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Objective: Fasting is considered to be a food structure that can improve body health. Several randomized clinical trials (RCTs) have investigated the effects of fasting in patients with metabolic syndrome (MS). In this review, we performed a meta-analysis to assess the effects of fasting on patients with MS. Methods: Following PRISMA guidelines, a systematic literature search was conducted in PubMed, Embase, and Cochrane Central updated to September 2021. The quality evaluation and heterogeneity detection of the included research literature were carried out by Revman and Stata software through a random-effects model. Results: A total of 268 subjects were included. The pooled results revealed that fasting significantly reduced body weight (WMD: −2.48 kg, 95% CI: −3.22, −1.74), BMI (WMD = −2.72 cm; 95%CI: −4.04, −1.40 cm), body fat percent (WMD: −1.57%, 95%CI: −2.47, −0.68), insulin level (WMD: −2.45 mmol/L; 95%CI: −4.40, −0.49 mmol/L) and HOMA-IR (WMD:-0.65 mmol/L; 95%CI: −0.90, −0.41 mmol/L) in patients with MS, whereas had no effect on glucose, blood pressure and lipids profile. Conclusions: Our findings provide insights into the effect of fasting on the anthropometric outcomes, insulin resistance, and gut microbiota in MS. [ABSTRACT FROM AUTHOR]

Summary: Deep‐frying oil intake is considered to destroy body health. In this review, a meta‐analysis was performed to assess the effects of deep‐frying oil intake on the risk of intestinal barrier dysfunction. Following Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines, a systematic literature search was conducted in PubMed, Embase and Cochrane Central updated till April 2022 (CRD42022326306). A total of nine studies were included. The pooled results revealed that deep‐frying oil intake significantly exaggerated crypt damage of colon [weighted mean difference (WMD) = 4.55; 95% CI: 2.87, 6.24, P < 0.05], increased proinflammatory cytokine expression in plasma and colon tissue, and enhanced intestinal permeability [lipopolysaccharides content (WMD: 10.11 μg mL−1, 95% CI: 7.44, 12.79 μg mL−1, P < 0.05)]. Moreover, deep‐frying oil intake could change the gut microbiota and decrease the content of microbiota‐derived short‐chain fatty acids. In conclusion, our findings provide insights into the effect of deep‐frying oil intake on the intestinal barrier dysfunction. [ABSTRACT FROM AUTHOR]

BACKGROUND The palm oil (PO), leaf lard oil (LO), rapeseed oil (RO), sunflower oil (SO) and linseed oil (LN) are five of the most typical dietary lipids in most Asian countries. However, their influences on gut health, and the connections between the fatty acid composition, the gut microbiota, and the bile acid metabolism are not fully understood. RESULTS: In the present study, results showed that compared with polyunsaturated fatty acid (PUFA)‐rich SO and LN, the saturated fatty acid (SFA)‐rich and monounsaturated fatty acid (MUFA)‐rich PO, LO and RO were more likely to decrease the re‐absorption of bile acid in the colon, which was probably caused by their different role in modulating the gut microbiota structure. LO consumption significantly up‐regulated the Cyp27a1, FXR and TGR5 gene expression level (P < 0.05). The correlation results suggested that the C18:0 was significantly positive correlated with these three genes, indicating that intake of SFA‐rich dietary lipids, especially for the C18:0, could specifically increase the bile acid production by stimulating the bile acid alternative synthesis pathway. Although the bile acid receptor expression in the colon was increased, the re‐absorption of bile acid did not show a significant increase (P > 0.05) as compared with other dietary lipids. Moreover, the C18:2‐rich SO maintained the bile acid metabolic balance probably by decreasing the Romboutsia, while increasing the Bifidobacterium abundance in the colon. CONCLUSIONS: The different dietary lipids showed different effects on the bile acid metabolism, which was probably connected with the alterations in the gut microbiota structure. The present study could provide basic understandings about the influences of the different dietary lipids consumption on gut homeostasis and bile acid metabolism. © 2021 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

The processing of dietary lipids in the intestinal lumen involves metabolic processes of the host and also of the microbial organisms that reside in the gut. Whereas, in the edible oil, there are also other minor content of components, such as fat-soluble micronutrients. The dietary oils and fats, as well as these accompanied components have different effects on the gut microbiota structure, which is also closely associated with gut inflammation, and the host health. This review of the literature highlights the effects of dietary oils and fats, as well as the minor content of accompanied components on the gut microbiota, and the gut inflammation, with special respect to illustrating the roles of high fat diet (HFD), fatty acid composition, the n6/n3 poly-unsaturated fatty acid (PUFA) ratio, the conjugated linoleic acids (CLAs), the fatty acid chain length and triacylglycerol (TAG) structure, the fat-soluble micronutrients, and some other minor content of components, such as trans -fatty acids (TFAs). The interactions between the dietary oils and fats and gut microbiota are also briefly discussed. The diversity in dietary oils and fats composition affects the gut microbiota structure, and the unhealthy dietary lipid pattern, such as HFD or diet rich in saturated fats may lead to the gut microbiota dysbiosis not only by decreasing their richness and diversity, but also by changing the Firmicutes to Bacteroidetes ratio, further raising the intestinal pro-inflammatory cytokines levels and permeability of the intestine mucosa. The balanced dietary oils and fats intake is recommended to achieve the appropriate fatty acid consumption ratio, especially for the n6/n3 PUFA ratio, thereafter, maintaining both of the gut microbiota homeostasis and host health. The accompanied minor content of fat-soluble bioactive components also showed positive roles for the overall gut health. However, more clinic evidence should be provided in future studies. [Display omitted] • Influences of dietary oils and fats composition on the gut microbiota and gut inflammation were elaborated. • The roles of the accompanied minor components in dietary oils and fats on gut homeostasis were reported. • Interactions between dietary oils and fats, and gut microbiota in the intestinal inflammation regulation were discussed. [ABSTRACT FROM AUTHOR]

The composition of the gastrointestinal microbiota and associated metabolites changes dramatically with diet and the development of obesity. Although many correlations have been described, specific mechanistic links between these changes and glucose homeostasis remain to be defined. Here we show that blood and intestinal levels of the microbiota-produced N-formyl peptide, formyl-methionyl-leucyl-phenylalanine, are elevated in high-fat diet-induced obese mice. Genetic or pharmacological inhibition of the N-formyl peptide receptor Fpr1 leads to increased insulin levels and improved glucose tolerance, dependent upon glucagon-like peptide 1. Obese Fpr1 knockout mice also display an altered microbiome, exemplifying the dynamic relationship between host metabolism and microbiota. Overall, we describe a new mechanism by which the gut microbiota can modulate glucose metabolism, providing a potential approach for the treatment of metabolic disease. [ABSTRACT FROM AUTHOR]

• The production mechanism of TMAO and the existing gut microbiota-mediated reduction of TMAO is discussed. • The relationship between dietary fatty acids, gut microbiota and cardiovascular disease (CVD) is described. • This review provides new insight into the association of dietary FAs and CVD, paving the way for dietary FAs therapy for CVD. Cardiovascular disease (CVD) is a serious disease that endangers human health and is one of the leading causes of death. Recent studies have reported that gut microbiota plays an important role in the development of CVD, especially its metabolite trimethylamine-N-oxide (TMAO). Dietary precursors, such as choline, L -carnitine, phosphatidylcholine and betaine were metabolized to trimethylamine (TMA) under the action of gut microbiota, and subsequently oxidized by hepatic flavin monooxygenases (FMOs) to form TMAO. Dietary fat is one of three major nutrients in food, has been found to have a positive or negative effect on the development of CVD. Multiple clinical and experimental evidences suggested that dietary fatty acids (FAs) can affect TMAO production through gut microbiota and/or FMO3 enzyme activity. This article summarizes the existing gut microbiota-mediated reduction of TMA, discusses the molecular mechanism of dietary FAs in the pathobiology of CVD from the view of TMAO. Therefore, this review provides new insight into the association of dietary FAs and CVD, paving the way for dietary FAs therapy for CVD. [ABSTRACT FROM AUTHOR]

Salecan, a natural β-glucan and one of the novel food ingredients approved in China, has been shown a variety of positive health effects, yet the mechanism of liver injury remains poorly understood. In addition, β-glucan could induce the shifts in gut microbiota, however, whether modulation of gut microbiota by β-glucan is associated with their positive health effects remain elusive. Here, the anti-inflammatory effects and the underlying mechanism of Salecan supplementation in CCl 4 -induced liver injury were investigated. After 8 weeks of treatment, we observed that Salecan alleviated liver injury by regulating inflammatory response and M2 macrophage polarization. In addition, Salecan treatment modulated the composition of gut microbiota and antibiotic cocktail treatment indicated that the hepatoprotective effect of Salecan was dependent on the gut microbiota. Fecal microbiota transplantation was used to further verify the mechanism, and we confirmed that microbial colonization partially alleviated liver injury. Besides, microbiota-derived metabolites of Salecan also contributed to the hepatoprotective and anti-inflammatory effect of Salecan against liver injury. These findings supported that Salecan intervention attenuated liver injury by regulating gut microbiota and its metabolites. [Display omitted] [ABSTRACT FROM AUTHOR]