
Torsoni A.S.
Velloso L.A.
Torsoni M.A.
Abstract: Endotoxic hypoglycaemia has an important role in the survival rates of septic patients. Previous studies have demonstrated that hypothalamic AMP-activated protein kinase (hyp-AMPK) activity is sufficient to modulate glucose homeostasis. However, the role of hyp-AMPK in hypoglycaemia associated with endotoxemia is unknown. The aims of this study were to examine hyp-AMPK dephosphorylation in lipopolysaccharide (LPS)-treated mice and to determine whether pharmacological hyp-AMPK activation could reduce the effects of endotoxemia on blood glucose levels. LPS-treated mice showed reduced food intake, diminished basal glycemia, increased serum TNF-α and IL-1β levels and increased hypothalamic p-TAK and TLR4/MyD88 association. These effects were accompanied by hyp-AMPK/ACC dephosphorylation. LPS-treated mice also showed diminished liver expression of PEPCK/G6Pase, reduction in p-FOXO1, p-AMPK, p-STAT3 and p-JNK level and glucose production. Pharmacological hyp-AMPK activation blocked the effects of LPS on the hyp-AMPK phosphorylation, liver PEPCK expression and glucose production. Furthermore, the effects of LPS were TLR4-dependent because hyp-AMPK phosphorylation, liver PEPCK expression and fasting glycemia were not affected in TLR4-mutant mice. These results suggest that hyp-AMPK activity may be an important pharmacological target to control glucose homeostasis during endotoxemia. © 2013 Elsevier Ireland Ltd.
Editor: 
Rights: fechado
Identifier DOI: 10.1016/j.mce.2013.07.018
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-84882737443&partnerID=40&md5=5447e6a6cb4d15a78af2bc70a81208be
Date Issue: 2013
Appears in Collections:Unicamp - Artigos e Outros Documentos

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