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Sato, F., et al

Together they produce a stronger, more sustained GH release than either compound alone, without the cortisol and prolactin spikes associated with older compounds like GHRP-2 or GHRP-6

It was later observed that mTORC1 was still inhibited by AICAR and the mitochondrial complex I inhibitor phenformin in TSC2 -null MEF cells, leading to the hypothesis that AMPK utilises alternate mechanisms to combat mTORC1 signal transduction during metabolic duress [25]