Abstract:BackgroundCoffee can regulate glucose homeostasis but the underlying mechanism is unclear. This study investigated the preventive and therapeutic effects of chlorogenic acid (CGA), a polyphenol that is found in coffee, on obesity and obesity-related metabolic endotoxemia.MethodMale 4-week-old C57BL/6 mice were fed either normal chow or a high-fat diet or 20 weeks and half the mice in each group were gavaged with CGA. Oral glucose tolerance tests (OGTTs) and insulin tolerance tests (ITTs) were performed. Marker… Show more
“…In our study, Ruminococcaceae were remarkably increased in Lepr −/− rats via LWE intervention. In addition, Faecalibaculum is a group of gram-positive obligate anaerobe that can produce short-chain fatty acids, more specifically butyrate, through fermentation [ 56 , 57 ]. Intestinimonas is a representative genus producing butyrate [ 58 ].…”
Metabolic syndrome is a chronic metabolic disorder that has turned into a severe health problem worldwide. A previous study reported that large yellow tea exhibited better anti-diabetic and lipid-lowering effects than green tea. Nevertheless, the potential mechanisms are not yet understood. In this study, we examined the prevention effects and mechanisms of large yellow tea water extract (LWE) on metabolic syndrome using leptin receptor knockout (Lepr−/−) rats. Seven-week-old male Lepr−/− and wild type (WT) littermate rats were divided into Lepr−/− control group (KO) (n = 5), Lepr−/− with LWE-treated group (KL) (n = 5), WT control group (WT) (n = 6), and WT with LWE intervention group (WL) (n = 6). Then, the rats were administered water or LWE (700 mg/kg BW) daily by oral gavage for 24 weeks, respectively. The results showed that the administration of LWE significantly reduced the serum concentrations of random blood glucose, total cholesterol, triglyceride, and free fatty acids, and increased glucose tolerance in Lepr−/− rats. Moreover, LWE remarkably reduced hepatic lipid accumulation and alleviated fatty liver formation in Lepr−/− rats. A mechanistic study showed that LWE obviously activated SIRT6 and decreased the expression of key lipogenesis-related molecules SREBP1, FAS, and DGAT1 in the livers of Lepr−/− rats. Furthermore, LWE significantly improved microbiota dysbiosis via an increase in gut microbiota diversity and an abundance of the microbiota that produce short chain fatty acids (SCFAs), such as Ruminococcaceae, Faecalibaculum, Intestinimonas, and Alistipes. Finally, LWE supplementation increased the concentrations of SCFAs in the feces of Lepr−/− rats. These results revealed that LWE attenuated metabolic syndrome of Lepr−/− rats via the reduction of hepatic lipid synthesis through the SIRT6/SREBP1 pathway and the modulation of gut microbiota.
“…In our study, Ruminococcaceae were remarkably increased in Lepr −/− rats via LWE intervention. In addition, Faecalibaculum is a group of gram-positive obligate anaerobe that can produce short-chain fatty acids, more specifically butyrate, through fermentation [ 56 , 57 ]. Intestinimonas is a representative genus producing butyrate [ 58 ].…”
Metabolic syndrome is a chronic metabolic disorder that has turned into a severe health problem worldwide. A previous study reported that large yellow tea exhibited better anti-diabetic and lipid-lowering effects than green tea. Nevertheless, the potential mechanisms are not yet understood. In this study, we examined the prevention effects and mechanisms of large yellow tea water extract (LWE) on metabolic syndrome using leptin receptor knockout (Lepr−/−) rats. Seven-week-old male Lepr−/− and wild type (WT) littermate rats were divided into Lepr−/− control group (KO) (n = 5), Lepr−/− with LWE-treated group (KL) (n = 5), WT control group (WT) (n = 6), and WT with LWE intervention group (WL) (n = 6). Then, the rats were administered water or LWE (700 mg/kg BW) daily by oral gavage for 24 weeks, respectively. The results showed that the administration of LWE significantly reduced the serum concentrations of random blood glucose, total cholesterol, triglyceride, and free fatty acids, and increased glucose tolerance in Lepr−/− rats. Moreover, LWE remarkably reduced hepatic lipid accumulation and alleviated fatty liver formation in Lepr−/− rats. A mechanistic study showed that LWE obviously activated SIRT6 and decreased the expression of key lipogenesis-related molecules SREBP1, FAS, and DGAT1 in the livers of Lepr−/− rats. Furthermore, LWE significantly improved microbiota dysbiosis via an increase in gut microbiota diversity and an abundance of the microbiota that produce short chain fatty acids (SCFAs), such as Ruminococcaceae, Faecalibaculum, Intestinimonas, and Alistipes. Finally, LWE supplementation increased the concentrations of SCFAs in the feces of Lepr−/− rats. These results revealed that LWE attenuated metabolic syndrome of Lepr−/− rats via the reduction of hepatic lipid synthesis through the SIRT6/SREBP1 pathway and the modulation of gut microbiota.
“…Frontiers in Microbiology frontiersin.org promising probiotics (Romano et 2021;Ye et al, 2021). Meanwhile, significant increases in Lachnospiraceae_NK4A136_ group (genus) and Firmicutes_bacterium_M10-2 (species) were also highlighted in the KO group compared with the WT group.…”
Section: Discussionmentioning
confidence: 95%
“…Similarly, when compared with WPbA, the biomarkers for KPbA included significantly increased Faecalibaculum (Faecalibaculum rodentium) and Dubosiell and decreased Akkermansia (Akkermansia_ muciniphila). Interestingly, these three genera/species microbiota were all beneficial for the production of short-chain fatty acids (SCFAs; Shen et al, 2021;Ye et al, 2021), which, as one of the safeguards for maintaining gut health, plays an important role in strengthening epithelial barrier integrity and inhibiting inflammation. However, a previous study found that oral administration of F. rodentium in antibiotic-treated resilient Ephx2 KO mice led to depression-like behaviors (Wang et al, 2021).…”
Cerebral malaria (CM), as one of the most common complications in severe malaria, has threatened millions of individuals’ neurological health and even their lives. Macrophage migration inhibitory factor (MIF), a pleiotropic proinflammatory factor in humans, seems to be a risk factor for death in patients with CM, but its functional mechanism remains unclear. To verify whether affecting the intestinal microbes of the host was one of the mechanisms by which MIF regulates CM, C57BL/6 mice, including WT + PbA, MIF-KO + PbA and their uninfected controls, were sent for 16S rRNA-based sequencing targeting the V4 region of the intestinal microbiota through the Illumina MiSeq platform. The results showed that OTU clustering, alpha and beta diversity in the four groups involved had evident variation. The relative abundance at different taxonomic levels, especially the dominant intestinal flora, was obviously changed. The LEfSe analysis screened out several biomarkers, including significantly reduced Ligilactobacillus (Lactobacillus murinus) in WPbA mice compared to the WT group and Akkermansia (Akkermansia_muciniphila) in KPbA mice compared to the WPbA group. For MIF KO groups, mice infected with PbA or uninfected showed significant enrichment of producers of short-chain fatty acids, including Dubosiella and Faecalibaculum (Faecalibaculum rodentium) in KPbA, and Lachnospiraceae_NK4A136_group and Firmicutes_bacterium_M10-2 in KO. This study not only further proved the gut microbiota changes in C57BL/6 mice caused by PbA infection, but also found that MIF deletion directly affected the changes in the gut microbiota of C57BL/6 mice before and after PbA infection. This finding reveals a potential mechanism by which MIF regulates CM. Combining MIF with potential microbial biomarkers will provide a promising idea to develop combined drugs for improving CM in the future.
“…Genus Dubosiella is a member of shortchain fatty acid (SCFA) producers (Mao et al, 2019;Bojovic et al, 2020). A previous study showed that chlorogenic acid increased the abundance of Dubosiella and improved metabolic endotoxemia (Ye et al, 2021). In contrast, the protective effects of yellow wine polyphenolic compounds were associated with a lower abundance of Dubosiella in Dox-treated rats (Lin et al, 2021).…”
ObjectivesDoxorubicin (Dox), a chemotherapeutic anthracycline agent for the treatment of a variety of malignancies, has a limitation in clinical application for dose-dependent cardiotoxicity. The purpose of this study was to explore the relationship between the composition/function of the gut microbiota and Dox-induced cardiotoxicity (DIC).MethodsC57BL/6J mice were injected intraperitoneally with 15 mg/kg of Dox, with or without antibiotics (Abs) administration. The M-mode echocardiograms were performed to assess cardiac function. The histopathological analysis was conducted by H&E staining and TUNEL kit assay. The serum levels of creatine kinase (CK), CK-MB (CK-MB), lactic dehydrogenase (LDH), and cardiac troponin T (cTnT) were analyzed by an automatic biochemical analyzer. 16S rRNA gene and metagenomic sequencing of fecal samples were used to explore the gut microbiota composition and function.Key FindingsDox caused left ventricular (LV) dilation and reduced LV contractility. The levels of cardiomyocyte apoptosis and myocardial enzymes were elevated in Dox-treated mice compared with the control (Con) group. 16S rRNA gene sequencing results revealed significant differences in microbial composition between the two groups. In the Dox group, the relative abundances of Allobaculum, Muribaculum, and Lachnoclostridium were significantly decreased, whereas Faecalibaculum, Dubosiella, and Lachnospiraceae were significantly increased compared with the Con group at the genus level. Functional enrichment with Cluster of orthologous groups of proteins (COG) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses showed that the Dox mice displayed different clusters of cellular processes and metabolism from the Con mice. The different species and their functions between the two groups were associated with the clinical factors of cardiac enzymes. Moreover, depletion of the gut microbiota could alleviate Dox-induced myocardial injury and cardiomyocyte apoptosis.ConclusionsThe study here shows that composition imbalance and functional changes of the gut microbiota can be one of the etiological mechanisms underlying DIC. The gut microbiota may serve as new targets for the treatment of cardiotoxicity and cardiovascular diseases.
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