The spread of antibiotic resistance to humans and potential protection strategies.

Metabolic syndrome (MetS) is a complex disease in which protein, fat, carbohydrates and other substances are metabolized in a disorderly way. Ferulic acid (FA) is a phenolic acid found in many vegetables, fruits, cereals and Chinese herbs that has a strong effect on ameliorating MetS. However, no review has summarized the mechanisms of FA in treating MetS. This review collected articles related to the effects of FA on ameliorating the common symptoms of MetS, such as diabetes, hyperlipidemia, hypertension and obesity, from different sources involving Web of Science, PubMed and Google Scholar, etc. This review summarizes the potential mechanisms of FA in improving various metabolic disorders according to the collected articles. FA ameliorates diabetes via the inhibition of the expressions of PEPCK, G6Pase and GP, the upregulation of the expressions of GK and GS, and the activation of the PI3K/Akt/GLUT4 signaling pathway. The decrease of blood pressure is related to the endothelial function of the aortas and RAAS. The improvement of the lipid spectrum is mediated via the suppression of the HMG-Co A reductase, by promoting the ACSL1 expression and by the regulation of the factors associated with lipid metabolism. Furthermore, FA inhibits obesity by upregulating the MEK/ERK pathway, the MAPK pathway and the AMPK signaling pathway and by inhibiting SREBP-1 expression. This review can be helpful for the development of FA as an appreciable agent for MetS treatment.

/pdf/protective-effects-of-ferulic-acid-on-metabolic-syndrome-a-1e0gv4az.pdf

Protective Effects of Ferulic Acid on Metabolic Syndrome: A Comprehensive Review

Epigallocatechin-3-gallate ameliorates polystyrene microplastics-induced anxiety-like behavior in mice by modulating gut microbe homeostasis.

Natural polyphenols provide numerous human-health promoting benefits, including gut microbiota regulation, microbial composition changes, and improvement of glycolipid-related metabolic disorders and insulin resistance. In fact, about 90–95% of the ingested polyphenols will reach the colon to interact with gut microbiota. On the one hand, polyphenols and their microbial metabolites affect glycolipid metabolism by enhancing intestinal barrier protection and reducing blood glucose and lipid level. On the other hand, polyphenol and its microbial metabolites influence glycolipid metabolism via gut-brain axis. This review focuses on the biotransformation of different types of polyphenols by gut microbiota and their metabolic pathways, as well as the mechanism of polyphenols or their microbial metabolites affecting glycolipid metabolism. The available evidence relating to natural polyphenols with different structures and sources as well as their metabolites produced by gut microbiota and the interaction between polyphenols and gut microbiota have been reported and discussed. Importantly, this review highlights the mechanism of polyphenols or their microbial metabolites affecting glycolipid metabolism via polyphenols-gut-brain axis. Polyphenols and their metabolites regulate blood glucose and lipid levels through the signaling pathways of inflammation-related factors, regulate glucose homeostasis, improve insulin resistance, reduce oxidative stress, and regulate the intestinal microbial composition. Besides, natural polyphenols affect glycolipid metabolism of the host via the gut-brain axis, including autonomic nervous system, neuroendocrine system, hypothalamic-pituitary-adrenal axis (HPA), and intestinal immune system pathways. It is still a challenging task to fully elucidate the mechanisms of the complex gut microbiota, and how different structural types of polyphenols and their metabolites regulate blood glucose and lipid levels. 

Natural polyphenols-gut microbiota interactions and effects on glycolipid metabolism via polyphenols-gut-brain axis: A state-of-the-art review

Internal clocks time behavior and physiology, including the gut microbiome, in a circadian (∼24 h) manner. Mismatch between internal and external time, e.g. during shift work, disrupts circadian system coordination promoting the development of obesity and type 2 diabetes (T2D). Conversely, body weight changes induce microbiota dysbiosis. The relationship between circadian disruption and microbiota dysbiosis in metabolic diseases, however, remains largely unknown.Core and accessory clock gene expression in different gastrointestinal (GI) tissues were determined by qPCR in two different models of circadian disruption - mice with Bmal1 deficiency in the circadian pacemaker, the suprachiasmatic nucleus (Bmal1SCNfl/-), and wild-type mice exposed to simulated shift work (SSW). Body composition and energy balance were evaluated by nuclear magnetic resonance (NMR), bomb calorimetry, food intake and running-wheel activity. Intestinal permeability was measured in an Ussing chamber. Microbiota composition and functionality were evaluated by 16S rRNA gene amplicon sequencing, PICRUST2.0 analysis and targeted metabolomics. Finally, microbiota transfer was conducted to evaluate the functional impact of SSW-associated microbiota on the host's physiology.Both chronodisruption models show desynchronization within and between peripheral clocks in GI tissues and reduced microbial rhythmicity, in particular in taxa involved in short-chain fatty acid (SCFA) fermentation and lipid metabolism. In Bmal1SCNfl/- mice, loss of rhythmicity in microbial functioning associates with previously shown increased body weight, dysfunctional glucose homeostasis and adiposity. Similarly, we observe an increase in body weight in SSW mice. Germ-free colonization experiments with SSW-associated microbiota mechanistically link body weight gain to microbial changes. Moreover, alterations in expression of peripheral clock genes as well as clock-controlled genes (CCGs) relevant for metabolic functioning of the host were observed in recipients, indicating a bidirectional relationship between microbiota rhythmicity and peripheral clock regulation.Collectively, our data suggest that loss of rhythmicity in bacteria taxa and their products, which likely originates in desynchronization of intestinal clocks, promotes metabolic abnormalities during shift work. 

https://doi.org/10.1016/j.molmet.2022.101628

Genetic and environmental circadian disruption induce weight gain through changes in the gut microbiome

Ferulic acid improves intestinal barrier function through altering gut microbiota composition in high-fat diet-induced mice

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Ferulic acid improves intestinal barrier function through altering gut microbiota composition in high-fat diet-induced mice