Glycocholic acid supplementation improved growth performance and alleviated tissue damage in the liver and intestine in Pelteobagrus fulvidraco fed a high-pectin diet

Yao, Shibin; Ren, Shengjie; Cai, Chen; Cao, Xiamin; Shi, Ye; Wu, Ping; Ye, Yuantu

doi:10.1007/s10695-022-01148-3

Cited by 6 publications

(2 citation statements)

References 63 publications

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“…( 42 ) reported that GCA effectively suppressed macrophage recruitment and the release of proinflammatory cytokines and chemokines induced by lipopolysaccharide in a mouse macrophage model. Several animal experiments have suggested that GCA may exert anti-inflammatory effects by promoting the expression of the Fxr gene ( 43 ). LCA is a natural agonist of the TGR5 receptor ( 44 ), and activation of TGR5 can reduce lipid uptake by macrophages and inhibit the secretion of proinflammatory cytokines, thus exerting anti-inflammatory effects ( 45 ).…”

Section: Discussionmentioning

confidence: 99%

Metabolomics and network pharmacology exploration of the effects of bile acids on carotid atherosclerosis and potential underlying mechanisms

Cheng,

Zhang,

et al. 2024

Front. Endocrinol.

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BackgroundBile acids (BAs), products of gut microbiota metabolism, have long been implicated in atherosclerotic disease pathogenesis. Characterizing the serum bile acid profile and exploring its potential role in carotid atherosclerosis (CAS) development are crucial tasks.MethodsIn this study, we recruited 73 patients with CAS as the disease group and 77 healthy individuals as the control group. We systematically measured the serum concentrations of 15 bile acids using ultrahigh-performance liquid chromatography-mass spectrometry (UPLC-MS/MS). Multivariate logistic regression and least absolute shrinkage and selection operator (LASSO) regression were applied to analyze the impact of bile acids on the disease and select the key BAs. The possible molecular mechanism was elucidated by network pharmacology.Results(1) The BA profile of patients with CAS significantly differed. (2) Multifactorial logistic regression analysis identified elevated levels of GCDCA (OR: 1.01, P < 0.001), DCA (OR: 1.01, P = 0.005), and TDCA (OR: 1.05, P = 0.002) as independent risk factors for CAS development. Conversely, GCA (OR: 0.99, P = 0.020), LCA (OR: 0.83, P = 0.002), and GUDCA (OR: 0.99, P = 0.003) were associated with protective effects against the disease. GCA, DCA, LCA, and TDCA were identified as the four key BAs. (3) TNF, FXR, GPBAR1, ESR1 and ACE were predicted to be targets of BAs against AS. These four BAs potentially impact AS progression by triggering signaling pathways, including cAMP, PPAR, and PI3K-AKT pathways, via their targets.ConclusionThis study offers valuable insights into potential therapeutic strategies for atherosclerosis that target bile acids.

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Section: Discussionmentioning

confidence: 99%

Metabolomics and network pharmacology exploration of the effects of bile acids on carotid atherosclerosis and potential underlying mechanisms

Cheng,

Zhang,

et al. 2024

Front. Endocrinol.

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“…Glycoholic acid is one of the naturally derived anti-in ammatory agents with high e cacy and safety [19] . Yao et al found that glycoholic acid improved growth performance and alleviated hepatic cholestasis and tissue damage to the liver and intestine induced by a high-pectin diet [20] . The above results suggest that glycoholic acid may also reduce in ammation and damage to vascular endothelium.…”

Section: Correlation Analysismentioning

confidence: 99%

Bile Acid Metabolism Analysis Insight into the Vascular Endothelial Injury in High Salt-Induced Hypertensive Rats

Zeng,

Peng,

Chen

et al. 2023

Preprint

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Background: High salt diet has become one of the leading risk factors for cardiovascular diseases worldwide. There is already research to prove that excessive salt intake can cause hypertension and endothelial damage. However, the potential mechanism requires further exploration. In the present study, we aimed to reveal the bile acid metabolism in high-salt-induced vascular endothelial injury in rats. Methods: A high-salt diet (HSD) induced rats model was established by evaluating the levels of blood pressure and vascular endothelial injury factors. Bile acid metabolism analysis was performed to identify differential bile acids between the normal group and the HSD group. Correlation analysis further detected the relevance between vascular endothelial injury factors and bile acids. Results: The results reflected that HSD can cause disorders in bile acid metabolism. 10 potential bile acids in plasma were found to be involved in the effects of high salt on vascular endothelium. Further correlation analysis indicated that endothelin-1 (ET-1) has a negative correlation with glycocholic acid, and nitric oxide (NO) has a positive correlation with ursocholic acid. Conclusion: This study identified which bile acids associated with high-salt-induced vascular endothelial injury, and provided a new idea for the prevention and treatment of high salt-induced cardiovascular diseases.

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Konjac supplementation can alleviate obesity induced by high-fat diet in mice by modulating gut microbiota and its metabolites

Wen,

Chen,

Huang

et al. 2024

Current Research in Food Science

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Glycocholic acid supplementation improved growth performance and alleviated tissue damage in the liver and intestine in Pelteobagrus fulvidraco fed a high-pectin diet

Cited by 6 publications

References 63 publications

Metabolomics and network pharmacology exploration of the effects of bile acids on carotid atherosclerosis and potential underlying mechanisms

Metabolomics and network pharmacology exploration of the effects of bile acids on carotid atherosclerosis and potential underlying mechanisms

Bile Acid Metabolism Analysis Insight into the Vascular Endothelial Injury in High Salt-Induced Hypertensive Rats

Konjac supplementation can alleviate obesity induced by high-fat diet in mice by modulating gut microbiota and its metabolites

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