We hypothesized that the recurrence of IH and the following reoxygenation (ROX) might result in cellular and systemic inflammation, which was manifested through the levels of proinflammatory cytokines and adipokines after IH exposure, and because IR and glucose intolerance are linked with inflammation tightly according to widely accepted previous studies, this inflammatory situation may implicate an IR status through the levels of leptin, adiponectin and some other mediators indirectly in 3T3-L1 adipocyte culture medium and rat model and through blood glucose and insulin levels in rat plasma. This evidence concerns the gene LEP and isolated hemihyperplasia.