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    Bile acids at the cross-roads of gut microbiome–host cardiometabolic interactions

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    Author
    Ryan, Paul M
    STANTON, CATHERINE cc
    Caplice, Noel M
    Keyword
    Microbiome –
    Bile acids
    Cardiovascular disease
    Metabolic syndrome
    Date
    28/12/2017
    
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    URI
    http://hdl.handle.net/11019/1529
    Citation
    Ryan PM, Stanton C, Caplice NM. Bile acids at the cross-roads of gut microbiome–host cardiometabolic interactions. Diabetology & Metabolic Syndrome 2017;9(1):102; doi 10.1186/s13098-017-0299-9.
    Abstract
    While basic and clinical research over the last several decades has recognized a number of modifiable risk factors associated with cardiometabolic disease progression, additional and alternative biological perspectives may offer novel targets for prevention and treatment of this disease set. There is mounting preclinical and emerging clinical evidence indicating that the mass of metabolically diverse microorganisms which inhabit the human gastrointestinal tract may be implicated in initiation and modulation of cardiovascular and metabolic disease outcomes. The following review will discuss this gut microbiome–host metabolism axis and address newly proposed bile-mediated signaling pathways through which dysregulation of this homeostatic axis may influence host cardiovascular risk. With a central focus on the major nuclear and membrane-bound bile acid receptor ligands, we aim to review the putative impact of microbial bile acid modification on several major phenotypes of metabolic syndrome, from obesity to heart failure. Finally, attempting to synthesize several separate but complementary hypotheses, we will review current directions in preclinical and clinical investigation in this evolving field.
    Funder
    Science Foundation Ireland; Enterprise Ireland
    Grant Number
    SFI/12/RC/2273; CF/2013/3030A/B
    ae974a485f413a2113503eed53cd6c53
    http://dx.doi.org/10.1186/s13098-017-0299-9
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    Teagasc publications in Biomed Central
    Teagasc publications in Biomed Central
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