HFD-induced Gut Microbiota Research Articles

Tea (Camellia sinensis L.) flower polysaccharide attenuates metabolic syndrome in high-fat diet induced mice in association with modulation of gut microbiota

There is a growing body of evidence suggesting that dietary polysaccharides play a crucial role in preventing metabolic syndrome (MetS) through their interaction with gut microbes. Tea (Camellia sinensis L.) flower polysacchride (TFPS) is a novel functional compound known for its diverse beneficial effects in both vivo and vitro. To further investigate the effects of TFPS on MetS and gut microbiota, and the possible association between gut microbiota and their activities, this study was carried out on mice that were fed a high-fat diet (HFD) and given oral TFPS at a dose of 400 and 800 mg/kg·body weight (BW)/d, respectively. TFPS treatment significantly mitigated HFD-induced MetS, evidenced by reductions in body weight, fat accumulation, plasma levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and IL-1β, along with an increase in plasma IL-10 levels. Furthermore, TFPS induced alterations in the diversity and composition of HFD-induced gut microbiota. Specifically, TFPS influenced the relative abundance of 11 genera, including Lactobacillus and Lactococcus, which showed strong correlations with metabolic improvements and likely contributed to the amelioration of MetS. In conclusion, TFPS exhibits promising prebiotic properties in preventing MetS and regulating gut microbiota.

Combined analysis of gut microbiota and metabolomics in high-fat model mice fed with Chlorella pyrenoidosa peptides

Chlorella pyrenoidosa peptides (SISISVAGGGR, T1) can effectively alleviate obesity and related metabolic disorders in high-fat mice. However, their lipid-lowering mechanism is still unclear. This research endeavor sought to delve into the potential mediators of T1 anti-obesity in high-fat mice through macrogenomics analyses combined with untargeted metabolomics analyses. The results showed that T1 alleviated HFD-induced increases in body weight, epididymal fat weight, TG, LDL, AST, TNF-α, and IL-1β levels, and increased HDL level. Moreover, T1 reversed the HFD-induced gut microbiota dysbiosis. Specifically, T1 resulted in a massive proliferation of Bacteroides, Parabacteroides, and Alistipes, as well as increased levels of metabolites such as DL-arginine, N-stearoyl GABA, and decreased levels of 7α,24(S)-dihydroxy-4-cholesten-3-one, and hexadecanedioic acid. Correlation analysis showed that T1 alleviated HFD-induced obesity metabolic syndrome and associated inflammation by modulating specific gut microbiota and related metabolites. This provides new ideas for the treatment of diet-induced obesity and related metabolic disorders.

Effects of semaglutide on gut microbiota, cognitive function and inflammation in obese mice.

This study aims to investigate the effects of semaglutide on gut microbiota, cognitive function, and inflammation in obese mice. Twenty-four C57BL/6J male mice were randomly assigned to three groups: a normal-chow diet group (NCD, n=8), high-fat diet group (HFD, n=8), and HFD+semaglutide group (Sema, n=8). The mice were fed a HFD to establish an animal model of obesity and then administered with semaglutide or saline for 12 weeks. Cognitive function was assessed using the Morris water maze test. Serum pro-inflammatory cytokines were measured. 16S rRNA gene sequencing technology was used to explore gut microbiota characteristics in obese mice. Obese mice showed significant cognitive impairment and inflammation. Semaglutide improved cognitive function and attenuated inflammation induced by a HFD diet. The abundance of gut microbiota was significantly changed in the HFD group, including decreased Akkermansia, Muribaculaceae, Coriobacteriaceae_UCG_002, Clostridia_UCG_014 and increased Romboutsia, Dubosiella, Enterorhabdus. Whereas semaglutide could dramatically reverse the relative abundance of these gut microbiota. Correlation analysis suggested that cognitive function was positively correlated with Muribaculaceae and Clostridia_UCG_014, and negatively associated with Romboutsia and Dubosiella. Romboutsia was positively correlated with TNFα, IL-6 and IL-1β. While Clostridia_UCG_014 was negatively related to TNFα, IL-6 and IL-1β. For the first time semaglutide displayed different regulatory effects on HFD-induced gut microbiota dysbiosis. Semaglutide could regulate the structure and composition of gut microbiota associated with cognitive function and inflammation. Thus, affecting gut microbiota might be a potential mechanism of semaglutide in attenuating cognitive function and inflammation.

Protective effects of catechin (C) and epigallocatechin gallate (EGCG) against high-fat diet (HFD)-exacerbated Salmonella infection in mice

Salmonella is one of the most prevalent foodborne pathogens. This study investigated the impact of HFD on Salmonella infection and the preventive effects of tea-derived polyphenols. Results showed that HFD decreased the survival rate of Salmonella-infected mice, while catechin (C) and epigallocatechin gallate (EGCG) supplementation increased survival rates, with EGCG being more effective. HFD promoted pro-inflammatory cytokines and inhibited intestinal epithelial barrier proteins, but catechins, especially EGCG, restored these levels. 16S rDNA sequencing revealed HFD-induced gut microbiota disruptions. Both catechins altered bacterial composition and diversity, with distinct profiles for C and EGCG. The relative abundance of Desulfovibrio and the Eubacterium coprostanoligenes group was modulated by both catechins, and nine bacteria were identified as biomarkers for EGCG treatment. In summary, Salmonella infection is exacerbated by HFD, but catechins, particularly EGCG, offer protective effects, providing valuable insights for controlling pathogenic infections by tea polyphenols or related functional foods.

Gymnemic acid alleviates gut barrier disruption and lipid dysmetabolism via regulating gut microbiota in HFD hamsters

Gut microbiota dysbiosis and gut barrier disruption are key events associated with high-fat diet (HFD)-induced systemic metabolic disorders. Gymnemic acid (GA) has been reported to have an important role in alleviating HFD-induced disorders of glycolipid metabolism, but its regulatory role in HFD-induced disorders of the gut microbiota and gut barrier function has not been elucidated. Here we showed that GA intervention in HFD-induced hamsters increased the relative abundance of short-chain fatty acid (SCFA)-producing microbes including Lactobacillus (P<.05) and Lachnoclostridium (P<.01) in the gut, and reduced the relative abundance of lipopolysaccharide (LPS)-producing microbes including Enterococcus (P<.05) and Bacteroides (P<.05), subsequently improving HFD-induced intestinal barrier dysfunction and systemic inflammation. Specifically, GA intervention reduced mRNA expression of inflammatory cytokines, including IL-1β, IL-6, and TNF-α (P<.01), increased mRNA expression of antioxidant-related genes, including Nfe2l2, Ho-1, and Nqo1 (P<.01), and increased mRNA expression of intestinal tight junction proteins, including Occludin and Claudin-1 (P<.01), thereby improving gut barrier function of HFD hamsters. This ameliorative effect of GA on the gut of HFD hamsters may further promote lipid metabolic balance in liver and adipose tissue by regulating the Toll-like receptor 4 (TLR4)-nuclear factor-κB (NF-κB) signaling pathway. Taken together, these results systematically revealed the important role of GA in regulating HFD-induced gut microbiota disturbance and gut barrier function impairment, providing a potential clinical theoretical basis for targeted treatment of HFD-induced microbiota dysbiosis.

Saccharina Japonica Polysaccharides Suppress High-Fat Diet-Induced Obesity and Modulate Gut Microbiota Composition and Function.

Recent studies have highlighted the potential of Saccharina japonica Polysaccharides (SJPs) in alleviating high-fat diet (HFD)-induced obesity by regulating gut microbiota, which warrants further exploration to elucidate the underlying structure-activity relationship. In this study, five polysaccharide fractions (Sj-T, Sj-T-1, Sj-T-2, Sj-T-3, and Sj-T-4) with different structure characteristics were prepared from S. japonica, and their effects on HFD-induced obesity and gut microbiota composition were investigated using C57BL/6J mice. The results revealed that oral administration of Sj-T considerably suppressed HFD-induced obesity, glucose metabolic dysfunction, and other disordered symptoms. While, Sj-T-2, which has the lowest molecular weight, was the most effective in alleviating HFD-induced obesity and had the second-best effect on improving HFD-induced impaired glucose tolerance among the five SJPs. Supplementation with SJPs significantly modulated HFD-induced gut microbiota dysbiosis both at the phylum and species levels, such as enriching Desulfobacterota and Actinobacteriota, while suppressing the abundance of Bacteroidota. Sj-T also dramatically restored the gut microbiota composition by modulating the abundance of many crucial gut bacterial taxa, including s_Bacteroides_acidifaciens, s_Lachnospiraceae _bacterium, and g_Lachnospiraceae_NK4A136_group. Besides, SJPs also dramatically altered the function of gut microbiota, including many carbohydrate-metabolism enzymes. This study highlights the potential of SJPs in preventing obesity and restoring intestinal homeostasis in obese individuals.

Chrysanthemum morifolium Ramat extract and probiotics combination ameliorates metabolic disorders through regulating gut microbiota and PPARα subcellular localization

BackgroundChrysanthemum morifolium Ramat, a traditional Chinese medicine, has the effects on liver clearing, vision improving, and anti-inflammation. C. morifolium and probiotics have been individually studied for their beneficial effects on metabolic diseases. However, the underlying molecular mechanisms were not completely elucidated. This study aims to elucidate the potential molecular mechanisms of C. morifolium and probiotics combination (CP) on alleviating nonalcoholic fatty liver disease (NAFLD) and the dysregulation of glucose metabolism in high-fat diet (HFD)-fed mice.MethodsThe therapeutic effect of CP on metabolism was evaluated by liver histology and serum biochemical analysis, as well as glucose tolerance test. The impact of CP on gut microbiota was analyzed by 16S rRNA sequencing and fecal microbiota transplantation. Hepatic transcriptomic analysis was performed with the key genes and proteins validated by RT-qPCR and western blotting. In addition, whole body Pparα knockout (Pparα−/−) mice were used to confirm the CP-mediated pathway.ResultsCP supplementation ameliorated metabolic disorders by reducing body weight and hepatic steatosis, and improving glucose intolerance and insulin resistance in HFD fed mice. CP intervention mitigated the HFD-induced gut microbiota dysbiosis, which contributed at least in part, to the beneficial effect of improving glucose metabolism. In addition, hepatic transcriptomic analysis showed that CP modulated the expression of genes associated with lipid metabolism. CP downregulated the mRNA level of lipid droplet-binding proteins, such as Cidea and Cidec in the liver, leading to more substrates for fatty acid oxidation (FAO). Meanwhile, the expression of CPT1α, the rate-limiting enzyme of FAO, was significantly increased upon CP treatment. Mechanistically, though CP didn’t affect the total PPARα level, it promoted the nuclear localization of PPARα, which contributed to the reduced expression of Cidea and Cidec, and increased expression of CPT1α, leading to activated FAO. Moreover, whole body PPARα deficiency abolished the anti-NAFLD effect of CP, suggesting the importance of PPARα in CP-mediated beneficial effect.ConclusionThis study revealed the hypoglycemic and hepatoprotective effect of CP by regulating gut microbiota composition and PPARα subcellular localization, highlighting its potential for therapeutic candidate for metabolic disorders.

Marine algae oils from Phaeodactylum tricornutum and Laminaria japonica alleviate obesity, insulin resistance, and gut microbiota dysbiosis in high-fat diet-fed mice

The present study was aimed to investigate the effects of Phaeodactylum tricornutum oil (PO) and Laminaria japonica oil (LO) against obesity and other metabolic disorders in a high-fat diet (HFD) induced obese mouse model. The results revealed that PO or LO supplementation significantly reduced HFD-induced body weight gain, hyperlipemia, and fat accumulation in mice. PO or LO supplementation also inhibited SREBP-1-mediated de novo lipogenesis and PPARγ-mediated adipogenesis, as well as enhanced PPARα-mediated fatty acid β-oxidation in the WAT and liver of HFD-fed mice. Moreover, PO or LO supplementation attenuated low-grade chronic inflammation, hyperglycemia and insulin resistance in obese mice. Furthermore, Dietary PO or LO also modulated HFD-induced gut microbiota dysbiosis and increased the SCFAs production. More importantly, our results also manifested that the ameliorative effect of PO and LO against HFD-induced obesity, IR and gut microbiota dysbiosis was comparable, but was superior than that of krill oil and fish oil.

Theabrownin as a Potential Prebiotic Compound Regulates Lipid Metabolism via the Gut Microbiota, Microbiota-Derived Metabolites, and Hepatic FoxO/PPAR Signaling Pathways.

The dysregulation of lipid metabolism poses a significant health threat, necessitating immediate dietary intervention. Our previous research unveiled the prebiotic-like properties of theabrownin. This study aimed to further investigate the theabrownin-gut microbiota interactions and their downstream effects on lipid metabolism using integrated physiological, genomic, metabolomic, and transcriptomic approaches. The results demonstrated that theabrownin significantly ameliorated dyslipidemia, hepatic steatosis, and systemic inflammation induced by a high-fat/high-cholesterol diet (HFD). Moreover, theabrownin significantly improved HFD-induced gut microbiota dysbiosis and induced significant alterations in microbiota-derived metabolites. Additionally, the detailed interplay between theabrownin and gut microbiota was revealed. Analysis of hepatic transcriptome indicated that FoxO and PPAR signaling pathways played pivotal roles in response to theabrownin-gut microbiota interactions, primarily through upregulating hepatic Foxo1, Prkaa1, Pck1, Cdkn1a, Bcl6, Klf2, Ppara, and Pparg, while downregulating Ccnb1, Ccnb2, Fabp3, and Plin1. These findings underscored the critical role of gut-liver axis in theabrownin-mediated improvements in lipid metabolism disorders and supported the potential of theabrownin as an effective prebiotic compound for targeted regulation of metabolic diseases.

Dietary intake of whole king oyster mushroom (Pleurotus eryngii) attenuated obesity via ameliorating lipid metabolism and alleviating gut microbiota dysbiosis

There is a growing interest in employing whole food-based strategies to prevent chronic diseases, owing to the potential synergistic interactions among various bioactive components found within whole foods. The current research aimed to determine inhibitory effects of the whole edible mushroom Pleurotus eryngii (WPE) on high-fat diet (HFD)-induced obesity in mice. Our results showed that dietary intake of WPE significantly inhibited the abnormal gain of body weight and adipose tissue weight, improved glucose tolerance, and ameliorated the serum biochemical parameters in HFD-fed mice. The histological analysis illustrated that the severity of non-alcoholic fatty liver induced by HFD was significantly reduced by WPE. Oral intake of WPE profoundly modulated the mRNA levels of hepatic genes involved in lipid metabolism and also increased the level of short-chain fatty acids in the mouse cecum. Moreover, WPE alleviated the HFD-induced gut microbiota dysbiosis, increasing the abundance of beneficial bacteria (Akkermansia, Lactobacillus, Bifidobacterium, and Sutteralla), and decreasing the harmful ones (rc4-4, Dorea, Coprococcus, Oscillospira, and Ruminococcus). These findings presented new evidence supporting that WPE could be used as a whole food-based strategy to protect against obesity and obesity-driven health problems.

Construction of nanoparticles from blueberry anthocyanins-lecithin/gum Arabic improves lipid droplet accumulation and gut microbiota disturbance in HFD-induced obese mice

The digestive instability of anthocyanins (ACNs) limits their application in food nutrition, especially precision nutrition. Blueberry ACNs-loaded nanoparticles (Lipo/GA-ACNs NPs) were prepared using gum arabic (GA) as the delivery carrier and liposomal vesicles (Lipo) prepared from soy lecithin as the targeting scaffold. The average particle size of the NPs was 99.4 nm, and the polydispersion index (PDI) was 0.46. The results showed that the presence of the Lipo-GA matrix enhanced the NPs' in vitro stability and antioxidant activity. In addition, the in vitro biocompatibility, uptake ability, lipid-lowering activity, and free-radical scavenging ability were improved to a certain extent. In a high-fat diet (HFD)-induced obese mouse model, oral administration of ACNs-LNP (LNP, liver-targeted nanoparticle) showed better effects on body weight, liver injury, and lipid droplet accumulation in the liver than ACNs. In addition, ACNs-LNP also played a role in regulating HFD-induced gut microbiota imbalance. These results provide a promising ACNs delivery strategy with the potential to be developed into a functional food that targets the liver to prevent fatty liver.

Amelioration of obesity and inflammation by polysaccharide from unripe fruits of raspberry via gut microbiota regulation

Raspberry, a traditional medicine food homology species, has important benefits in patients with metabolic syndrome. However, the mechanism of raspberry polysaccharides (RP) on obesity remains unclear. In our study, we showed that RP intervention is negatively associated with body weight gain, hyperlipidemia, inflammation, and fat accumulation in obese mice. RP ameliorated HFD-induced gut microbiota dysbiosis, produced short-chain fatty acids, maintained intestinal barrier integrity, and prevented metabolic endotoxemia, manifested by decreased host lipopolysaccharide level, and increased colon expression of tight junction proteins. These effects might be related with driven by a SCFAs-producing bacterium and downregulation of TLR4/NF-κB signaling transduction. Notably, the abundance of Ruminococcaceae_UCG − 014, Lactobacillus taiwanensis, Bifidobacterium pseudolongum, and Turicibacter are markedly correlated with enhanced intestinal barrier function induced by RP treatment. Thus, we believe that RP could be as a potential health supplement or prebiotic for obesity therapy.

Pomelo peel dietary fiber ameliorates alterations in obesity-related features and gut microbiota dysbiosis in mice fed on a high-fat diet

Pomelo peel has abundance of dietary fiber and various biological activities but is often discarded as waste. This study evaluated the biological activities of pomelo peel dietary fiber (PPDF) in preventing obesity and regulating intestinal microbiota in obese mouse model induced using a high-fat diet (HFD). As for the composition, the prepared PPDF contained 89.64% of total dietary fiber, 53.27% of insoluble dietary fiber, and 36.37% of soluble dietary fiber. PPDF treatment significantly reduced weight gain and fat accumulation in the liver and epididymal tissues of obese mice; significantly alleviated HFD-induced dyslipidemia; and restored the levels of triglycerides, low-density lipoprotein–cholesterol, and high-density lipoprotein–-cholesterol to control levels, and the PPDF 5% dose restored total cholesterol to the control level. Furthermore, PPDF ameliorated HFD-induced gut microbiota dysbiosis by increasing intestinal microbial diversity, decreasing the Firmicutes/Bacteroidetes ratio, increasing beneficial bacteria (Bifidobacterium, Alloprevotella, and Lactobacillus), and decreasing harmful bacteria (Staphylococcus and Corynebacterium_1). This study provided a new idea to use PPDF as functional food to prevent obesity, alleviate dyslipidemia, or a potential probiotic to ameliorate gut microbiota dysbiosis.

Orm2 Deficiency Aggravates High-Fat Diet-Induced Obesity through Gut Microbial Dysbiosis and Intestinal Inflammation.

Orosomucoid 2 (Orm2) is a hepatocyte-secreted protein that plays a crucial role in regulating obesity-type metabolic disease and immunity. The imbalance of gut microbiota is one of the causes of obesity, but the mechanism of the relationship between Orm2 and gut microbiota in obesity remains unclear. Orm2-/- (Orm2 knockout) mice on a normal diet developed spontaneous obesity and metabolic disturbances at the 20th week. Through 16S rRNA gene sequencing, the study finds that the gut microbiota of Orm2-/- mice has a different microbial composition compared to wild type (WT) mice. Furthermore, a high-fat diet (HFD) for 16 weeks exacerbates obesity in Orm2-/- mice. Lack of Orm2 promotes dysregulation of gut microbiota under the HFD, especially a reduction of Clostridium spp. Supplementation with Clostridium butyricum alleviates obesity and alters the gut microbial composition in WTmice, but has minimal effects on Orm2-/- mice. In contrast, co-housing of Orm2-/- mice with WT mice rescues Orm2-/- obesity by reducing pathogenic bacteria and mitigating intestinal inflammation. These findings suggest Orm2 deficiency exacerbates HFD-induced gut microbiota disturbance and intestinal inflammation, providing a novel insight into the complex bacterial flora but not a single probiotic administration in the therapeutic strategy of obesity.

Alterations of gut microbiome and metabolism induced by inulin associated with weight loss in obese female mice

Our previous work revealed the microbiota-dependent beneficial effects of inulin in obese male mice, but the effects in obese female mice were not determined. High-fat diet (HFD)-induced obese female mice were switched to normal diets and gavaged with normal saline or inulin for 10 weeks. Inulin supplementation significantly accelerated weight loss and reversed HFD-induced gut microbiota dysbiosis in obese female mice, and also reduced the ratio of Firmicutes/Bacteroidetes and enriched the abundance of norank_f_Muribaculaceae and Alistipes. In addition, 52 key serum metabolites were distinctly altered after inulin supplementation. Among them, andrographolide and monoacylglycerols (18:4) increased more than 9-fold and 14-fold, respectively, while phosphatidylcholine (PC) (18:1e/2:0), PC (20:1/20:2) and PC (19:1/19:1) decreased. In conclusion, gut microbiota and metabolites were closely associated with the beneficial effects of inulin in accelerating weight loss in obese female mice.

High-fat diet-induced gut microbiota alteration promotes lipogenesis by butyric acid/miR-204/ACSS2 axis in chickens

The gut microbiota is known to have significant involvement in the regulation of lipogenesis and adipogenesis, yet the mechanisms responsible for this relationship remain poorly understood. The current study aims to provide insight into the potential mechanisms by which the gut microbiota modulates lipogenesis in chickens. Using chickens fed with a normal-fat diet (NFD, n=5) and high-fat diet (HFD, n=5), we analyzed the correlation between gut microbiota, cecal metabolomics, and lipogenesis by 16s rRNA sequencing, miRNA and mRNA sequencing as well as targeted metabolomics analysis. The potential metabolite/miRNA/mRNA axis regulated by gut microbiota was identified using chickens treated with antibiotics (ABX, n=5). The possible mechanism of gut microbiota regulating chicken lipogenesis was confirmed by fecal microbiota transplantation (FMT) from chickens fed with NFD to chickens fed with HFD (n=5). The results showed that HFD significantly altered gut microbiota composition and enhanced chicken lipogenesis, with a significant correlation between 3. Furthermore, HFD significantly altered the hepatic miRNA expression profiles and reduced the abundance of hepatic butyric acid. Procrustes analysis indicated that the HFD-induced dysbiosis of the gut microbiota might affect the expression profiles of hepatic miRNA. Specifically, HFD-induced gut microbiota dysbiosis may reduce the abundance of butyric acid and downregulate the expression of miR-204 in the liver. Multiomics analysis identified ACSS2 as a target gene of miR-204. Gut microbiota depletion by an antibiotic cocktail (ABX) showed a gut microbiota-dependent manner in the abundance of butyric acid and the expression of miR-204/ACSS2, which have been observed to be significantly correlated. Fecal microbiota transplantation from NFD chickens into HFD chickens effectively attenuated the HFD-induced excessive lipogenesis, elevated the abundance of butyric acid and the relative expression of miR-204, and reduced the expression of ACSS2 in the liver. Mechanistically, our results showed that the gut microbiota plays an antiobesity role by regulating the butyric acid/miR-204/ACSS2 axis in chickens. This work contributed to a better understanding of the functions of gut microbiota in regulating chicken lipogenesis.

MicroRNA-29a Compromises Hepatic Adiposis and Gut Dysbiosis in High Fat Diet-Fed Mice via Downregulating Inflammation.

miR-29a expression patterns influence numerous physiological phenomena. Of note, upregulation of miR-29a ameliorates high-fat diet (HFD)-induced liver dysfunctions in mice. However, the miR-29a effect on gut microbiome composition and HFD-induced gut microbiota changes during metabolic disturbances remains unclear. We provide compelling evidence for the protective role of miR-29a in gut barrier dysfunction and steatohepatitis. We bred miR-29a overexpressed mice (miR-29aTg) to characterize intestinal, serum biochemical, and fecal microbiota profiling features compared to wild-type mice (WT). Mice were fed an HFD for 8 months to induce steatohepatitis, and intestinal dysfunction was determined via histopathological analysis. miR-29aTg had better lipid metabolism capability that decreased total cholesterol and triglyceride levels in serum than WT of the same age. We further demonstrated that miR-29aTg contributes to intestinal integrity by maintaining periodic acid Schiff positive cell numbers and diversity of fecal microorganisms. HFD-induced bacterial community disturbance and steatohepatitis resulted in more severe WT than miR-29aTg. Gut microorganism profiling revealed Lactobacillus, Ruminiclostridium_9, and Lachnoclostridium enrichment in miR-29aTg and significantly decreased interleukin-6 expression in the liver and intestinal tract. This study provides new evidence that sheds light on the host genetic background of miR-29a, which protects against steatohepatitis and other intestinal disorders. This article is protected by copyright. All rights reserved.

Perilla, sunflower, and tea seed oils as potential dietary supplements with anti-obesity effects by modulating the gut microbiota composition in mice fed a high-fat diet.

Obesity has become a serious public health problem with its alarmingly increasing prevalence worldwide, prompting researchers to create and develop several anti-obesity drugs. Here, we aimed to investigate the protective effects of perilla seed oil (PSO), sunflower oil (SFO), and tea seed oil (TSO) against obesity through the modulation of the gut microbiota composition and related metabolic changes in mice fed a high-fat diet (HFD). Mice were divided into six equal groups: ND (normal diet); HFD; ORL (HFD supplemented with 20mg/kg body weight of orlistat); PSO, SFO, and TSO (HFD supplemented with 2g/kg body weight of PSO, SFO, and TSO, respectively). Our findings showed that PSO, SFO, and TSO supplementation significantly reduced body weight, organ weight, blood glucose, lipopolysaccharides (LPS), insulin resistance, and improved serum lipid levels (TG, TC, LDL-C, and HDL-C). Meanwhile, the three treatments alleviated oxidative stress and hepatic steatosis and reduced liver lipid accumulation. Relative mRNA expression levels of inflammatory cytokines (TNF-α, IL-1β, IL-6, and MCP-1) and lipid synthesis-related genes (PPAR-γ, FAS, and SREBP-1) were down-regulated, while β-oxidation-related genes (PPAR-α, CPT1a, and CPT1b) were up-regulated in the liver tissue of treated mice. Besides, dietary oil supplementation alleviated HFD-induced gut microbiota dysbiosis by promoting gut microbiota richness and diversity, decreasing the Firmicutes-to-Bacteroidetes ratio, and boosting the abundance of some healthy bacteria, like Akkermansia. PSO, SFO, and TSO supplementation could alleviate inflammation, oxidative stress, and hepatic steatosis, likely by modulating the gut microbiota composition in HFD-fed mice.

Tibetan highland barley fiber improves obesity and regulates gut microbiota in high-fat diet-fed mice

Tibetan highland barley fiber (T-Fiber) contains high dietary fiber (DF) and beta-glucose. Highland barley has been shown to reduce the risk of diseases associated with high-fat diets (HFD). In the present research, we studied whether T-Fiber could ameliorate HFD-induced obesity in mice and explored its regulatory effects on intestinal microbes. Our findings revealed that T-Fiber feeding significantly reduced weight gain and dyslipidemia, improved glucose tolerance and insulin resistance, alleviated chronic systemic inflammation, and increased short-chain fatty acids (SCFA) in feces in mice. Histological observations confirmed that T-Fiber alleviated Epididymal fat (EF) and lipid accumulation in the liver. In addition, 16s rRNA sequencing analysis of mice cecum contents showed that T-Fiber restored the HFD-induced gut microbiota. T-Fiber supplementation increased the abundance of potentially beneficial bacteria Muribaculaceae, Akkermansiaceae, and Lachnospiraceae_NK4A136_groups, while significantly reducing the abundance of Bacteroidaceae, Prevotellaceae, Rikenellaceae, and Alloprevotella. Furthermore, the increase in the production of SCFA may be related to the abundance of Lachnospiraceae_NK4A136_group. In conclusion, T-Fiber has some anti-obesity abilities under high-fat feeding and can be developed as a relevant anti-obesity product.

Vitamin D alleviates non-alcoholic fatty liver disease via restoring gut microbiota and metabolism.

Non-alcoholic fatty liver disease (NAFLD) represents a severe public health problem. Dysbiosis of gut microbiome has been identified as one of the key environmental factors contributing to NAFLD. As an essential nutrition, Vitamin D (VD) plays an important role in regulating gut microbiota based on its receptor (Vitamin D Receptor, VDR) which is highly expressed in the gastrointestinal tract. Rats were fed with HFD (high-fat diet) for 12 weeks. And the rats were treated with VD two times a week by intraperitoneal injection for 12 weeks. H&E staining combined with plasma biochemical index was performed to characterize pathological changes and function of the liver. Fecal microbiota 16S rRNA gene sequencing and metabolomics were taken to reveal the altered gut microbiota and metabolites. The VD alleviates the HFD-induced lipid accumulation in the liver as well as decreases the levels of amlodipine besylate (ALT) and amlodipine aspartate (AST). VD supplement decreased the ratio of phylum Firmicutes/Bacteroidetes (F/B) but increased alpha diversity. In addition, the VD treatment improved the HFD-induced gut microbiota by increasing the Prevotella and Porphyromonadaceae and decreasing Mucispirillum, Acetatifactor, Desulfovibrio, and Oscillospira abundance. Furthermore, the capability of tyrosine metabolism, tryptophan metabolism, arginine biosynthesis, and sphingolipid metabolism was enhanced after VD treatment. Consistently, Prevotella positively correlated with tryptophan metabolism and sphingolipid metabolism. Importantly, the Prevotella abundance was positively associated with serotonin, melatonin, tryptamine, L-arginine, and 3-dehydrosphinganine which synthesize from tryptophan, tyrosine, arginosuccinate, and serine, respectively. VD treatment inhibited HFD-induced NAFLD accompany by dysbiosis gut microbiota and metabolites, suggesting that VD supplement could be a potential intervention used for NAFLD treatment by targeting the specific microbiota.