Lactitol Reduces Renal Dysfunction and a Senescence Marker in Aged Mice with Adenine-Induced CKD

Abstract

Senescent cells, which accumulate with age and contribute to age-related diseases such as chronic kidney disease (CKD), have emerged as therapeutic targets. In this study, we investigated the effects of lactitol, a food-derived compound, in aged mice with adenine-induced CKD. We hypothesized that oral administration of lactitol would reduce senescence-associated cellular burden and improve renal function in aged mice with adenine-induced CKD. Oral administration of lactitol significantly reduced cecal and fecal pH, accompanied by marked decreases in renal expression of the stress-, senescence-, and fibrosis-related markers p21, Acta2, and Col1a1. Furthermore, serum levels of urea nitrogen and creatinine—key indicators of kidney dysfunction—were significantly improved in the lactitol-treated group. These findings suggest that lactitol intake may contribute to the suppression of CKD progression by modulating the intestinal environment and attenuating senescence- and fibrosis-associated responses. While senolytics are gaining attention as novel anti-aging therapies, our findings support the potential of food-based interventions as a safer and more accessible approach that may help reduce senescent cell burden in age-related disease contexts.