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This mechanism is critical because neurons have a limited ability to synthesize endogenous GS (Dringen and Arend, 2025)

This distinguishes it from full-length GH and means that at research-relevant concentrations, the fragment does not produce the insulin resistance, glucose dysregulation, or tissue proliferation associated with GHR-mediated GH signalling allowing isolated study of the GH lipolytic mechanism without these confounding effects

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