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A Rare Sugar, D-Allulose, Attenuates Cognitive Impairment and Brain Pathologies in D-Galactose-Accelerated Aging Rats
Yanmei Huang1, Chanisa Thonusin2, Donglin Lu2
1Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai 50200, Thailand.
Background:
Aging is the major risk factor for cognitive impairment via aging-induced neuronal dysfunction. D-allulose, a low-calorie rare sugar, has been shown to provide beneficial effects in the obese-insulin-resistant brain. However, its beneficial effects on the aging brain have never been investigated.
Objective:
This study investigated whether D-allulose could attenuate cognitive impairment and brain pathological alterations in a D-galactose-accelerated aging model.
Methods:
Thirty-two 5-month-old male Wistar rats were randomly allocated by cage drawing lots into four groups (n = 8 rats/group): control (Con), D-galactose (D-gal), D-galactose + inulin (D-gal + Inu), and D-galactose + D-allulose (D-gal + Allu). The control group received normal saline solution (NSS; 1 mL/kg/day, s.c.), whereas the other three groups received D-galactose (150 mg/kg/day, s.c.) for 20 weeks. Beginning at week 9, the D-gal-treated groups additionally received NSS, inulin (2.0 g/kg/day), or D-allulose (1.9 g/kg/day), respectively, by oral gavage for 12 weeks. Following the treatment, spatial learning and memory were assessed using the Morris water maze. Brain pathological alterations were evaluated using Western blot, RT-qPCR, immunofluorescence staining, mitochondrial functional assessments, and electrophysiological recordings.
Results:
D-galactose exposure reduced target quadrant entries in the Morris Water Maze (5.6 ± 0.89 vs 7.6 ± 0.42, P = 0.021) and lowered the mean normalized hippocampal fEPSP slope (99.0% ± 1.86% vs 162.0% ± 21.79%, P = 0.009) compared with controls. D-allulose increased target quadrant entries (7.4 ± 0.50 vs 5.6 ± 0.89, P = 0.042) and the mean normalized hippocampal fEPSP slope (155.5% ± 8.95% vs 99.0% ± 1.86%, P = 0.018) compared with the D-gal group. However, inulin did not significantly alter these outcomes. Mitochondrial ROS production and brain MDA levels were also lower in D-gal + Allu group than in D-gal group (P = 0.023 and P = 0.013, respectively).
Conclusion:
D-allulose mitigates aging-associated brain dysfunction and pathological alterations in D-galactose-accelerated aging model.
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