Gut Microbial Profile Changes in Patients with Gallbladder Stones after UDCA/CDCA Treatment

Lee, Jungnam; Lee, Sohee; Kim, Hanul; Bae, Jaewoong; Park, Jin-Seok

doi:10.3390/biomedicines11030777

Cited by 4 publications

(3 citation statements)

References 35 publications

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“…Excessive xanthin can cause hyperuricemia and then lead to NAFLD and NASH (Nishikawa et al, 2020). CDCA can be converted into secondary bile acids, such as deoxycholic acid (DCA), and regulate intestinal flora including Faecalibacterium, Roseburia, and Lachnospira, thus, interfering with NASH (Jiao et al, 2018;Lee et al, 2023). In our experiment, SA can maintain the metabolic balance by regulating metabolites such as xanthine, CDCA, and 3a,7a,12a-Trihydroxy-5b-cholestan-26al etc.…”

Section: Discussionmentioning

confidence: 79%

The alleviating effect of Scutellaria amoena extract on the regulation of gut microbiota and its metabolites in NASH rats by inhibiting the NLRP3/ASC/caspase-1 axis

Lin,

Fang,

et al. 2023

Front. Pharmacol.

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Background:Scutellaria amoena (SA) is the root of S. amoena C.H. Wright of Labiatae, also known as Scutellaria southwestern. This is mainly distributed in Sichuan, Yunnan, and Guizhou in China. In southwest China, SA is used as an alternative method to genuine medicine for the treatment of allergy, diarrhea, inflammation, hepatitis, and bronchitis. Thus far, studies on the effects of SA on non-alcoholic steatohepatitis (NASH) are lacking. This paper investigated the effect of SA on the regulation of gut microbiota and its metabolites in NASH rats by inhibiting the NOD-like receptor 3 (NLRP3)/apoptosis-associated speck-like protein (ASC)/caspase-1 axis.Methods: A NASH rat model was induced by a high-fat diet (HFD) for 12 weeks, and rats were orally given different doses of SA extracts (150 and 300 mg/kg/d) for 6 weeks. Changes in histological parameters, body weight, organ indexes, cytokines, and biochemical parameters related to NLRP3 in NASH rats were checked. 16S rRNA gene sequencing and UPLC-MS/MS technology were used to analyze the changes in the gut microbiota composition and its metabolites in NASH rats.Results: SA significantly inhibited the HFD-induced increase in body weight, lipid levels, and inflammatory infiltration. SA notably inhibited the HFD-induced increase in the upper and lower factors of NLRP3, such as transforming growth factor (TGF)-β, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-18, pro-IL-18, IL-1β, pro-IL-1β, NLRP3, ASC, and caspase-1. Additionally, mRNA expressions of caspase-1, NLRP3, and ASC were significantly downregulated after SA treatment. The results of the intestinal flora showed that SA could increase the diversity of flora and change its structure and composition in NASH rats by reducing Firmicutes/Bacteroidetes (F/B) ratio, Blautia (genus), Lachospiraceae (family), and Christensenellaceae R-7 group (genus), and increasing Muribaculaceae (family) and Bacteroides (genus). The metabolomics revealed that 24 metabolites were possibly the key metabolites for SA to regulate the metabolic balance of NASH rats, including chenodeoxycholic acid, xanthine, and 9-OxoODE. Nine metabolic pathways were identified, including primary bile acid biosynthesis, bile secretion, purine metabolism, and secondary bile acid biosynthesis.Conclusion: SA can regulate the intestinal microbial balance and metabolic disorder by inhibiting the NLRP3/ASC/caspase-1 axis to relieve NASH.

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Section: Discussionmentioning

confidence: 79%

The alleviating effect of Scutellaria amoena extract on the regulation of gut microbiota and its metabolites in NASH rats by inhibiting the NLRP3/ASC/caspase-1 axis

Lin,

Fang,

et al. 2023

Front. Pharmacol.

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“…Other side, SPBs, such as UDCA, DCA and especially LCA, were decreased under high-sucrose condition. UDCA, usually is used for treating cholestatic liver disease with its ability to promote the secretion of bile aids 44 . Recently, a famous study found that UDCA could protect from SARS-CoV-2 infection by reducing ACE2 45 .…”

Section: Discussionmentioning

confidence: 99%

Long-time high-sucrose intake induced metabolic dysfunction via disrupting the balance of intestinal microenvironment

Wang,

Li,

Zhang

et al. 2024

Preprint

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Sucrose, a common sweeter, is frequently added to drink and food, and excess intake of sucrose is really harmful to our health. This study aimed to reveal the potential mechanisms of high-sucrose induced metabolic dysfunction. Sixty mice were divided into two groups, respectively, the normal group (Nor group) and high-sucrose group (HS group). 16S rDNA and untargeted metabolomics technologies were used to analyzed the dynamic changes of gut microbiota and metabolites in colon contents of young mice, middle age mice and old mice. Long-time high-sucrose intake induced fat deposition and metabolic disorder, along with a completely different gut microbiota map. The energy metabolism related gene expression of the gut microbiome was downregulated, but potential pathogen gene expression was upregulated by long-time high-sucrose intake. Furthermore, mice in the HS were utilized less amino acids and long chain fatty acids, with effecting tryptophan metabolism by producing less indole, more 5-HT and kynurenine. Also less secondary bile acids, and more TMA/TMAO were produced by gut microbes in HS group. These results demonstrated that long-time high-sucrose intake leads to fat deposition and metabolic disorder via disrupting the balance of intestinal microenvironment.

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“…These aspects were also associated with an important increase in the secondary BAs from the enterohepatic cycle. The authors suggested that some bacteria, such as Ruminococcus gnavus spp., could even be used as biomarkers to point to the group that is exposed to GS formation [ 57 , 58 , 59 , 60 , 61 , 62 ].…”

Section: Discussionmentioning

confidence: 99%

Cholesterol Gallstones and Long-Term Use of Statins: Is Gut Microbiota Dysbiosis Bridging over Uncertainties?

Georgescu,

Lighezan,

Ionita

et al. 2024

Diagnostics

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A total of 300 research participants—200 consecutive patients diagnosed with dyslipidemia (100 statin (+), treated for at least five years, and 100 statin (−)) and 100 healthy controls—were included in this observational study. The aim of the study was to deliver insights into the relationship between the long-term use of statins for dyslipidemia and gallstone disease (GSD), as well as insights into the background particularities of the gut microbiota. All study participants underwent clinical examination, laboratory workups, stool microbiology/stool 16S r RNA, next-generation sequencing, and abdominal ultrasound/CT exams. Results: The research participants presented with similarities related to age, gender, and location. Patients displayed comparable heredity for GSs, metabolic issues, and related co-morbidities. Gut dysbiosis (DB) was present in 54% of the statin (−) patients vs. 35% of the statin (+) patients (p = 0.0070). GSs were present in 14% of patients in the statin (−) group vs. 5% of patients in the statin (+) group (p = 0.0304). Severe dysbiosis, with a significant reduction in biodiversity, an increase in LPS (+) bacteria, and a notable decrease in mucin-degrading bacteria, mucosa-protective bacteria, and butyrate-producing bacteria were observed in the statin (−) group. Strong positive correlations between GSD and diabetes/impaired glucose tolerance (r = 0.3368, p = 0.0006), obesity (r = 0.3923, p < 0.0001), nonalcoholic fatty liver disease (r = 0.3219, p = 0.0011), and DB (r = 0.7343, p < 0.0001), as well as significant negative correlations between GSD and alcohol use (r = −0.2305, p = 0.0211), were observed. The multiple regression equation demonstrated that only DB (95% CI: 0.3163 to 0.5670; p < 0.0001) and obesity (95% CI: 0.01431 to 0.2578; p = 0.0289) were independent risk factors predicting GSD in the group of patients treated with statins. Conclusion: The long-term use of statins in dyslipidemic patients was associated with a low risk of developing GSs. The gut microbiota associated with a long-term use of statins in dyslipidemic patients was characterized by a low risk of developing an imbalance of various functional bacteria and alterations in the metabolic microbiota. DB and obesity were found to be independent risk factors predicting GSD in statin (+) patients.

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Gut Microbial Profile Changes in Patients with Gallbladder Stones after UDCA/CDCA Treatment

Cited by 4 publications

References 35 publications

The alleviating effect of Scutellaria amoena extract on the regulation of gut microbiota and its metabolites in NASH rats by inhibiting the NLRP3/ASC/caspase-1 axis

The alleviating effect of Scutellaria amoena extract on the regulation of gut microbiota and its metabolites in NASH rats by inhibiting the NLRP3/ASC/caspase-1 axis

Long-time high-sucrose intake induced metabolic dysfunction via disrupting the balance of intestinal microenvironment

Cholesterol Gallstones and Long-Term Use of Statins: Is Gut Microbiota Dysbiosis Bridging over Uncertainties?

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