The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease

Qaradakhi, Tawar; Gadanec, Laura Kate; McSweeney, Kristen Renee; Abraham, Jemma Rose; Apostolopoulos, Vasso; Zulli, Anthony

doi:10.3390/nu12092847

Cited by 81 publications

(49 citation statements)

References 220 publications

(325 reference statements)

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“…Taurine is known to be involved in osmoregulation [12], protection from cardiac dysfunction [13] and renal development, and has anti-oxidant properties. In addition, taurine has anti-inflammatory effects, which improve diabetes [14], and may have a crucial role in regulating insulin release [15]. Simplified metabolic pathways for taurine (modified from Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway map 00430) (A) and sulfoquinovose (modified from Denger et al [6] and Felux et al [16]) (B).…”

Section: Introductionmentioning

confidence: 99%

Multiplexed Quantitative Assessment of the Fate of Taurine and Sulfoquinovose in the Intestinal Microbiome

et al. 2020

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(1) Introduction: Sulfonates, which can be diet- or host-derived, are a class of compounds detected in the gut, are involved in host–microbiome interactions and have several health effects. Our aim was to develop a method to quantify five of the sulfonates in the intestine and apply it in a simplified human microbiome model. These were taurine, its metabolic precursor cysteate and one of its degradation products isethionate, as well as sulfoquinovose and one of its most relevant degradation products 2,3-dihydroxy-1-propanesulfonate. (2) Methods: An extraction and sample preparation method was developed, without the need for derivatization. To detect and quantify the extracted sulfonates, a multiplexed LC-MS/MS-MRM method was established. (3) Results: The accuracy and precision of the method were within GLP-accepted parameters. To apply this method in a pilot study, we spiked either taurine or sulfoquinovose into an in vitro simplified human microbiota model with and without Bilophila wadsworthia, a known sulfonate utilizer. The results revealed that only the culture with B. wadsworthia was able to degrade taurine, with isethionate as an intermediate. After spiking the communities with sulfoquinovose, the results revealed that the simplified human microbiome model was able to degrade sulfoquinovose to 2,3-dihydroxypropane-1-sulfonate, which was probably catalyzed by Escherichia coli. In the community with B. wadsworthia, the 2,3-dihydroxypropane-1-sulfonate produced was further degraded by B. wadsworthia to sulfide. (4) Conclusions: We successfully developed a method for sulfonate quantification and applied it in a first pilot study.

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Section: Introductionmentioning

confidence: 99%

Multiplexed Quantitative Assessment of the Fate of Taurine and Sulfoquinovose in the Intestinal Microbiome

et al. 2020

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“…Though taurine has been extensively investigated with regards to its anti-inflamma tory and antioxidative effects [ 8 , 9 , 10 , 28 , 29 , 30 ], there is paucity of data demonstrating the tissue-protective potential of TauCl in vivo. This may be partly due to the limitations on the availability of relatively large amounts of the compound.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Taurine Chloramine on Experimentally Induced Colitis: NFκB, STAT3, and Nrf2 as Potential Targets

et al. 2021

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Taurine chloramine (TauCl) is an endogenous anti-inflammatory substance which is derived from taurine, a semi-essential sulfur-containing β-amino acid found in some foods including meat, fish, eggs and milk. In general, TauCl as well as its parent compound taurine downregulates production of tissue-damaging proinflammatory mediators, such as chemokines and cytokines in many different types of cells. In the present study, we investigated the protective effects of TauCl on experimentally induced colon inflammation. Oral administration of TauCl protected against mouse colitis caused by 2,4,6-trinitrobenzene sulfonic acid (TNBS). TauCl administration attenuated apoptosis in the colonic mucosa of TNBS-treated mice. This was accompanied by reduced expression of an oxidative stress marker, 4-hydroxy-2-nonenal and proinflammatory molecules including tumor necrosis factor-α, interleukin-6 and cyclooxygenase-2 in mouse colon. TauCl also inhibited activation of NFκB and STAT3, two key transcription factors mediating proinflammatory signaling. Notably, the protective effect of TauCl on oxidative stress and inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding heme oxygenase-1, NAD(P)H:quinone oxidoreductase, glutamate cysteine ligase catalytic subunit, and glutathione S-transferase. Taken together, these results suggest that TauCl exerts the protective effect against colitis through upregulation of Nrf2-dependent cytoprotective gene expression while blocking the proinflammatory signaling mediated by NFκB and STAT3.

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“…In mammals, the susceptibility to taurine deficiency varies by species: while taurine can be synthesized endogenously and is considered non-essential or conditionally-essential in humans, rodents, and dogs, it is essential for cats (91,(124)(125)(126)(127). Taurine has been implicated in the maintenance of normal contractile function, modulation of myocardial calcium homeostasis, and potentially acts as an antioxidant and anti-inflammatory agent (123,128). Schaffer et al demonstrated that the taurine-deficient heart is associated with reduced ATP generation and is energy starved, possibly due to impaired mitochondrial respiratory chain activity, and NADH utilization (129).…”

Section: Taurinementioning

confidence: 99%

Metabolic Reprogramming, Gut Dysbiosis, and Nutrition Intervention in Canine Heart Disease

Li¹

2022

Front. Vet. Sci.

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This review provides a state-of-the-art overview on recent advances in systems biology in canine cardiac disease, with a focus on our current understanding of bioenergetics and amino acid metabolism in myxomatous mitral valve disease (MMVD). Cross-species comparison is drawn to highlight the similarities between human and canine heart diseases. The adult mammalian heart exhibits a remarkable metabolic flexibility and shifts its energy substrate preference according to different physiological and pathological conditions. The failing heart suffers up to 40% ATP deficit and is compared to an engine running out of fuel. Bioenergetics and metabolic readaptations are among the major research topics in cardiac research today. Myocardial energy metabolism consists of three interconnected components: substrate utilization, oxidative phosphorylation, and ATP transport and utilization. Any disruption or uncoupling of these processes can result in deranged energy metabolism leading to heart failure (HF). The review describes the changes occurring in each of the three components of energy metabolism in MMVD and HF. It also provides an overview on the changes in circulating and myocardial glutathione, taurine, carnitines, branched-chain amino acid catabolism and tryptophan metabolic pathways. In addition, the review summarizes the potential role of the gut microbiome in MMVD and HF. As our knowledge and understanding in these molecular and metabolic processes increase, it becomes possible to use nutrition to address these changes and to slow the progression of the common heart diseases in dogs.

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The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease

Cited by 81 publications

References 220 publications

Multiplexed Quantitative Assessment of the Fate of Taurine and Sulfoquinovose in the Intestinal Microbiome

Multiplexed Quantitative Assessment of the Fate of Taurine and Sulfoquinovose in the Intestinal Microbiome

Protective Effects of Taurine Chloramine on Experimentally Induced Colitis: NFκB, STAT3, and Nrf2 as Potential Targets

Metabolic Reprogramming, Gut Dysbiosis, and Nutrition Intervention in Canine Heart Disease

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