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Polycystic ovary syndrome (PCOS) represents a common endocrine—metabolic disorder disease with chronic low-grade inflammation and alteration of intestinal flora. Serving as functional food, flaxseed oil (FO), which is rich in plant-derived α-linolenic acid of omega-3 polyunsaturated fatty acids, has been proven to benefit for chronic metabolic diseases. However, the exact role of dietary FO on PCOS remains largely unclear. In the present study, 6-week-old female Sprague–Dawley rats were randomly divided into four groups (eight rats/group), including (a) pair-fed (PF) control (CON) group (PF/CON), (b) FO-fed CON group (FO/CON), (c) PF with letrozole-induced PCOS model (MOD) group (PF/MOD), and (d) FO-fed MOD group (FO/MOD). All rats were fed a standard diet. After 3 weeks of modeling and subsequent 8 weeks of treatment, the rats in diverse groups were euthanized and associated indications were investigated. The results showed that dietary FO ameliorated the disorder of estrous cycle and ovarian morphology. In parallel, dietary FO improved the sex steroid hormone disturbance (luteinizing hormone/follicle-stimulating hormone, estrogen, testosterone, and progesterone), body weights, dyslipidemia, and insulin resistance. Moreover, FO treatment improved plasma and ovary inflammatory interleukin (IL)-1β, IL-6, IL-10, and IL-17A, tumor necrosis factor-α, and monocyte chemoattractant protein-1. Additionally, FO intervention significantly modulated the composition of gut microbiota and vaginal microbiota by increasing the abundances of Allobaculum, Lactobacillus, Butyrivibrio, Desulfovibrio, Bifidobacterium, Faecalibacterium, Parabacteroides as well as decreasing the abundances of Actinobacteria, Bacteroides, Proteobacteria , and Streptococcus , the ratio of Firmicutes / Bacteroidetes. A decrease in plasma lipopolysaccharide level and an increase in short-chain fatty acids, including acetic acid, propionic acid, butyric acid and pentanoic acid, were determined after dietary FO supplementation. Correlation analysis revealed close relationships among sex steroid hormones, inflammation, and gut/vaginal microbiota. Collectively, this study demonstrated that dietary FO ameliorated PCOS through the sex steroid hormones—microbiota—inflammation axis in rats, which may contribute to the understanding of pathogenesis and potentially serve as an inexpensive intervention in the control of PCOS. [ABSTRACT FROM AUTHOR]

Background: Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disease worldwide with chronic low-grade inflammation and alteration of gut microbiota. Inulin (INU) has been confirmed to exhibit benefit for metabolic diseases. The aim of this study was to clarify the effects and mechanism of INU on NAFLD inflammation via gut-liver axis. Methods: C57BL/6 mice were randomly divided into four groups: normal diet group (ND); high-fat diet group (HFD); ND with INU group (ND-INU); HFD with INU group (HFD-INU). After 14 weeks of feeding, mice were sacrificed and associated indications were investigated. Results: Significant increases of body weight, liver weight, liver biochemical aspartate aminotransferase, alanine aminotransferase, triglyceride, total cholesterol and pro-inflammatory indicators (Lipopolysaccharide, interleukin (IL)-18, IL-1β, TNF-α and IL-6), as well as a reduction of plasma IL-10 were observed in HFD group, while INU treatment restored these abnormal indicators. The ratio of hepatic macrophages (Mψs) and Toll-like receptor 4+ Mψs were both reduced with INU intervention. Nuclear factor-κB, nod-like receptor protein 3, apoptosis-associated speck-like protein and caspase-1 were decreased in HFD-INU group. Additionally, the results of 16S rRNA sequencing and analysis showed that INU administration modulated the composition of gut microbial community in NAFLD mice by up-regulating the abundances of Akkermansia and Bifidobacterium as well as down-regulating the abundances of Blautia and the ratio of Firmicutes/Bacteroidetes. Short-chain fatty acids including acetic acid, propionic acid and butyric acid, were increased with INU treatment. Correlation analysis revealed close relationships among inflammatory indicators, metabolic indicators as well as gut microbiota/its metabolite short-chain fatty acids. Conclusion: INU prevents NAFLD via modulating gut microbiota and suppressing Lipopolysaccharide-Toll-like receptor 4-Mψ-Nuclear factor-κB-nod-like receptor protein 3 inflammatory pathway via the gut-liver axis. [ABSTRACT FROM AUTHOR]