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This is similar as our previous results in DIRKO mice, which have both GIP and GLP-1 receptor gene deletion ( The reason why GIP receptor KO mice had glucose intolerance at higher glucose levels seems to be explained by the failure to further increase insulin levels

Additionally, the absence of cortisol elevation reduces glucocorticoid-driven catabolic interference, allowing structured evaluation of recovery-linked GH physiology while maintaining endocrine stability across experimental timelines

In reconstitution practices, this property aligns with the need for safety and efficiency

So just kind of like, yeah, the whole, Dr