Mechanism and effects of fructose diphosphate on anti-hypoxia fatigue and learning memory ability

This study aims to investigate the mechanisms through which Fructose Diphosphate (FDP) causes the anti-hypoxia and anti-fatigue effects, and improves learning and memory. Mice were divided into three groups: FDP-L，FDP-H and a control group. Acute toxic hypoxia induced by carbon monoxide, sodium nitrite and potassium cyanide, and acute cerebral ischemic hypoxia, were used to investigate the anti-hypoxia ability of FDP. The tests of rod-rotating, mouse-tail suspension and swimming endurance were used to explore the anti-fatigue effects of FDP. The Morris water maze experiment was used to determine the impact of FDP on learning and memory ability. Poisoning-induced hypoxic tests showed that mouse survival time was significantly prolonged in the FDP-L and FDP-H groups compared with the control group (p < 0.05). In the exhaustive swimming test, FDP significantly shortened struggling time and prolonged the time of weight-loaded swimming; the rod-rotating test showed that endurance time was significantly prolonged by using FDP (p < 0.05). FDP significantly decreased lactate and urea nitrogen levels, increased hepatic and muscle glycogen, and glucose transporter-4 and Na+-K+-ATPase (p < 0.05). To conclude, FDP enhances hypoxia tolerance and fatigue resistance and improves learning and memory ability through regulating glucose and energy metabolism.