Hypothalamic AMPK activation blocks lipopolysaccharide inhibition of glucose production in mice liver

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MetadadosDescriçãoIdioma
Autor(es): dc.creatorSantos, G. A.-
Autor(es): dc.creatorMoura, R. F.-
Autor(es): dc.creatorVitorino, D. C.-
Autor(es): dc.creatorRoman, E. A. F. R.-
Autor(es): dc.creatorTorsoni, A. S.-
Autor(es): dc.creatorVelloso, L. A.-
Autor(es): dc.creatorTorsoni, M. A.-
Data de aceite: dc.date.accessioned2026-02-09T12:45:27Z-
Data de disponibilização: dc.date.available2026-02-09T12:45:27Z-
Data de envio: dc.date.issued2021-01-03-
Data de envio: dc.date.issued2021-01-03-
Data de envio: dc.date.issued2013-12-05-
Fonte completa do material: dc.identifierhttps://repositorio.ufla.br/handle/1/45957-
Fonte completa do material: dc.identifierhttps://www.sciencedirect.com/science/article/pii/S0303720713003122?via%3Dihub#!-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/capes/1167670-
Descrição: dc.descriptionEndotoxic 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.-
Idioma: dc.languageen-
Publicador: dc.publisherElsevier-
Direitos: dc.rightsrestrictAccess-
???dc.source???: dc.sourceMolecular and Cellular Endocrinology-
Palavras-chave: dc.subjectLipopolysaccharide-
Palavras-chave: dc.subjectGlucose production-
Palavras-chave: dc.subjectHypothalamus-
Palavras-chave: dc.subjectGlucose homeostasis-
Palavras-chave: dc.subjectLipopolissacarídeo-
Palavras-chave: dc.subjectProdução de glicose-
Palavras-chave: dc.subjectHipotálamo-
Palavras-chave: dc.subjectHomeostase da glicose-
Título: dc.titleHypothalamic AMPK activation blocks lipopolysaccharide inhibition of glucose production in mice liver-
Tipo de arquivo: dc.typeArtigo-
Aparece nas coleções:Repositório Institucional da Universidade Federal de Lavras (RIUFLA)

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