Ptgs2 activation by endotoxin mediates the decrease in Igf1, but not in Igfbp3, gene expression in the liver

Martín, Ana Isabel Morales; López-Menduiña, María; Castillero, Estíbaliz; Granado, Miriam; Villanúa, María de los Ángeles; López-Calderón, Asunción

doi:10.1677/joe-08-0205

Cited by 5 publications

(3 citation statements)

References 54 publications

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“…D-Trp(8)-γMSH treatment was able to prevent the effects of LPS on IGF-I levels, whereas it was unable to modify the IGFBP-3 response to LPS injections. The effect of LPS on IGF-I seems to be due, among other mechanisms, to a direct inhibitory action on liver cells [ 43 ], through the induction of COX-2 and iNOS [ 44 , 45 ]. Taking into account that D-Trp(8)-γMSH had an anti-inflammatory effect in the liver, it is not surprising that it prevents the effects of LPS on serum and liver IGF-I levels.…”

Section: Discussionmentioning

confidence: 99%

D-TRP(8)-γMSH Prevents the Effects of Endotoxin in Rat Skeletal Muscle Cells through TNFα/NF-KB Signalling Pathway

et al. 2016

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Sepsis induces anorexia and muscle wasting secondary to an increase in muscle proteolysis. Melanocyte stimulating hormones (MSH) is a family of peptides that have potent anti-inflammatory effects. Melanocortin receptor-3 (MC3-R) has been reported as the predominant anti-inflammatory receptor for melanocortins. The aim of this work was to analyse whether activation of MC3-R, by administration of its agonist D-Trp(8)-γMSH, is able to modify the response of skeletal muscle to inflammation induced by lipopolysaccharide endotoxin (LPS) or TNFα. Adult male rats were injected with 250 μg/kg LPS and/or 500 μg/kg D-Trp(8)-γMSH 17:00 h and at 8:00 h the following day, and euthanized 4 hours afterwards. D-Trp(8)-γMSH decreased LPS-induced anorexia and prevented the stimulatory effect of LPS on hypothalamic IL-1β, COX-2 and CRH as well as on serum ACTH and corticosterone. Serum IGF-I and its expression in liver and gastrocnemius were decreased in rats injected with LPS, but not in those that also received D-Trp(8)-γMSH. However, D-Trp(8)-γMSH was unable to modify the effect of LPS on IGFBP-3. In the gastrocnemius D-Trp(8)-γMSH blocked LPS-induced decrease in pAkt, pmTOR, MHC I and MCH II, as well as the increase in pNF-κB(p65), FoxO1, FoxO3, LC3b, Bnip-3, Gabarap1, atrogin-1, MuRF1 and in LC3a/b lipidation. In L6 myotube cultures, D-Trp(8)-γMSH was able to prevent TNFα-induced increase of NF-κB(p65) phosphorylation and decrease of Akt phosphorylation as well as of IGF-I and MHC I expression. These data suggest that MC3-R activation prevents the effect of endotoxin on skeletal wasting by modifying inflammation, corticosterone and IGF-I responses and also by directly acting on muscle cells through the TNFα/NF-κB(p65) pathway.

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Section: Discussionmentioning

confidence: 99%

D-TRP(8)-γMSH Prevents the Effects of Endotoxin in Rat Skeletal Muscle Cells through TNFα/NF-KB Signalling Pathway

et al. 2016

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“…The effects of α MSH treatment on serum levels of IGF-I and IGFBP3 in rats injected with LPS were different, since α MSH was not able to modify the inhibitory effect of LPS on IGF-I, whereas it prevented the LPS-induced decrease in serum IGFBP3 and its expression in the liver. The different responses of both proteins to α MSH treatment may be due to the fact that they are regulated differently [38–40]. In addition, they are produced by different liver cells, whereas IGF-I is mainly produced in hepatocytes, IGFBP3 expression is only found in nonparenchymal cells [38, 41].…”

Section: Discussionmentioning

confidence: 99%

αMSH Blunts Endotoxin-Induced MuRF1 and Atrogin-1 Upregulation in Skeletal Muscle by Modulating NF-κB and Akt/FoxO1 Pathway

Martín

Gómez-SanMiguel

Gómez-Moreira

et al. 2014

Mediators of Inflammation

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Alpha melanocyte stimulating hormone (αMSH) has been shown to have anti-inflammatory and anticachectic actions. We hypothesized that αMSH administration could attenuate the effect of lipopolysaccharide (LPS) on the skeletal muscle through modifications in IGF-Akt-FoxO1 pathway, or/and in serum corticosterone. Adult male Wistar rats were injected with LPS and/or αMSH. αMSH administration reduced LPS-induced increase in liver TNFα and serum nitrites as well as NF-κB activation in skeletal muscle. In contrast, αMSH was not able to prevent the stimulatory effect of LPS on serum concentration of ACTH and corticosterone. LPS decreased serum levels of IGF-I and IGFBP3 and their expression in the liver (P < 0.01). However IGFBP3 expression in the gastrocnemius was increased by LPS. Treatment with αMSH prevented the effects of LPS on IGFBP3 but not on IGF-I. In the gastrocnemius αMSH blocked LPS-induced decrease in pAkt as well as the increase in pNF-κB(p65), FoxO1, atrogin-1, and MuRF1 levels. These results suggest that αMSH blunts skeletal muscle response to endotoxin by downregulating atrogenes and FoxO1 at least in part by controlling NF-κB activation and Akt signalling, but not through modifications in the secretion of corticosterone or IGF-I.

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“…TNF-α suppresses GH receptor (GHR) expression by reduction of transactivators Sp1/Sp3 binding to a GHR promotor (Denson et al, 2001), IL-6 up-regulates strong inhibitor of GH intracellular signal transduction, SOCS-3 (Wang et al, 2002a;Denson et al, 2003). Other mechanisms of LPS-dependent GH resistance are: decrease in IGF-1 concentration caused by liver cyclooxyganase-2 activation (Briard et al, 2000;Wang et al, 2002b;Martín et al, 2008), direct suppression of GHR expression by MyD88-dependent and -independent TLR4 signaling pathways (Dejkhamron et al, 2007) and promotion of proteolytic GHR cleavage (Wang et al, 2008). Moreover, the ability of GH to promote phosphorylation of signal transducer and activator of transcription (STAT) in the liver is reduced during sepsis (Hong-Brown et al, 2003).…”

Section: Growth Hormonementioning

confidence: 99%

Microbiome impact on metabolism and function of sex, thyroid, growth and parathyroid hormones.

2015

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Commensal bacteria and their genes associated with host are known as microbiome. In recent years, microbial influence on host endocrine system has been under detailed investigation. The role of microbiome in the pathogenesis of insulin resistance and obesity, the function of hypothalamic-pituitary-adrenal axis and secretion of hormones regulating appetite is well described in world literature. In this article we discuss poorly reviewed issues: the microbiome role in modulation of non-peptide (sex and thyroid) and peptide (growth hormone and parathyroid hormone) functions. Understanding complex bidirectional relations between host endocrine system and bacteria is of fundamental importance to understanding microbial impact on host reproduction, risk of endocrine-related cancers, pathogenesis of non-thyroidal illness syndrome, growth failure in children and hormonal changes during chronic kidney disease. This article also highlights effects of dietary compounds on microbiome composition and bacterial enzymes activity, and thus host hormonal status.

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Ptgs2 activation by endotoxin mediates the decrease in Igf1, but not in Igfbp3, gene expression in the liver

Cited by 5 publications

References 54 publications

D-TRP(8)-γMSH Prevents the Effects of Endotoxin in Rat Skeletal Muscle Cells through TNFα/NF-KB Signalling Pathway

D-TRP(8)-γMSH Prevents the Effects of Endotoxin in Rat Skeletal Muscle Cells through TNFα/NF-KB Signalling Pathway

αMSH Blunts Endotoxin-Induced MuRF1 and Atrogin-1 Upregulation in Skeletal Muscle by Modulating NF-κB and Akt/FoxO1 Pathway

Microbiome impact on metabolism and function of sex, thyroid, growth and parathyroid hormones.

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