Please use this identifier to cite or link to this item: http://repositorio.ufla.br/jspui/handle/1/45957
Title: Hypothalamic AMPK activation blocks lipopolysaccharide inhibition of glucose production in mice liver
Keywords: Lipopolysaccharide
Glucose production
Hypothalamus
Glucose homeostasis
Lipopolissacarídeo
Produção de glicose
Hipotálamo
Homeostase da glicose
Issue Date: 5-Dec-2013
Publisher: Elsevier
Citation: SANTOS, G. A. et al. Hypothalamic AMPK activation blocks lipopolysaccharide inhibition of glucose production in mice liver. Molecular and Cellular Endocrinology, [S. l.], v. 381, n. 1-2, p. 88-96, 5 Dec. 2013.
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.
URI: https://www.sciencedirect.com/science/article/pii/S0303720713003122?via%3Dihub#!
http://repositorio.ufla.br/jspui/handle/1/45957
Appears in Collections:DME - Artigos publicados em periódicos

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