Impaired fertility during periods of heat stress is the culmination of several physiological responses to heat stress, ranging from reduced estrus expression and altered follicular function to early embryonic death. Furthermore, heat-stressed dairy cattle exhibit a unique metabolic status that likely contributes to the observed reduction in fertility. An understanding of this unique metabolic status can be used as a basis for improving cow management and feeding strategies, thereby reducing the negative effects of heat stress on reproduction. One potential opportunity for improved management during heat stress requires investigation of altered insulin and glucose dynamics and their effects on fertility. During heat stress, adipose responsiveness to an adrenergic stimulus is blunted, indicating that cows experiencing a thermal load reprioritize fuel selection in favor of glucose. Thus, heat-stressed dairy cattle have higher circulating concentrations of insulin while circulating glucose is lower (compared with pair-fed counterparts). Despite some reported positive effects on aspects of reproductive performance, insulin damages oocyte quality, even in the absence of heat stress. Altered mitochondrial function, organelle distribution and cytoskeletal components have been described in oocytes exposed to elevated insulin and purportedly induce metabolic stress at the molecular level. These changes are particularly concerning because if fertilization does occur, the resulting embryo is reliant on the organelles and cytoplasmic machinery contributed by the oocyte. For these reasons, it is likely that insulin-mediated damage to oocyte quality is manifested in both the immediate reduction in fertility and the characteristic delay in return to full fertility following a heat-stress event. Previous studies indicate that dietary interventions could alleviate insulin-mediated damage to the oocyte, thereby improving the fertility of dairy cattle during and after a heat stress event.