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Taking all this data together it seems logical or appropriate to conclude that, because IGF1-R has a different signalling pathway that can maintain lipid oxidation in the liver, FFA uptake in muscle, and activates mTORC1 could reactivate IR through tyrosine kinase activity on IRS, thus displacing serine phosphorylation, reinstituting insulin signalling

It can, mostly because of what it does for consistency

If you want a broader overview of its role in the body, What is Glutathione and Why It Matters for Our Health is a helpful next read

The peptides for menopause guide and hormone balance peptide research address these specific considerations in detail