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If the abovementioned is occurring, it could mean that IGF-1 administration could also lower glucose levels by suppressing hepatic gluconeogenesis, as well as improving insulin signalling in this organ, leading to IGFBP-1 suppression and overall improvement of the IGF-1/GH/insulin axis

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Briefly, these studies revealed that DSePA treatment (at concentrations which are non-toxic for normal cells) inhibited the growth of lung cancer cells by causing reductive stress (marked by the increase in the levels of GSH and GPx) followed by mitochondrial and endoplasmic reticulum-dependent apoptosis [92]