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The pathophysiological mechanisms of MASLD, particularly in patients with comorbid T2DM, involve a cascade of metabolic-inflammatory-fibrotic vicious cycles driven by insulin resistance

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This effect was reportedly greater than the results observed when either GHK-Cu or HA was studied independently

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Moreover, hippocampal DA also regulates appetitive memory formation as evidenced by the finding that the D1R blockade prior to a cocaine-conditioning session in a conditioned place preference task impairs short and long-term memory formation [52]

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