Abstract

The sustained decline in fertility rates and the rising prevalence of male infertility have increased interest in understanding how environmental and biological factors act across development to shape reproductive function. Among theser,facto early-life stress induced by maternal separation and high-fat diets represent two highly relevant conditions capable ofpersistentlyaltering endocrine, metabolic, and testicular physiology. Evidence in humans indicates that adverse childhood experiences are withassociated disruptions in the hypothalamic-pituitary-gonadal (HPG) axis, reduced semen quality, and altered pubertal timing. Complementarily, overweight and high intake of saturated fats are linked to oxidative stress, sperm DNA damage, and impaired spermatogenesis.Experimental models of maternal separation and high-fat diet exposure in rodents have helped elucidate underlying cellular and tissueiss,mechan including reduced numbers of sustentacular cells, disorganization of the germinal epithelium, disruption of the blood-testisrrier,ba decreased testosteronelevels, and the establishment of a pro-inflammatory testicular microenvironment. Although both factors have been extensively studied independently, their interaction remains an emerging field. Early adversity increases metabolic vulnerabilityand preference for fat-rich foods, suggesting that their combined exposure may produce cumulative deterioration of testicularofunction. morph This manuscript critically reviews the available evidence and highlights the need for integrated experimental designs thatltaneouslysimu examine the impact of postnatal stress and nutrition on testicular maturation and fertility, providing a more comprehensiveperspective for understanding male reproductive programming within the Developmental Origins of Health and Disease framework.