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Another proposed mechanism involves competing interactions at growth factor receptor sites

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Such phosphorylation leads to the blockade of the tyrosine residues in IRSs, to which the insulin and IGF-1 receptors phosphorylate to activate IRSs and consequently commence the signalling cascade [185, 192], as comprehensively discussed above

Investigations commonly evaluate how peptide fragments derived from human growth hormone interact with metabolic pathways involved in energy regulation

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