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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

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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

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