Bile acid signaling in the regulation of whole body metabolic and immunological homeostasis

Wang, Jia; Li, Yitao; Cheung, Kenneth C. P.; Zheng, Xiaojiao

doi:10.1007/s11427-023-2353-0

Cited by 25 publications

(12 citation statements)

References 157 publications

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“…The most abundant secondary BAs in the body are DCA and LCA. They are formed by microbial reactions, involving bile salt hydrolase (BSH) and 7α-dehydroxylation, using CA and CDCA conjugated with glycine or taurine as substrates . Excessive accumulation of DCA inhibits the growth of Clostridium difficile in the intestine, impairing the enterohepatic circulation of BAs. , This disruption leads to an increased production of reactive oxygen species, exacerbated DNA damage, and a shift in the secretion phenotype toward aging, thereby promoting the growth of hepatocellular carcinoma induced by a high-fat diet .…”

Section: Discussionmentioning

confidence: 99%

Lactiplantibacillus plantarum ATCC8014 Alleviates Postmenopausal Hypercholesterolemia in Mice by Remodeling Intestinal Microbiota to Increase Secondary Bile Acid Excretion

Zhang,

Liu,

et al. 2024

J. Agric. Food Chem.

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Hypercholesterolemia poses a significant cardiovascular risk, particularly in postmenopausal women. The antihypercholesterolemic properties of Lactiplantibacillus plantarum ATCC8014 (LP) are well recognized; however, its improving symptoms on postmenopausal hypercholesterolemia and the possible mechanisms have yet to be elucidated. Here, we utilized female ApoE-deficient (ApoE −/− ) mice undergoing bilateral ovariectomy, fed a high-fat diet, and administered 10 9 colony-forming units (CFU) of LP for 13 consecutive weeks. LP intervention reduces total cholesterol (TC) and triglyceride (TG) accumulation in the serum and liver and accelerates their fecal excretion, which is mainly accomplished by increasing the excretion of fecal secondary bile acids (BAs), thereby facilitating cholesterol conversion. Correlation analysis revealed that lithocholic acid (LCA) is an important regulator of postmenopausal lipid abnormalities. LP can reduce LCA accumulation in the liver and serum while enhancing its fecal excretion, accomplished by elevating the relative abundances of Allobaculum and Olsenella in the ileum. Our findings demonstrate that postmenopausal lipid dysfunction is accompanied by abnormalities in BA metabolism and dysbiosis of the intestinal microbiota. LP holds therapeutic potential for postmenopausal hypercholesterolemia. Its effectiveness in ameliorating lipid dysregulation is primarily achieved through reshaping the diversity and abundance of the intestinal microbiota to correct BA abnormalities.

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Section: Discussionmentioning

confidence: 99%

Lactiplantibacillus plantarum ATCC8014 Alleviates Postmenopausal Hypercholesterolemia in Mice by Remodeling Intestinal Microbiota to Increase Secondary Bile Acid Excretion

Zhang,

Liu,

et al. 2024

J. Agric. Food Chem.

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“…Bile acids play a role through the activation of nuclear hormone farnesol X receptor) and G protein‐coupled bile acid receptor 5. 55 GM is an important regulator of bile acid metabolism. The diversity of bile acid is decreased in germ‐free and antibiotic‐treated rats, and bile acid metabolites can activate receptors and act as signal molecules in the host, which can affect HPA axis and play a role in the brain.…”

Section: Potential Mechanisms By Which Gut Microbiota Affects Neurode...mentioning

confidence: 99%

Treatment of preterm brain injury via gut‐microbiota–metabolite–brain axis

Li,

Liu,

Shi

2023

CNS Neurosci Ther

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BackgroundBrain injury in preterm infants potentially disrupts critical structural and functional connective networks in the brain. It is a major cause of neurological sequelae and developmental deficits in preterm infants. Interesting findings suggest that the gut microbiota (GM) and their metabolites contribute to the programming of the central nervous system (CNS) during developmental stages and may exert structural and functional effects throughout the lifespan.AimTo summarize the existing knowledge of the potential mechanisms related to immune, endocrine, neural, and blood–brain barrier (BBB) mediated by GM and its metabolites in neural development and function.MethodsWe review the recent literature and included 150 articles to summarize the mechanisms through which GM and their metabolites work on the nervous system. Potential health benefits and challenges of relevant treatments are also discussed.ResultsThis review discusses the direct and indirect ways through which the GM may act on the nervous system. Treatment of preterm brain injury with GM or related derivatives, including probiotics, prebiotics, synbiotics, dietary interventions, and fecal transplants are also included.ConclusionThis review summarizes mechanisms underlying microbiota‐gut‐brain axis and novel therapeutic opportunities for neurological sequelae in preterm infants. Optimizing the initial colonization and microbiota development in preterm infants may represent a novel therapy to promote brain development and reduce long‐term sequelae.

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“…Bile acids play pivotal roles not only in lipid digestion, absorption of fat-soluble vitamins, cholesterol metabolism, and bile excretion, but also in modulation of gut microbiota and regulation of glucose metabolism ( 13 ). Intriguingly, emerging research has illuminated that bile acid signaling contributes to immunological homeostasis via both innate and adaptive immune responses, functioning as the pro-inflammatory or anti-inflammatory role ( 14 ). Che et al.…”

Section: Introductionmentioning

confidence: 99%

USP50 regulates NLRP3 inflammasome activation in duodenogastric reflux-induced gastric tumorigenesis

Zhao,

Mu,

et al. 2024

Front. Immunol.

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Duodenogastric reflux (DGR) has been linked to the onset of gastric cancer (GC), although the precise mechanism is yet obscure. Herein, we aimed to investigate how refluxed bile acids (BAs) and macrophages are involved in gastric carcinogenesis. In both active human bile reflux gastritis and the murine DGR model, ubiquitin specific protease 50 (USP50) was dramatically raised, and macrophages were the principal leukocyte subset that upregulated USP50 expression. Enhancing USP50 expression amplified bile acid-induced NLR family pyrin domain containing 3 (NLRP3) inflammasome activation and subsequent high-mobility group box protein 1 (HMGB1) release, while USP50 deficiency resulted in the reversed alteration. Mechanistically, USP50 interacted with and deubiquitinated apoptosis-associated speck-like protein containing CARD (ASC) to activate NLRP3 inflammasome. The release of HMGB1 contributes to gastric tumorigenesis by PI3K/AKT and MAPK/ERK pathways. These results may provide new insights into bile reflux-related gastric carcinogenesis and options for the prevention of DGR-associated GC.

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Bile acid signaling in the regulation of whole body metabolic and immunological homeostasis

Cited by 25 publications

References 157 publications

Lactiplantibacillus plantarum ATCC8014 Alleviates Postmenopausal Hypercholesterolemia in Mice by Remodeling Intestinal Microbiota to Increase Secondary Bile Acid Excretion

Lactiplantibacillus plantarum ATCC8014 Alleviates Postmenopausal Hypercholesterolemia in Mice by Remodeling Intestinal Microbiota to Increase Secondary Bile Acid Excretion

Treatment of preterm brain injury via gut‐microbiota–metabolite–brain axis

USP50 regulates NLRP3 inflammasome activation in duodenogastric reflux-induced gastric tumorigenesis

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