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Open AccessJournal ArticleDOI

Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk.

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TLDR
Gut microbes, through generation of trimethylamine N-oxide (TMAO), directly contribute to platelet hyperreactivity and enhanced thrombosis potential, revealing a previously unrecognized mechanistic link between specific dietary nutrients, gut microbes, platelet function, and thromBosis risk.
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This article is published in Cell.The article was published on 2016-03-24 and is currently open access. It has received 1219 citations till now. The article focuses on the topics: Platelet activation & Trimethylamine N-oxide.

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Emerging targetome and signalome landscape of gut microbial metabolites.

TL;DR: In this article , the authors present an updated understanding of how microbial metabolite interaction with host targets finely orchestrates and integrates multiple signals to pathophysiological phenotypes, contributing new insights into organ crosstalk and holistic homeostasis maintenance in biological systems.
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Targeting the human microbiome and its metabolite TMAO in cardiovascular prevention and therapy.

TL;DR: The effects of changes in the gut microbiota as well as the important metabolite Trimethylamine-N-oxide (TMAO) are focused on.
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Is increased plasma TMAO a compensatory response to hydrostatic and osmotic stress in cardiovascular diseases

TL;DR: It is hypothesized that increased plasma TMAO serves as a compensatory response mechanism which protects cells from hydrostatic and osmotic stresses and is present in humans consuming seafood-rich diet which is thought to be health-beneficial.
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Gut Microbiota Alteration After Long-Term Consumption of Probiotics in the Elderly

TL;DR: It is demonstrated that the long-time intake of probiotics caused significant changes in the gut microbiota structure, including an increase in the composition of beneficial microorganisms, which might contribute to the maintenance of host health and homeostasis of microenvironment.
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Intestinal microbiota dysbiosis play a role in pathogenesis of patients with primary immune thrombocytopenia.

TL;DR: It is suggested that the distinct microbiota dysbiosis in ITP characterized by alterations in biodiversity and composition, which could provide insights for diet therapy and fecal microbiota transplantation treatment to cure ITP.
References
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Journal ArticleDOI

An obesity-associated gut microbiome with increased capacity for energy harvest

TL;DR: It is demonstrated through metagenomic and biochemical analyses that changes in the relative abundance of the Bacteroidetes and Firmicutes affect the metabolic potential of the mouse gut microbiota and indicates that the obese microbiome has an increased capacity to harvest energy from the diet.
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The gut microbiota as an environmental factor that regulates fat storage

TL;DR: In this article, the authors found that conventionalization of adult germ-free C57BL/6 mice with a normal microbiota harvested from the distal intestine (cecum) of conventionally raised animals produces a 60% increase in body fat content and insulin resistance within 14 days despite reduced food intake.
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Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease

TL;DR: Discovery of a relationship between gut-flora-dependent metabolism of dietary phosphatidylcholine and CVD pathogenesis provides opportunities for the development of new diagnostic tests and therapeutic approaches for atherosclerotic heart disease.
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Intestinal Microbial Metabolism of Phosphatidylcholine and Cardiovascular Risk

TL;DR: The production of TMAO from dietary phosphatidylcholine is dependent on metabolism by the intestinal microbiota and increased levels are associated with an increased risk of incident major adverse cardiovascular events.
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