As insulin resistance was found to be positively correlated with mean escape latency, they suggested that fructose-induced peripheral insulin resistance may contribute to hippocampal-dependent cognitive function, either because chronic hyperinsulinemia might determine a reduced insulin transport into the brain or because a fructose diet induces an increase in plasma TG, which penetrate the BBB and promote hippocampal-dependent memory deficits [99]. This evidence concerns the gene INS and Insulin resistance.