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Studies in Crat knockout mice demonstrated that CrAT deficiency leads to abnormal fuel selection, which results in a perturbation of glucose homeostasis and suggest that deficits in CrAT activity might contribute to diet-induced metabolic inflexibility by exacerbating the Randle glucose-fatty acid cycle 66

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Consistent with the in vitro findings, GHK-Cu increased antioxidant enzymes and decreased pro-inflammatory cytokines in vivo

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Metabolic rebound after GLP-1 receptor agonist discontinuation