Endotoxemia can be caused by obesity, environmental chemical exposure, abiotic stressors, and bacterial infection. Circumstances that deleteriously impact intestinal barrier integrity can induce endotoxemia and controlled experiments have identified negative impacts of lipopolysaccharide (LPS; an endotoxin mimetic) on folliculogenesis, puberty onset, estrus behavior, ovulation, meiotic competence, luteal function and ovarian steroidogenesis. In addition, neonatal LPS exposures have transgenerational female reproductive impacts, raising concern about early life contacts to this endogenous reproductive toxicant. Aims of this review are to identify physiological stressors causing endotoxemia, to highlight potential mechanism(s) by which LPS compromises female reproduction, and identify knowledge gaps regarding how acute and/or metabolic endotoxemia influence(s) female reproduction.