Non-alcoholic fatty liver disease (NAFLD) and sarcopenia are common age-related chronic comorbidities that share many common pathophysiological factors. However, their underlying mechanisms have not been fully elucidated. In recent years, cuproptosis has been discovered as a new cell death mode, and the potential functional role of copper homeostasis in a variety of chronic diseases has become a research focus. Loss of copper in the liver is closely related to the occurrence of early NAFLD, and copper overload in skeletal muscles may promote the occurrence of sarcopenia through various signaling pathways. As indicated by ceruloplasmin levels in serum, extracellular copper overload may play a potential functional role in this process. This review discusses the possible mechanism of copper homeostasis imbalance and the onset of early NAFLD combined with sarcopenia from the perspective of copper metabolism, in order to provide molecular targets and theoretical basis for early clinical improvement or even reversal of these two metabolic diseases.