Abstract
The occurrence of diarrhea-predominant irritable bowel syndrome (IBS-D) is the result of multiple factors, and its pathogenesis has not yet been clarified. Emerging evidence indicates abnormal changes in gut microbiota and bile acid (BA) metabolism have a close relationship with IBS-D. Gut microbiota is involved in the secondary BA production via deconjugation, 7α-dehydroxylation, oxidation, epimerization, desulfation, and esterification reactions respectively. Changes in the composition and quantity of gut microbiota have an important impact on the metabolism of BAs, which can lead to the occurrence of gastrointestinal diseases. BAs, synthesized in the hepatocytes, play an important role in maintaining the homeostasis of gut microbiota and the balance of glucose and lipid metabolism. In consideration of the complex biological functional connections among gut microbiota, BAs, and IBS-D, it is urgent to review the latest research progress in this field. In this review, we summarized the alterations of gut microbiota in IBS-D and discussed the mechanistic connections between gut microbiota and BA metabolism in IBS-D, which may be involved in activating two important bile acid receptors, G-protein coupled bile acid receptor 1 (TGR5) and farnesoid X receptor (FXR). We also highlight the strategies of prevention and treatment of IBS-D via regulating gut microbiota-bile acid axis, including probiotics, fecal microbiota transplantation (FMT), cholestyramine, and the cutting-edge technology about bacteria genetic engineering.
Highlights
Irritable bowel syndrome (IBS) is the most common functional bowel disease, which can be categorized into diarrheapredominant IBS (IBS-D), constipation-predominant IBS (IBS-C), mixed diarrhea and constipation IBS (IBS-M) and unspecified IBS (IBS-U), mainly symptoms including abdominal pain accompanied by increased defecation, loose stool, or mucus, without obvious organic abnormalities [1, 2]
BAs are synthesized in the liver, converted from the primary bile acids to secondary bile acids in the intestine where the microbiota make a significant impact on the process such as deconjugation and dihydroxylation
There is considerable and growing evidence indicating the significance of interactions between gut microbiota and BAs in patients and animal models with irritable bowel syndrome (IBS-D) during recent years, but still, many blind spots about gut microbiota-bile acid axis with IBS-D should need to be explored
Summary
Irritable bowel syndrome (IBS) is the most common functional bowel disease, which can be categorized into diarrheapredominant IBS (IBS-D), constipation-predominant IBS (IBS-C), mixed diarrhea and constipation IBS (IBS-M) and unspecified IBS (IBS-U), mainly symptoms including abdominal pain accompanied by increased defecation, loose stool, or mucus, without obvious organic abnormalities [1, 2]. The pathogenesis of IBS involves extensive and complex disturbances in the gut microbiota-bile acid metabolic axis [5]. Under the interaction of host and microorganism, a lot of metabolic substances are produced, including BAs, choline, neurotransmitters, short-chain fatty acids (SCFAs), and other signaling factors and energy substrates, which are involved in gastrointestinal inflammation and carcinogenesis, liver disease, metabolic syndrome, IBS, and chronic diseases [8, 9]. In the past few years, most previous studies have paid attention to the field of gut microbiota-bile acid axis in gastrointestinal carcinogenesis and inflammation; few have focused on IBS-D. We discuss the effects of BAs, gut microbiota, and their interactions on IBS-D depending on current evidence from clinical and animal experiments, and present the potential future directions for the prevention and treatment of IBS-D by targeting the gut microbiota-bile acid axis
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