High-fiber diet mitigates maternal obesity-induced cognitive and social dysfunction in the offspring via gut-brain axis

Gut microbes play significant roles in colitis development. The current study was aimed to uncover the preventive effects of lycopene (LYC), a functional carotenoid component, on colitis and the accompanied behavior disorders. The current study demonstrated that LYC treatment (50 mg/kg body weight/day) for 40 days prevented the dextran sulfate sodium (DSS)-induced gut barrier damages and inflammatory responses in male mice. LYC improved DSS-induced depression and anxiety-like behavioral disorders by suppressing neuroinflammation and prevented synaptic ultrastructure damages by upregulating the expressions of neurotrophic factor and postsynaptic-density protein. Moreover, LYC reshaped the gut microbiome in colitis mice by decreasing the relative abundance of proteobacteria and increasing the relative abundance of Bifidobacterium and Lactobacillus. LYC also elevated the generation of short-chain fatty acids and inhibited the permeability of lipopolysaccharide in colitis mice. In conclusion, LYC ameliorate DSS-induced colitis and behavioral disorders via mediating microbes–gut–brain axis balance.

Sesamol, a liposoluble lignan extract, has already been proved to possess potent anti-inflammatory properties, and it could also regulate gut dysfunction. The purpose of the present research is to explore the protective effect of sesamol on colitis mice. In the current research, sesamol treatment (100 mg/kg bodyweight/day) for 6 weeks inhibited the dextran sulphate sodium (DSS)induced bodyweight loss of mice. Transmission electron microscopy and hematoxylin and eosin staining results showed that the DSS-induced histopathological changes of mice were also recovered by sesamol supplementation. In addition, DSS-induced inflammatory responses were inhibited by sesamol supplementation via the NF-κB signaling pathway in mice colon. Moreover, sesamol treatment prevented gut barrier damages by enhancing the expression of tight junction proteins (occludin, claudin-1, and ZO-1) and recovering the loss of gut mucus layer. Furthermore, sesamol supplementation also increased the short-chain fatty acid (SCFAs) contents of acetate, propionate, and butyrate. Furthermore, sesamol supplementation changed the gut microbiome structure by enhancing the relative abundance of Coprococcuscus, Butyricicoccus, Odoribacter, and AF12 in colitis mice. In conclusion, sesamol could effectively ameliorate DSS-induced colitis by promoting gut microecology.

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The carotenoid pigment lycopene (LYC) possesses several properties, including antioxidative, anti-inflammatory, and neuroprotective properties. This study examined the effects of dietary supplementation with LYC on age-induced cognitive impairment, and the potential underlying mechanisms. Behavioral tests revealed that chronic LYC supplementation alleviated age-associated memory loss and cognitive defects. Histological and immunofluorescence-staining results indicated that LYC treatment reversed age-associated neuronal damage and synaptic dysfunctions in the brain. Additionally, LYC supplementation decreased age-associated oxidative stress via suppression of malondialdehyde levels, which increased glutathione, catalase, and superoxide dismutase activities and the levels of antioxidant-enzyme mRNAs, including those of heme oxygenase 1 and NAD-(P)-H-quinone oxidoreductase-1. Furthermore, LYC supplementation significantly reduced age-associated neuroinflammation by inhibiting microgliosis (Iba-1) and downregulating related inflammatory mediators. Moreover, LYC lowered the accumulation of Aβ in the brains of aged CD-1 mice. Therefore, LYC has the potential for use in the treatment of several age-associated chronic diseases.

Scope Methionine restriction (MR) is known to potently alleviate inflammation and improve gut microbiome in obese mice. The gut microbiome exhibits diurnal rhythmicity in composition and function, and this, in turn, drives oscillations in host metabolism. High‐fat diet (HFD) strongly altered microbiome diurnal rhythmicity, however, the role of microbiome diurnal rhythmicity in mediating the improvement effects of MR on obesity‐related metabolic disorders remains unclear. Methods and results 10‐week‐old male C57BL/6J mice are fed a low‐fat diet or HFD for 4 weeks, followed with a full diet (0.86% methionine, w/w) or a methionine‐restricted diet (0.17% methionine, w/w) for 8 weeks. Analyzing microbiome diurnal rhythmicity at six time points, the results show that HFD disrupts the cyclical fluctuations of the gut microbiome in mice. MR partially restores these cyclical fluctuations, which lead to time‐specifically enhance the abundance of short‐chain fatty acids producing bacteria, increases the acetate and butyric, and dampens the oscillation of inflammation‐related Desulfovibrionales and Staphylococcaceae over the course of 1 day. Notably, MR, which protects against systemic inflammation, influences brain function and synaptic plasticity. Conclusion MR could serve as a potential nutritional intervention for attenuating obesity‐induced cognitive impairments by balancing the circadian rhythm in microbiome‐gut‐brain homeostasis.

Cichoric acid (CA), a polyphenol component from Echinacea purpurea, exhibits preventive effects on liver lipid-metabolism disorders in obesity. This research aimed to determine the role of circadian rhythm signaling during the process of CA-attenuated lipid accumulation in hepatocytes. In the current study, CA treatments improved cell morphology changes and hepatic lipid levels, which were triggered by free fatty acids (2:1, oleate: palmitate) in a dose-dependent way. Besides, CA (200 μM) regulated the circadian rhythm expressions of clock genes and the relatively shallow daily oscillations. Moreover, silencing Bmal1 significantly blocked the p-Akt/Akt pathway to 80.1% ± 1.5% and the p-GSK3β/GSK3β pathway to 64.7% ± 2.8% ( p < 0.05). Furthermore, silencing Bmal1 elevated the expressions of FAS and ACC to 122.4% ± 5.6% and 114.9% ± 1.7% in protein levels ( p < 0.05) and to 166.5% ± 18.5% and 131.4% ± 5.5% in mRNA levels ( p < 0.05). Therefore, our results demonstrated that CA has a Bmal1 resistance to lipid accumulation by enhancing the Akt/GSK3β signaling pathways and modulating the downstream expressions related to lipid metabolism, which indicated that CA might be useful as a natural and promising nonalcoholic fatty liver diseases (NAFLD) modulator.