A diet high in sugar and fat influences neurotransmitter metabolism and then affects brain function by altering the gut microbiota.
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ABSTRACT:
SUBMITTER: Guo Y
PROVIDER: S-EPMC8160265 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Multiple lines of evidence suggest that the gut microbiota plays vital roles in metabolic diseases such as hyperlipidemia. Previous studies have confirmed that krill oil can alleviate hyperlipidemia, but the underlying mechanism remains unclear. To discern whether krill oil changes the structure of the gut microbiota during the hyperlipidemia treatment, 72 mice were acclimatized with a standard chow diet for 2 weeks and then randomly allocated to receive a standard chow diet (control group, n = 12) or a high-sugar-high-fat (HSHF) diet supplemented with a low (100 μg/g·d, HSHF+LD group, n = 12), moderate (200 μg/g·d, HSHF+MD group, n = 12) or high dosage of krill oil (600 μg/g·d, HSHF+HD group, n = 12), simvastatin (HSHF+S group, n = 12) or saline (HSHF group, n = 12) continuously for 12 weeks. The resulting weight gains were attenuated, the liver index and the low-density lipoprotein, total cholesterol and triglyceride concentrations showed a stepwise reduction in the treated groups compared with those of the control group. A dose-dependent modulation of the gut microbiota was observed after treatment with krill oil. Low- and moderate- doses of krill oil increased the similarity between the composition of the HSHF diet-induced gut microbiota and that of the control, whereas the mice fed the high-dose exhibited a unique gut microbiota structure that was different from that of the control and HSHF groups. Sixty-five key operational taxonomic units (OTUs) that responded to the krill oil treatment were identified using redundancy analysis, of which 26 OTUs were increased and 39 OTUs were decreased compared with those of the HSHF group. In conclusion, the results obtained in this study suggest that the structural alterations in the gut microbiota induced by krill oil treatment were dose-dependent and associated with the alleviation of hyperlipidemia. Additionally, the high-dose krill oil treatment showed combined effects on the alleviation of hyperlipidemia and obesity.
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Project description:Background:Gut microbiota dysbiosis has been linked to obesity-associated chronic inflammation. Microbiota manipulation may therefore affect obesity-related comorbidities. Blueberries are rich in anthocyanins, which have anti-inflammatory properties and may alter the gut microbiota. Objective:We hypothesized that blueberry supplementation would alter the gut microbiota, reduce systemic inflammation, and improve insulin resistance in high-fat (HF)-diet-fed rats. Methods:Twenty-four male Wistar rats (260-270 g; n = 8/group) were fed low-fat (LF; 10% fat), HF (45% fat), or HF with 10% by weight blueberry powder (HF_BB) diets for 8 wk. LF rats were fed ad libitum, whereas HF and HF_BB rats were pair-fed with diets matched for fiber and sugar contents. Glucose tolerance, microbiota composition (16S ribosomal RNA sequencing), intestinal integrity [villus height, gene expression of mucin 2 (Muc2) and ?-defensin 2 (Defb2)], and inflammation (gene expression of proinflammatory cytokines) were assessed. Results:Blueberry altered microbiota composition with an increase in Gammaproteobacteria abundance (P < 0.001) compared with LF and HF rats. HF feeding led to an ?15% decrease in ileal villus height compared with LF rats (P < 0.05), which was restored by blueberry supplementation. Ileal gene expression of Muc2 was ?150% higher in HF_BB rats compared with HF rats (P < 0.05), with expression in the LF group not being different from that in either the HF or HF_BB groups. Tumor necrosis factor ? (Tnfa) and interleukin 1? (Il1b) gene expression in visceral fat was increased by HF feeding when compared with the LF group (by 300% and 500%, respectively; P < 0.05) and normalized by blueberry supplementation. Finally, blueberry improved markers of insulin sensitivity. Hepatic insulin receptor substrate 1 (IRS1) phosphorylation at serine 307:IRS1 ratio was ?35% higher in HF rats compared with LF rats (P < 0.05) and HF_BB rats. Conclusion:In HF-diet-fed male rats, blueberry supplementation led to compositional changes in the gut microbiota associated with improvements in systemic inflammation and insulin signaling.
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Project description:Allicin, naturally present in the bulbs of the lily family, has anticancer, blood pressure lowering, blood fat lowering and diabetes improving effects. Recent studies have shown that allicin promotes the browning of white adipocytes and reduces the weight gain of mice induced by high-fat diet. While the gut microbiota has a strong relationship with obesity and energy metabolism, the effect of allicin on weight loss via gut microorganisms is still unclear. In this study, we treated obese mice induced by high-fat diet with allicin to determine its effects on fat deposition, blood metabolic parameters and intestinal morphology. Furthermore, we used high-throughput sequencing on a MiSeq Illumina platform to determine the gut microorganisms' species. We found that allicin significantly reduced the weight gain of obese mice by promoting lipolysis and thermogenesis, as well as blood metabolism and intestinal morphology, and suppressing hepatic lipid synthesis and transport. In addition, allicin changed the composition of the intestinal microbiota and increased the proportion of beneficial bacteria. In conclusion, our study showed that allicin improves metabolism in high-fat induced obese mice by modulating the gut microbiota. Our findings provide a theoretical basis for further elucidation of the weight loss mechanism of allicin.
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Project description:Obesity is associated with gastrointestinal (GI) tract and central nervous system (CNS) disorders. High-fat diet (HFD) feeding-induced obesity in mice induces dysbiosis, causing a shift toward bacteria-derived metabolites with detrimental effects on metabolism and inflammation: events often contributing to the onset and progression of both GI and CNS disorders. Palmitoylethanolamide (PEA) is an endogenous lipid mediator with beneficial effects in mouse models of GI and CNS disorders. However, the mechanisms underlining its enteroprotective and neuroprotective effects still need to be fully understood. Here, we aimed to study the effects of PEA on intestinal inflammation and microbiota alterations resulting from lipid overnutrition. Ultramicronized PEA (30 mg/kg/die per os) was administered to HFD-fed mice for 7 weeks starting at the 12th week of HFD regimen. At the termination of the study, the effects of PEA on inflammatory factors and cells, gut microbial features and tryptophan (TRP)-kynurenine metabolism were evaluated. PEA regulates the crosstalk between the host immune system and gut microbiota via rebalancing colonic TRP metabolites. PEA treatment reduced intestinal immune cell recruitment, inflammatory response triggered by HFD feeding, and corticotropin-releasing hormone levels. In particular, PEA modulated HFD-altered TRP metabolism in the colon, rebalancing serotonin (5-HT) turnover and reducing kynurenine levels. These effects were associated with a reshaping of gut microbiota composition through increased butyrate-promoting/producing bacteria, such as Bifidobacterium, Oscillospiraceae and Turicibacter sanguinis, with the latter also described as 5-HT sensor. These data indicate that the rebuilding of gut microbiota following PEA supplementation promotes host 5-HT biosynthesis, which is crucial in regulating intestinal function.
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Project description:Metabolic disorders and intestinal flora imbalance usually accompany obesity. Due to its diverse biological activities, Lactobacillus plantarum is widely used to alleviate various diseases as a probiotic. Here, we show that L. plantarum can reduce the body weight of mice fed high-fat diets, reduce fat accumulation, and enhance mice glucose tolerance. Our results show that L. plantarum can significantly reduce the expression of DGAT1 and DGAT2, increase the expression of Cpt1a, and promote the process of lipid metabolism. Further data show that L. plantarum can increase the SCFA content in the colon and reverse the intestinal flora disorder caused by HFD, increase the abundance of Bacteroides, and Bifidobacteriales, and reduce the abundance of Firmicutes and Clostridiales. Finally, through Pearson correlation analysis, we found that Bacteroides and SCFAs are positively correlated, while Clostridiales are negatively correlated with SCFAs. Therefore, we believe that L. plantarum can regulate the structure of the intestinal microbial community, increase the production of SCFAs and thus regulate lipid metabolism.
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Project description:The intestinal microbiota is known to regulate host energy homeostasis and can be influenced by high-calorie diets. However, changes affecting the ecosystem at the functional level are still not well characterized. We measured shifts in cecal bacterial communities in mice fed a carbohydrate or high-fat (HF) diet for 12 weeks at the level of the following: (i) diversity and taxa distribution by high-throughput 16S ribosomal RNA gene sequencing; (ii) bulk and single-cell chemical composition by Fourier-transform infrared- (FT-IR) and Raman micro-spectroscopy and (iii) metaproteome and metabolome via high-resolution mass spectrometry. High-fat diet caused shifts in the diversity of dominant gut bacteria and altered the proportion of Ruminococcaceae (decrease) and Rikenellaceae (increase). FT-IR spectroscopy revealed that the impact of the diet on cecal chemical fingerprints is greater than the impact of microbiota composition. Diet-driven changes in biochemical fingerprints of members of the Bacteroidales and Lachnospiraceae were also observed at the level of single cells, indicating that there were distinct differences in cellular composition of dominant phylotypes under different diets. Metaproteome and metabolome analyses based on the occurrence of 1760 bacterial proteins and 86 annotated metabolites revealed distinct HF diet-specific profiles. Alteration of hormonal and anti-microbial networks, bile acid and bilirubin metabolism and shifts towards amino acid and simple sugars metabolism were observed. We conclude that a HF diet markedly affects the gut bacterial ecosystem at the functional level.
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Project description:Previous studies proved that heavy metals could increase the risk of disease by acting on the gut microbiota. Meanwhile, gut microbiota played important roles in detoxifying heavy metals. However, the response of gut microbiota to heavy metals and which microbes dominated this detoxification processes are still unclear. This study investigated the difference of high-fat-diet (HFD) and normal-diet (ND) gut microbiota and their response to and detoxification effects on arsenic (As), cadmium (Cd), and lead (Pb) exposure. Results showed that gut microbiota of ND and HFD was significantly different and responded to As, Pb, and Cd exposure differently, too. When exposed to 100 ppm As, Cd, or Pb, HFD-fed mice accumulated more heavy metals in the liver and kidney along with more severe functional damage than ND-fed mice, indicated by a more dramatic increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and urinary total protein (TPU), urinary uric acid (UUA), and urinary creatinine (Ucrea) content. Among ND gut microbiota, relative abundance of Bacteroides, Lactobacillus, Butyricimonas, and Dorea was significantly increased by arsenic (As) exposure; relative abundance of Faecoccus and Lactobacillus was significantly increased by Cd exposure; relative abundance of Desulfovibrio, Plasmodium, and Roseburia were significantly increased by Pb exposure. However, among HFD gut microbiota, those microbes were not significantly changed. Bivariate association analysis found weak positive correlations between content of fecal excreted heavy metals and richness of total fecal microbiota as well as abundance of some of the heavy metal-enriched microbes. Our study concluded that HFD increased disease risk of heavy metal exposure probably via its gut microbiota which excreted less heavy metal through feces.
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Project description:BACKGROUND:As the gut microbiota contributes to metabolic health, it is important to determine specific diet-microbiota interactions that influence host metabolism. Bile acids and dietary fat source can alter phenotypes of diet-induced obesity, but the interplay with intestinal microorganisms is unclear. Here, we investigated metabolic consequences of diets enriched in primary bile acids with or without addition of lard or palm oil, and studied gut microbiota structure and functions in mice. RESULTS:In combination with bile acids, dietary lard fed to male C57BL/6N mice for a period of 8 weeks enhanced fat mass accumulation in colonized, but not in germ-free mice when compared to palm oil. This was associated with impaired glucose tolerance, lower fasting insulin levels, lower counts of enteroendocrine cells, fatty liver, and elevated amounts of hepatic triglycerides, cholesteryl esters, and monounsaturated fatty acids. Lard- and bile acid-fed mice were characterized by shifts in dominant gut bacterial communities, including decreased relative abundances of Lachnospiraceae and increased occurrence of Desulfovibrionaceae and the species Clostridium lactatifermentans and Flintibacter butyricus. Metatranscriptomic analysis revealed shifts in microbial functions, including lipid and amino acid metabolism. CONCLUSIONS:Caution is required when interpreting data from diet-induced obesity models due to varying effects of dietary fat source. Detrimental metabolic consequences of a diet enriched with lard and primary bile acids were dependent on microbial colonization of the host and were linked to hepatic lipid rearrangements and to alterations of dominant bacterial communities in the cecum.
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Project description:Bamboo shoots (BS) have a variety of nutritional benefits; however, their anti-obesity effect and its underlying mechanism of action are still unclear. In this study, we investigated the protective effect of BS against high-fat diet (HFD)-induced gut dysbiosis in mice. After 12 weeks of feeding C57BL/6J mice either on a normal or an HFD with or without BS, metabolic indicators, including blood lipids and glucose tolerance, were measured. 16S rRNA gene sequencing and metabolomics were used to identify alterations in gut microbiota composition and fecal metabolic profiling. The results demonstrated that BS supplementation reduced body weight by 30.56%, mitigated liver damage, and improved insulin resistance and inflammation in obese mice. In addition, BS increased short-chain fatty acid (SCFA) levels and SCFA-producing bacteria (e.g., Lachnospiraceae_NK4A136_group and Norank_f_Muribaculaceae), and reduced levels of harmful bacteria (e.g., Blautia and Burkholderia-Paraburkholderia). Finally, BS increased many beneficial fecal metabolites, such as fatty acids and bile acids, which are highly relevant to the altered gut microbiota. Based on the modulatory effect of BS on microbiota composition and gut metabolite levels observed in this study, we suggest that BS may be beneficial in treating obesity and its related complications.
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