Abstract
The aim was to determine whether gum Arabic (GA) supplementation prevents cognitive decline in type 2 diabetes, through stimulation of mitochondrial function in the hippocampus. Type 2 diabetic rats and controls were assigned to following groups for 16 weeks: Control + Water; Control + GA 10% w/v; Diabetes + Water; Diabetes + GA 10% w/v. Latency in water maze was shorter for Diabetes + GA compared to Diabetes + Water (P < 0.05). Diabetes + GA group had a higher expression density per cell of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) compared to Diabetes + Water (P < 0.05). A similar trend was observed for ATP synthase β-subunit expression (ATPB). Number of PGC-1α positive cells was higher in diabetes compared to control groups (p < 0.05). The GA prevented learning and memory loss in type 2 diabetes. This was associated with greater expression of PGC-1a and a trend for greater ATBP protein expression in the hippocampus.
Highlights
There were no differences in fasting blood glucose either between groups (p > 0.05)
Body weight was greater in the diabetic groups (Dia betes + Water = 286.60 ± 15.4 g; Diabetes + gum Arabic (GA) = 263.250 ± 29.8 g) compared to the control groups (Control + Water = 226.30 ± 48.01 g; Control + GA = 227.08 ± 24.38 g) (F = 2.74, df = 3, p = 8.42 × 10-5; p < 0.05)
Comparison of average body weight showed that these differ ences between the diabetes and control groups were maintained during the course of the study (F = 28.21, p = 4.42 × 10-18; Diabetes + Water = 378.41 ± 34.38 g vs Control + Water = 365.82 ± 58.10 g, p = 3.4 × 1010; Diabetes + GA = 384.14 ± 96.87 g vs Control + GA = 362.98 ± 60.45 g, p = 8.26 × 10-12)
Summary
Type 2 diabetes is a heterogeneous metabolic disorder characterised by long-term hyperglycaemia that causes vascular complications, which damage various organ systems including the brain (Chatter jee et al, 2017). Insulin receptors are found in areas of the brain asso ciated with learning and memory, such as the hippocampus (Agrawal et al, 2009). Brain insulin resistance, impaired glucose utilisation and energy metabolism drives oxidative stress, mitochondrial dysfunction, and further insulin resistance (de la Monte, 2014). These changes lead to hippocampal atrophy and cognitive impairment, driving a pathological process of early ageing of the brain, which in the long-term may predispose to dementia and Alzheimer’s disease (Carvalho et al, 2015; Arnold et al, 2018)
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