β-Glucan from Lentinula edodes prevents cognitive impairments in high-fat diet-induced obese mice: involvement of colon-brain axis

BackgroundLong-term high fat (HF) diet intake can cause neuroinflammation and cognitive decline through the gut-brain axis. (1, 3)/(1, 6)-beta -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 beta -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 beta -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 beta -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 beta -glucan supplementation prevented the gut microbial composition shift induced by the HF diet. Long-term L. edodes beta -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 beta -glucan supplementation ameliorated the alteration of synaptic ultrastructure, neuroinflammation and brain-derived neurotrophic factor (BDNF) deficits induced by HF diet. Furthermore, the beta -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 beta -glucan prevents cognitive impairments induced by the HF diet, which may occur via colon-brain axis improvement. The finding suggested that dietary L. edodes beta -glucan supplementation may be an effective nutritional strategy to prevent obesity-associated cognitive decline.

Automated summary

The study found that both short-term and long-term supplementation of L. edodes beta-glucan prevented gut microbial composition shifts induced by a high-fat diet. Long-term supplementation also prevented cognitive impairments induced by the high-fat diet, improved synaptic ultrastructure, reduced neuroinflammation, and ameliorated brain-derived neurotrophic factor deficits in the prefrontal cortex and hippocampus. Additionally, beta-glucan supplementation increased mucosal thickness, upregulated tight junction protein expression, decreased plasma LPS levels, and inhibited proinflammatory macrophage accumulation in the colon of high-fat diet-fed mice.