As an essential trace element, copper (Cu) plays a critical role in numerous physiological processes associated with aging, and its involvement in the aging process has attracted increasing attention. In this study, we investigated the mechanisms underlying copper imbalance during aging. Analysis of blood copper concentrations in healthy individuals revealed an age-dependent increase in circulating copper levels. To further elucidate this phenomenon, we employed a mouse model to explore age-related changes in copper metabolism. Compared with young controls, aged mice exhibited elevated plasma copper concentrations and an enrichment of the lighter copper isotope (⁶³Cu). We propose that aged mice exhibit an abnormally high demand for copper intake, potentially due to deregulated nutrient sensing. This dysregulation may enhance the expression of copper reductases and transport proteins, thereby promoting excessive intestinal absorption of exogenous copper. Collectively, this study provides a copper-centric perspective on the connection between deregulated nutrient sensing and aging, thus shedding light on the aspect of aging and copper overexposure.
 

copper,,aging,stable isotopic analysis