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Antenatal obesity increases the risk of postpartum depression. Previous research found that dietary fiber supplementation could alleviate mental behavioral disorders. The present study aims to uncover the effects of high-dietary fiber intake on high-fat diet (HFD)-induced depressive-like behaviors and its underlying mechanism. Female C57BL6/J mice were fed with HFD to establish an antenatal obese model. A high-dietary fiber intake (inulin, 0.037 g/kcal) significantly attenuated cognitive deficits and depressive-like behaviors in the maternal mice after the offspring weaning. High-dietary fiber intake upregulated the expression of 5-hydroxytryptamine (5-HT) and norepinephrine (NE) and suppressed neuroinflammation. Furthermore, high-dietary fiber intake restructured the gut microbiome and elevated the formation of short-chain fatty acids (SCFAs). Correlation analysis indicated that the increase in microbes such as Lactobacillus and S24-7, and SCFAs’ levels were positively correlated with behavioral improvements. In conclusion, high-dietary fiber intake is a promising nutritional intervention strategy to prevent antenatal obesity-induced behavioral disorders via a microbiota–gut–brain axis.

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Scope Obesity is associated with gut microbiome dysbiosis. Mannose oligosaccharide (MOS) has been reported to be a potential prebiotic. The present study is aimed to determine the effects of MOS on western‐diet‐induced obesity and to uncover the mediating roles of the gut microbiota and microbial metabolites. Methods and results Three‐month‐old male ICR mice are fed with a high‐fat and high‐fructose diet for 8 weeks. The diet‐induced obese mice are then orally administrated with MOS (100 and 200 mg kg–1 d–1) for 4 weeks. MOS significantly reduces bodyweight gain, insulin resistance, fatty liver, and inflammatory responses in obese mice. MOS also stimulates lipolysis and inhibits lipogenesis in the adipose tissues. Moreover, MOS restructures the gut microbiome by enhancing the abundance of Bifidobacterium and Lactobacillus in obese mice. The microbial metabolite SCFAs are also increased in the feces and serum. Correlation analysis indicates that the appetite suppression and lipid‐lowering effects of MOS are highly correlated with the butyrate levels. Conclusion MOS suppresses the appetite, which results in less lipid deposition. The lower appetite is likely due to an altered gut microbiome and elevated SCFAs production. MOS may be a potential nutraceutical used in body weight management and gut health improvement.

Sea-buckthorn flavonoids (SFs) have been used as functional food components for their bioactive potential in preventing metabolic complications caused by diet, such as obesity and inflammation. However, the protective effect of SFs on cognitive functions is not fully clear. In this study, a high-fat and high-fructose diet (HFFD)-induced obese mice model was treated with SFs for 14 weeks. It was found that the oral SF administration (0.06% and 0.31% w/w, mixed in diet) significantly reduced bodyweight gain and insulin resistance in the HFFD-fed mice. SFs significantly prevented HFFD-induced neuronal loss and memory impairment in behavioral tests. Additionally, SFs also suppressed the HFFD-induced synaptic dysfunction and neuronal damages by increasing the protein expressions of PSD-95. Furthermore, SF treatment activated the ERK/CREB/BDNF and IRS-1/AKT pathways and inactivated the NF-κB signaling and its downstream inflammatory mediator expressions. In conclusion, SFs are a potential nutraceutical to prevent high-energy density diet-induced cognitive impairments, which could be possibly explained by their mediating effects on insulin signaling and inflammatory responses in the brain.