Improved insulin sensitivity by rapamycin is associated with reduction of mTOR and S6K1 activities in L6 myotubes

“…Another important set of findings was that the activation of AMPK down-regulated the mTORC1 activity and attenuated the UPR in vivo, and administration of the mTORC1-specific inhibitor rapamycin suppressed the high glucose-induced ER stress response (Li et al, 2014b). On the contrary, Hwang et al (2012) found that the inhibition of mTOR by rapamycin had no effect on the ER-stress markers in L6 myotubes. These observations suggest that the mTOR signal pathway does not always have relationships with the ER stress.…”

Section: Discussionmentioning

confidence: 99%

PI3K-Akt-mTOR signal inhibition affects expression of genes related to endoplasmic reticulum stress

et al. 2016

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ABSTRACT. PI3K-Akt-mTOR signaling pathway is associated with endoplasmic reticulum (ER) stress. However, it is not clear how this signaling pathway affects the ER stress. The present study aimed to determine whether the PI3K-Akt-mTOR signaling pathway regulates tunicamycin (TM)-induced increases in mRNA levels of genes involved in the ER stress, to help elucidate the mechanism by which this pathway affects the ER stress in primary goose hepatocytes. Primary hepatocytes were isolated from geese and cultured in vitro. After 12 h in a serumfree medium, the hepatocytes were incubated for 24 h in a medium with either no addition (control) or with supplementation of TM or TM together with PI3K-Akt-mTOR signaling pathway inhibitors (LY294002, rapamycin, NVP-BEZ235). Thereafter, the expression levels of genes involved in the ER stress (BIP, EIF2a, ATF6, and XBP1) were assessed. The results indicated that the mRNA level of BIP 2 Q. Song et al. Genetics and Molecular Research 15 (3): gmr.15037868 was up-regulated in 0.2, 2, and 20 µM TM treatment group (P < 0.05), whereas the mRNA levels of EIF2a, ATF6, and XBP1 were up-regulated in the 2 µM TM treatment group (P < 0.05). However, the TM mediated induction of mRNA levels of genes involved in the ER stress (BIP, EIF2a, ATF6, and XBP1) was down-regulated after the treatment with PI3K-Akt-mTOR pathway inhibitors (LY294002, NVP-BEZ235, and rapamycin). Therefore, our results strongly suggest that the PI3K-AktmTOR signaling pathway might be involved in the down-regulation of the TM-induced ER stress in primary goose hepatocytes.

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“…Eckert et al(2007) demonstrated that at least two pathways are required for glucose signaling inHL1C hepatomas, one of which is dependent on a non-Pl3-kinase intermediary, which is inhibited by LY294002 and LY303511. Another work suggested that treatment of L6 myotubes with 100nM insulin can increase Akt and mTOR phosphorylation (Hwang et al, 2012). Saltiel & Kahn (2001) showed that glucose metabolism can be regulated by insulin through the PI3K signal transduction cascade.…”

Section: Discussionmentioning

confidence: 99%

Insulin Promotes the Expression of the Gluconeogenic Rate-Limiting Enzymes Phosphoenolpyruvate Carboxykinase (Pepck) and Glucose 6-Phosphatase (G6pase) through PI3k/Akt/mTOR Signaling Pathway in Goose Hepatocytes

Xiong

Song

Han

et al. 2016

Rev. Bras. Cienc. Avic.

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Improved insulin sensitivity by rapamycin is associated with reduction of mTOR and S6K1 activities in L6 myotubes

Cited by 23 publications

References 30 publications

Circulating mesencephalic astrocyte-derived neurotrophic factor is increased in newly diagnosed prediabetic and diabetic patients, and is associated with insulin resistance

Circulating mesencephalic astrocyte-derived neurotrophic factor is increased in newly diagnosed prediabetic and diabetic patients, and is associated with insulin resistance

PI3K-Akt-mTOR signal inhibition affects expression of genes related to endoplasmic reticulum stress

Insulin Promotes the Expression of the Gluconeogenic Rate-Limiting Enzymes Phosphoenolpyruvate Carboxykinase (Pepck) and Glucose 6-Phosphatase (G6pase) through PI3k/Akt/mTOR Signaling Pathway in Goose Hepatocytes

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