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Thus, it is possible that the combination of low GH and normal IGF-I serves as a physiological mechanism aimed at preserving the GH/IGF-I anabolic effects and minimizing the insulin-antagonistic effects of GH without compromising the positive IGF-I metabolic effects

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Then, how do tumor cells sustain rapid proliferation when a large portion of glutamine is shunted toward GSH synthesis via GGCT-mediated regulation, consequently reducing glutamine flux into TCA cycle