The proportion of aged individuals in the general population is increasing, and non-communicable diseases like obesity are major contributors to mortality in older individuals. The WNIN/Ob obese rat exhibits a significantly reduced average lifespan of 15 months. Exploring molecular and biochemical characteristics of these rats can establish them as appropriate model for studying the neurobiology of aging and obesity.We investigated the growth characteristics and lifespan of WNIN/Obobese rats, examined neuronal-glial changes, levels of oxidative stress, antioxidant enzyme activity, and DNA damage in various brain regions.Our findings revealed a significant decrease in brain weights and a 60% reduction in total lifespan in WNIN/Ob obese rats. We observed neuronal-glial changes resembling those seen in the aging brain. Moreover, young WNIN/Ob rats exhibited significantly higher levels of oxidative stress and DNA damage in brain, comparable to 15-month-old normal rats. Additionally, antioxidant enzyme activity was significantly lower in WNIN/Ob rats.The onset of degenerative features such as increased oxidative stress, astrogliosis, DNA damage, and decreased antioxidant levels in different brain regions of WNIN/Ob obese rats at a much younger age may contribute to the reduced longevity observed in this animal model, which holds promise for studying the intricate connection between obesity and aging.Our study sheds light on the altered brain metabolism and oxidative stress as potential underlying causes of metabolic syndrome and premature aging in WNIN/Ob rat model. It provides insights into interplay between obesity-aging, and associated disorders.This model may aid in the development of therapeutic strategies to mitigate obesity impact on aging-related health outcomes.