Regulation of Hepatic Insulin-Like Growth Factor-Binding Protein-1 Gene Expression by Insulin: Central Role for Mammalian Target of Rapamycin Independent of Forkhead Box O Proteins

Mounier, Cathérine; Dumas, Víctor; Posner, Barry I.

doi:10.1210/en.2005-0902

Cited by 24 publications

(14 citation statements)

References 67 publications

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“…7). Recent reports suggest that in hepatocytes, the inhibition of PI3K activity by both specific inhibitors (Wortmannin and LY294002) abrogated FOXO1/3 phosphorylation by insulin (Mounier et al 2006). Moreover, insulin modulates many aspects of the inflammatory network (Dandona et al 2002).…”

Section: Discussionmentioning

confidence: 99%

The activation of NF-κB through Akt-induced FOXO1 phosphorylation during aging and its modulation by calorie restriction

Kim

et al. 2007

Biogerontology

102

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Insulin-induced PI3K/Akt activation is known to inhibit a family of Forkhead transcription factors (FOXO), which can lead to increased oxidative stress in several model organisms. One of major transcription factors activated by oxidative stress and responsible for the production of many proinflammatory cytokines is NF-kappaB. In the present study, We were carried out to determine the relationship between FOXO1 and NF-kappaB activation using HEK293T cells and aged kidney isolated from ad libitum fed (AL) and 40% calorie restriction (CR) rats. Results showed that phosphorylation of FOXO1 and NF-kappaB activation were significantly increased in old rats. Moreover, FOXO1 phosphorylation and NF-kappaB activation were shown to be significantly lower in the CR rats compared with 24-month-old AL rats. To further explore the molecular link between FOXO and NF-kappaB, we performed transfection experiments with FOXO-mutant plasmid in cultured HEK293T cells. Treatment of the cell with insulin led to NF-kappaB activation through the phosphorylation of FOXO via the PI3K/Akt pathway. These results indicate that insulin promoted NF-kappaB activation through phosphorylation of FOXO1 by upregulating PI3K/Akt signaling. We conclude that the phosphorylation of FOXO1 regulates NF-kappaB nuclear translocation by activating PI3K/Akt during aging, which was suppressed by the hypoinsulinemic action of CR.

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Section: Discussionmentioning

confidence: 99%

The activation of NF-κB through Akt-induced FOXO1 phosphorylation during aging and its modulation by calorie restriction

Kim

et al. 2007

Biogerontology

102

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“…However, in these studies, the effects on IGFBP1 expression were observed in the context of overexpressed FoxO1. Under more physiological conditions, insulin may not act through FoxO1, but rather through mammalian target of rapamycin, to regulate IGFBP1 expression (Mounier et al, 2006).…”

Section: Insulin Sensitivitymentioning

confidence: 99%

The role of FoxO in the regulation of metabolism

2008

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“…Alterations in the exposure to growth factors, hormones, or mitogens (Carriere et al , 2008; Mounier et al , 2006; Shang et al , 2012) as well as changes in cellular metabolism (Gwinn et al , 2008) can influence the expression and activity of mTOR through its multiple domains. mTOR is ubiquitously expressed in most cells and tissues.…”

Section: Molecular Domains and Cellular Expression Of Mtormentioning

confidence: 99%

Shedding new light on neurodegenerative diseases through the mammalian target of rapamycin

Chong¹,

Shang

Wang

et al. 2012

Progress in Neurobiology

105

118

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Neurodegenerative disorders affect a significant portion of the world's population leading to either disability or death for almost 30 million individuals worldwide. One novel therapeutic target that may offer promise for multiple disease entities that involve Alzheimer's disease, Parkinson's disease, epilepsy, trauma, stroke, and tumors of the nervous system is the mammalian target of rapamycin (mTOR). mTOR signaling is dependent upon the mTORC1 and mTORC2 complexes that are composed of mTOR and several regulatory proteins including the tuberous sclerosis complex (TSC1, hamartin/ TSC2, tuberin). Through a number of integrated cell signaling pathways that involve those of mTORC1 and mTORC2 as well as more novel signaling tied to cytokines, Wnt, and forkhead, mTOR can foster stem cellular proliferation, tissue repair and longevity, and synaptic growth by modulating mechanisms that foster both apoptosis and autophagy. Yet, mTOR through its proliferative capacity may sometimes be detrimental to central nervous system recovery and even promote tumorigenesis. Further knowledge of mTOR and the critical pathways governed by this serine/threonine protein kinase can bring new light for neurodegeneration and other related diseases that currently require new and robust treatments.

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Regulation of Hepatic Insulin-Like Growth Factor-Binding Protein-1 Gene Expression by Insulin: Central Role for Mammalian Target of Rapamycin Independent of Forkhead Box O Proteins

Cited by 24 publications

References 67 publications

The activation of NF-κB through Akt-induced FOXO1 phosphorylation during aging and its modulation by calorie restriction

The activation of NF-κB through Akt-induced FOXO1 phosphorylation during aging and its modulation by calorie restriction

The role of FoxO in the regulation of metabolism

Shedding new light on neurodegenerative diseases through the mammalian target of rapamycin

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