: Insulin resistance (IR) is a state of decreased sensitivity or responsiveness of target tissues to metabolic actions of circulating insulin. IR can be selective, involving only certain aspects of insulin action, i.e. only its impact on hepatic glucose disposal. Plasma insulin concentration is a continuous variable, dependent upon several physiological stimuli, thus the thresholds used to diagnose IR are arbitrary. Insulin resistance (impaired insulin action) may occur due to derangements on three levels: pre-receptor (antibodies against insulin, defected insulin molecule), receptor (defects of insulin receptor, anti-receptor antibodies) and post-receptor (disregulated intracellular pathways). The aim of the study has been promoting the opinion that IR itself cannot be considered only a harmful phenomenon. Detrimental effect is rather chronic hyperinsulinemia related to IR. IR appears important physiological mechanism responsible for adaptation to various stresses: physical, as well as emotional/physiological. Diurnal, seasonal, age-related, pregnancy-associated, and illness-induced fluctuations in food intake and energy expenditure necessitate homeostatic versatility, including the capacity to vary insulin sensitivity, so as to optimize partitioning between tissues of a variable nutrient supply. IR has positively been selected during evolution for the short-lived energy-consuming activation of the brain or immune system. Physiologic situations that require organisms to reserve priority nutrient access for an emerging metabolic requirement, for example immune system activation or foetal development, promote the decrease of systemic insulin sensitivity, reducing nutrient uptake by non-priority tissues and reserving glucose for priority cells. It has been suggested that IR is a mechanism of antioxidant defence in conditions of nutrient energy excess.