Orexin A activates the PI3K/Akt/mTOR pathway in Hep3B cells. Orexin A increases GLUT1 protein and glucose uptake via PI3K/Akt/mTOR. Orexin A facilitates metabolic flux towards TCA cycle independent of PI3K/Akt/mTOR.
Book Title: Effects of Orexin A on Glucose Metabolism in Human Hepatocellular Carcinoma Invitro Via PI3K/Akt/mTOR-dependent and -independent Mechanism
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Published on 2016 by
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Book is About: Carcinoma
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Abstract: Orexins are hypothalamic neuropeptides that regulate food intake, energy homeostasis, reward system and sleep/wakefulness states. The purpose of this study was to investigate the effects of orexin A on glucose metabolism in human hepatocellular carcinoma cell line, Hep3B, and determine the possible mechanisms. Hep3B cells were incubated with different concentrations of orexin A (10 −9 –10 −7 M) invitro in the presence or absence of the orexin receptor 1 (OX1R) inhibitor (SB334867), Akt inhibitor (PF-04691502) and mammalian target of rapamycin (mTOR) inhibitor (temsirolimus). Subsequently, OX1R protein expression, glucose transporter 1 (GLUT1) expression, glucose uptake, the mRNA expression of lactate dehydrogenase (LDHA), pyruvate dehydrogenase kinase 1 (PDK1) and pyruvate dehydrogenase B (PDHB), lactate generation and mitochondrial pyruvate dehydrogenase (PDH) enzyme activity were measured. The activity of phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling was also determined. OX1R was expressed in hepatoma tissues and Hep3B cells. Stimulation of the Hep3B cells with orexin A resulted in a dose-dependent increase of GLUT1 expression and glucose uptake, which was associated with the activation of PI3K/Akt/mTOR pathway. Further, orexin A increased PDHB expression and PDH enzyme activity, decreased LDHA, PDK1 mRNA levels and lactate generation independent of PI3K/Akt/mTOR pathway. Our results demonstrated that orexin A directed the cellular metabolism towards mitochondrial glucose oxidation rather than glycolysis. These findings provide functional evidence of the metabolic actions of orexin A in hepatocellular carcinoma cells. Highlights: Orexin receptor 1 is expressed in human hepatocellular carcinoma tissues and cells. Orexin A activates the PI3K/Akt/mTOR pathway in Hep3B cells. Orexin A increases GLUT1 protein and glucose uptake via PI3K/Akt/mTOR. Orexin A facilitates metabolic flux towards TCA cycle independent of PI3K/Akt/mTOR.
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