Abstract
BackgroundLong-term high fat (HF) diet intake can cause neuroinflammation and cognitive decline through the gut-brain axis. (1, 3)/(1, 6)-β-glucan, an edible polysaccharide isolated from medical mushroom, Lentinula edodes (L. edodes), has the potential to remodel gut microbiota. However, the effects of L. edodes derived β-glucan against HF diet-induced neuroinflammation and cognitive decline remain unknown. This study aimed to evaluate the neuroprotective effect and mechanism of dietary L edodes β-glucan supplementation against the obesity-associated cognitive decline in mice fed by a HF diet.MethodsC57BL/6J male mice were fed with either a lab chow (LC), HF or HF with L. edodes β-glucan supplementation diets for 7 days (short-term) or 15 weeks (long-term). Cognitive behavior was examined; blood, cecum content, colon and brain were collected to evaluate metabolic parameters, endotoxin, gut microbiota, colon, and brain pathology.ResultsWe reported that short-term and long-term L. edodes β-glucan supplementation prevented the gut microbial composition shift induced by the HF diet. Long-term L. edodes β-glucan supplementation prevented the HF diet-induced recognition memory impairment assessed by behavioral tests (the temporal order memory, novel object recognition and Y-maze tests). In the prefrontal cortex and hippocampus, the β-glucan supplementation ameliorated the alteration of synaptic ultrastructure, neuroinflammation and brain-derived neurotrophic factor (BDNF) deficits induced by HF diet. Furthermore, the β-glucan supplementation increased the mucosal thickness, upregulated the expression of tight junction protein occludin, decreased the plasma LPS level, and inhibited the proinflammatory macrophage accumulation in the colon of mice fed by HF diet.ConclusionsThis study revealed that L. edodes β-glucan prevents cognitive impairments induced by the HF diet, which may occur via colon-brain axis improvement. The finding suggested that dietary L. edodes β-glucan supplementation may be an effective nutritional strategy to prevent obesity-associated cognitive decline.
Highlights
Long-term high fat (HF) diet intake can cause neuroinflammation and cognitive decline through the gut-brain axis. (1, 3)/(1, 6)-β-glucan, an edible polysaccharide isolated from medical mushroom, Lentinula edodes (L. edodes), has the potential to remodel gut microbiota
Short‐term L. edodes derived β‐glucan supplementation attenuated the gut microbiota dysbiosis induced by high-fat diet group (HF) diet Our previous studies have shown that chronic HF diet led to microbial dysbiosis with regards to diversity and composition [15, 16]
The mean proportion of Proteobacteria and Actinobacteria was significantly decreased by the HF diet, while short-term L. edodes supplementation improved the abundance of (See figure on page.) Fig. 1 Short-term L. edodes derived β-glucan supplementation attenuated the gut microbiota dysbiosis induced by HF diet. a The relative abundance of Firmicutes, b the relative abundance of Bacteroidetes, c the ratio of Firmicutes (FM) to Bacteroidetes (BO), d the relative abundance of Proteobacteria, e the relative abundance of Actinobacteria, f the Shannon index, g the linear discriminant analysis (LDA) effect size results on mice gut microbiomes, h the plasma LPS levels in the sera, i body weight, j energy intake
Summary
Long-term high fat (HF) diet intake can cause neuroinflammation and cognitive decline through the gut-brain axis. (1, 3)/(1, 6)-β-glucan, an edible polysaccharide isolated from medical mushroom, Lentinula edodes (L. edodes), has the potential to remodel gut microbiota. Long-term high fat (HF) diet intake can cause neuroinflammation and cognitive decline through the gut-brain axis. The effects of L. edodes derived β-glucan against HF diet-induced neuroinflammation and cognitive decline remain unknown. This study aimed to evaluate the neuropro‐ tective effect and mechanism of dietary L edodes β-glucan supplementation against the obesity-associated cognitive decline in mice fed by a HF diet. Evidence shows that obesity and/or high fat feeding are associated with deficits in learning, memory, and executive functioning [4, 5] and potentially brain atrophy [6]. It is urgent to clarify the underlying mechanism of obesity-induced cognitive decline and develop a targeted therapeutic strategy. Neuroinflammation is proposed to be an important pathophysiological hallmark underlying cognitive decline [7]. Addressing neuroinflammation mediated by microglia bears great promise as a novel treatment strategy to reduce neuronal damage and to foster a permissive environment for further regeneration effort [9]
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