MS4A1-PTGS2 axis induces taurine metabolic reprogramming to exacerbate abdominal aortic aneurysm progression.

This study unveils the pivotal roles of taurine metabolic reprogramming and its implications in the development and progression of Abdominal Aortic Aneurysm (AAA). Leveraging an integrated approach that combines single-cell RNA sequencing (scRNA-seq) and Weighted Gene Co-expression Network Analysis (WGCNA), our research investigates the intricate transcriptional and gene expression dynamics crucial to AAA. Our findings uniquely link metabolic shifts to the integrity of the extracellular matrix (ECM) and the functionality of smooth muscle cells (SMCs), key elements in the pathology of AAA. Utilizing scRNA-seq data from a mouse model (GSE152583 dataset), we identified critical alterations in cellular composition during AAA progression, particularly highlighting shifts in fibroblasts and inflammatory cells. Concurrently, WGCNA of human AAA tissue samples has outlined distinct gene expression patterns correlated with disease severity and progression, offering comprehensive insights into both molecular and cellular disease mechanisms. Moreover, this study introduces innovative metabolic profiling techniques to identify differential metabolites in AAA, integrating extensive metabolomic analyses with pathway enrichment strategies. This novel approach has pinpointed potential biomarkers and therapeutic targets, notably within taurine metabolism pathways, crucial for crafting non-surgical interventions. By merging state-of-the-art bioinformatics with thorough molecular analysis, our study not only enhances the understanding of AAA's complex pathophysiology but also catalyzes the development of targeted therapeutic strategies. This research represents a significant advancement in the molecular characterization of AAA, with substantial implications for its future diagnosis and treatment strategies.

Serum taurine affects lung cancer progression by regulating tumor immune escape mediated by the immune microenvironment.

INTRODUCTION: Taurine is a naturally occurring sulfonic acid involved in various physiological and pathological processes, such as the regulation of calcium signaling, immune function, inflammatory response, and cellular aging. It has the potential to predict tumor malignant transformation and formation. Our previous work discovered the elevated taurine in lung cancer patients. However, the precise impact and mechanism of elevated serum taurine levels on lung cancer progression and the suitability of taurine or taurine-containing drinks for lung cancer patients remain unclear. OBJECTIVES: Our study aimed to systematically investigate the role of taurine in lung cancer, with the ultimate goal of contributing novel strategies for lung cancer treatment. METHODS: Lung cancer C57 and nude mice models, RNA sequencing, and stable transfection were applied to explored the effects and mechanisms of taurine on lung cancer. Tissues of 129 non-small cell lung cancer (NSCLC) patients derived from 2014 to 2017 for immunohistochemistry were collected in Taihe Hospital. RESULTS: Low doses of taurine, as well as taurine-infused beverages at equivalent doses, significantly enhanced lung tumor growth. Equally intriguing is that the promoting effect of taurine on lung cancer progression wanes as the dosage increases. The Nuclear factor erythroid 2-like 1 (Nfe2l1 or Nrf1)-reactive oxygen species (ROS)-PD-1 axis may be a potential mechanism for dual role of taurine in lung cancer progression. However, taurine's impacts on lung cancer progression and the anti-tumor function of Nfe2l1 were mainly determined by the immune competence. Taurine inhitited lung tumor growth probably by inhibiting NF-κB-mediated inflammatory responses in nude mice rather than by affecting Nfe2l1 function. As patients age increased, Nfe2l1 gene and protein gradually returned to the levels observed in healthy individuals, but lost its anti-lung cancer effects. CONCLUSIONS: Taurine emerges as a potential biomarker for lung cancer progression, predicting poor prognosis and unsuitability for specific patients. Lung cancer patients, especially young patients, should be conscious of potential effects of taurine-containing drinks. Conversely, taurine or its drinks may be more suitable for older or immune-deficient patients.

Taurine exhibits antioxidant, anti-inflammatory, and antiapoptotic effects against pyraclostrobin exposure in rats.

Pyraclostrobin, a strobilurin-derived fungicide, causes oxidative stress and DNA damage in the organism. Taurine plays an important role in metabolic processes such as osmoregulatory, cytoprotective, and antioxidant effects. The study aimed to investigate the protective effect of taurine in Sprague Dawley male rats exposed to pyraclostrobin. The rats were separated into 6 groups and were found 8 animals in each group. Rats were given 30 mg/kg pyraclostrobin and pyraclostrobin together with three different taurine concentrations (50, 100, and 200 mg/kg) via oral gavage for 28 days. While pyraclostrobin increased biochemical parameters, lipid peroxidation, and DNA damage, it decreased glutathione levels and enzyme activities of catalase and superoxide dismutase. Pyraclostrobin increased apoptotic, proinflammatory, and CYP2E1 mRNA expression levels, whereas antiapoptotic gene Bcl-2 mRNA expression levels decreased in liver tissue. Additionally, pyraclostrobin caused histopathological alterations in tissues. Taurine in a dose-dependent manner reversed the changes caused by pyraclostrobin. As a result, taurine exhibited a cytoprotective effect by showing antioxidant, anti-inflammatory, and antiapoptotic activities against oxidative damage caused by pyraclostrobin.

A narrative review and new insights into the protective effects of taurine against drug side effects.

Taurine, a non-essential amino acid produced from cysteine, is abundant in body tissues and blood plasma. It plays vital roles in growth, osmosis, lipid metabolism, and neurohormonal modulation. Taurine has antioxidant, anti-apoptotic, and anti-inflammatory properties, and its deficiency can lead to various diseases including cardiovascular, diabetic, renal, and liver disorders. This report provides a comprehensive review of the functional properties of taurine in counteracting pharmaceutical-induced side effects. A search across databases such as Scopus, PubMed, MEDLINE, and Web of Science yielded 109 articles, of which 75 were included in the study. These results suggest that the protective effects of taurine involve mechanisms such as influencing pathways of Nrf2/OH-1, PI3-kinase/AKT and ERK2, boosting antioxidants (SOD, GPx and CAT), and suppression of inflammatory cytokines (TNF-α, IL-1ß and IL-6). Overall, supplementation with taurine along with medications with significant side effects may mitigate these effects and enhance their efficacy. Further investigation of the interactions between taurine and other nutrients or compounds may provide insights into synergistic effects and novel therapeutic approaches.

Enhancing the antioxidant properties of functional herbal beverages using Ultrasonic-Assisted extraction: Optimized formulation and synergistic combinations of taurine and vit. C.

Functional herbal beverages are gaining popularity in the beverage industry due to their natural antioxidants. However, the high concentration of antioxidants in these beverages can lead to increased toxicity, limiting their use. Moreover, the composition of tap water, including mineral salts and hydrogen carbonate ions, hampers the extraction process of polyphenolic compounds, thereby reducing the antioxidant properties. This study aims to address these challenges by enhancing antioxidant properties, reducing toxic effects, and improving the extraction process. Low-dose herbal extracts of green tea, rosemary, milk thistle, and sage were extracted using 100 ml of boiling water as a solvent, with ultrasonication employed for 20 min. Taurine, vit. C, and their combination were added to the extracts. The antioxidant properties, polyphenol, and flavonoid content were evaluated. The results demonstrated that the low-dose herbal tea combined with taurine and vit. C exhibited higher antioxidant activity compared to high-dose tea. Notably, the combination of taurine and vit. C showed the strongest synergistic effect. The addition of vit. C to these combinations eliminated any antagonism and resulted in a robust synergistic effect. The optimal conditions for enhancing antioxidant properties were determined as follows: an herbal type of 0.030 ≈ 0 (sage), vit. C concentration of 0.045 g/100 ml, and taurine concentration of 0.179 g/100 ml. The measured responses for reducing power, DPPH, and ABTS were 0.152 µg vit. C equivalent/ml, 67.778 %, and 87.630 %, respectively. This study provides valuable insights into optimizing the antioxidant properties of herbal beverages through the synergistic combinations of taurine and vit. C. By employing proper preparation techniques and including taurine and vit. C, the antioxidant capacity of these beverages can be significantly improved, potentially offering health benefits against degenerative diseases.

Effects of taurine on the growth performance, diarrhea, oxidative stress and intestinal barrier function of weanling piglets.

Oxidative damage resulting from weaning stress significantly impacts the growth performance and health status of piglets. Taurine, a dietary antioxidant with diverse functions, was investigated in this study for its protective role against weaning stress-induced oxidative damage and its underlying mechanism. Forty 28-day-old male castrated weaned piglets were randomly assigned to four groups. The control group received the basal diet, while the experimental groups were fed the basal diet supplemented with 0.1, 0.2%, or 0.3% taurine over a 28-day period. In vitro, H2O2 was utilized to induce oxidative damage to the jejunal mucosa of piglets via IPEC-J2 cells. The results demonstrated that taurine supplementation reduced the incidence of diarrhea in piglets compared to that in the control group (p < 0.05); the addition of 0.2 and 0.3% taurine led to increased average daily gain and improved feed conversion efficiency in weaned piglets, showing a linear dose-response correlation (p < 0.05). Taurine supplementation at 0.2 and 0.3% enhanced the activities of serum CAT and GSH-Px while decreasing the levels of serum NO, XOD, GSSG, and MDA (p < 0.05). Moreover, it significantly elevated the levels of GSS, Trx, POD, complex I, mt-nd5, and mt-nd6, enhancing superoxide anion scavenging capacity and the hydroxyl-free scavenging rate in the livers of weaned piglets while reducing NO levels in the liver (p < 0.05). Additionally, 0.2 and 0.3% taurine supplementation decreased serum IL-6 levels and elevated the concentrations of IgA, IgG, and IL-10 in weaned piglets (p < 0.05). The levels of occludin, claudin, and ZO-1 in the jejunum mucosa of weaned piglets increased with 0.2 and 0.3% taurine supplementation (p < 0.05). In IPEC-J2 cells, pretreatment with 25 mM taurine for 24 h enhanced the activities of SOD and CAT; reduced the MDA content; upregulated the mRNA expression of various genes, including ZO-1, occludin, claudin-1, Nrf2, and HO-1; and reversed the oxidative damage induced by H2O2 exposure (p < 0.05). Overall, the findings suggest that the inclusion of 2 and 3% taurine in the diet can enhance growth performance, reduce diarrhea rates, ameliorate oxidative stress and inflammation, and promote intestinal barrier function in weaned piglets.

Inhibition of mitophagy via the EIF2S1-ATF4-PRKN pathway contributes to viral encephalitis.

INTRODUCTION: Mitophagy, a selective form of autophagy responsible for maintaining mitochondrial homeostasis, regulates the antiviral immune response and acts as viral replication platforms to facilitate infection with various viruses. However, its precise role in herpes simplex virus 1 (HSV-1) infection and herpes simplex encephalitis (HSE) remains largely unknown. OBJECTIVES: We aimed to investigate the regulation of mitophagy by HSV-1 neurotropic infection and its role in viral encephalitis, and to identify small compounds that regulate mitophagy to affect HSV-1 infection. METHODS: The antiviral effects of compounds were investigated by Western blot, RT-PCR and plaque assay. The changes of Parkin (PRKN)-mediated mitophagy and Nuclear Factor kappa B (NFKB)-mediated neuroinflammation were examined by TEM, RT-qPCR, Western blot and ELISA. The therapeutic effect of taurine or PRKN-overexpression was confirmed in the HSE mouse model by evaluating survival rate, eye damage, neurodegenerative symptoms, immunohistochemistry analysis and histopathology. RESULTS: HSV-1 infection caused the accumulation of damaged mitochondria in neuronal cells and in the brain tissue of HSE mice. Early HSV-1 infection led to mitophagy activation, followed by inhibition in the later viral infection. The HSV-1 proteins ICP34.5 or US11 deregulated the EIF2S1-ATF4 axis to suppress PRKN/Parkin mRNA expression, thereby impeding PRKN-dependent mitophagy. Consequently, inhibition of mitophagy by specific inhibitor midiv-1 promoted HSV-1 infection, whereas mitophagy activation by PRKN overexpression or agonists (CCCP and rotenone) attenuated HSV-1 infection and reduced the NF-κB-mediated neuroinflammation. Moreover, PRKN-overexpressing mice showed enhanced resistance to HSV-1 infection and ameliorated HSE pathogenesis. Furthermore, taurine, a differentially regulated gut microbial metabolite upon HSV-1 infection, acted as a mitophagy activator that transcriptionally promotes PRKN expression to stimulate mitophagy and to limit HSV-1 infection both in vitro and in vivo. CONCLUSION: These results reveal the protective function of mitophagy in HSE pathogenesis and highlight mitophagy activation as a potential antiviral therapeutic strategy for HSV-1-related diseases.

Taurine, alpha lipoic acid and vitamin B6 ameliorate the reduced developmental competence of immature mouse oocytes exposed to methylglyoxal.

Advanced glycation end products (AGEs) are the final products of the Maillard reaction, formed through the interaction of carbohydrates and proteins. Reactive dicarbonyl compounds such as methylglyoxal (MGO) serve as precursors for AGEs formation. Elevated levels of MGO/AGEs are observed in conditions like obesity, polycystic ovarian syndrome (PCOS), and diabetes, negatively impacting oocyte development. Previous studies have shown that hydrogen sulfide, a gasotransmitter with anti-AGEs effects, is produced in a process influenced by vitamin B6. R-α-lipoic acid (ALA) inhibits protein glycation and AGEs formation while stimulating glutathione (GSH) production. Taurine mitigates oxidative stress and acts as an anti-glycation compound, preventing in vitro glycation and AGEs accumulation. This study aimed to explore the ameliorative effects of a micronutrient support (Taurine, ALA and B6: TAB) on mouse oocytes challenged with MGO. Our results indicate that MGO reduces oocyte developmental competence, while TAB supplementation improves maturation, fertilization, and blastocyst formation rates. TAB also restores cell lineage allocation, redox balance and mitigates mitochondrial dysfunction in MGO-challenged oocytes. Furthermore, cumulus cells express key enzymes in the transsulfuration pathway, and TAB enhances their mRNA expression. However, TAB does not rescue MGO-induced damage in denuded oocytes, emphasizing the supportive role of cumulus cells. Overall, these findings suggest that TAB interventions may have significant implications for addressing reproductive dysfunctions associated with elevated MGO/AGEs levels. This study highlights the potential of TAB supplementation in preserving the developmental competence of COCs exposed to MGO stress, providing insights into mitigating the impact of dicarbonyl stress on oocyte quality and reproductive outcomes.

Sarcobesity: new paradigms for healthy aging related to taurine supplementation, gut microbiota and exercise.

Enigmatic sarcopenic obesity is still a challenge for science and adds to the global public health burden. The progressive accumulation of body fat combined with a dysfunctional skeletal muscle structure and composition, oxidative stress, mitochondrial dysfunction, and anabolic resistance, among other aggravating factors, together represent the seriousness and complexity of treating the metabolic disorder of sarcobesity in aging. For this reason, further studies are needed that encourage the support of therapeutic management. It is along these lines that we direct the reader to therapeutic approaches that demonstrate important, but still obscure, outcomes in the physiological conditions of sarcobesity, such as the role of taurine in modulating inflammatory and antioxidant mechanisms in muscle and adipose tissue, as well as the management of gut microbiota, able to systemically re-establish the structure and function of the gut-muscle axis, in addition to the merits of physical exercise as an instrument to improve muscular health and lifestyle quality.

Investigation of the anti-skin aging effects of taurine through mendelian randomization analysis of its relationship with immune cells.

BACKGROUND: Aging skin, exacerbated by external factors like UV radiation and pollutants, is a major cosmetic concern. Taurine, renowned for its antioxidant and anti-inflammatory properties, may combat skin aging. We performed mendelian randomization (MR) analysis to investigate the causal link between taurine and immune cells linked to skin aging. OBJECTIVES: To investigate the association between taurine and immune cells using mendelian randomization, to thereby explore the mechanism through which taurine exerts anti-aging effects on the skin via immune modulation. METHODS: A MR approach was employed using taurine-level data from the Ieu Open GWAS Project and immunocyte traits from a large European cohort. MR-Egger regression, weighted median estimation, and inverse variance weighting all provided statistical insights into causality. Sensitivity analyses assessed the heterogeneity and pleiotropy among the genetic instruments used. RESULTS: MR analysis identified a causal relationship between taurine levels and 10 immunocyte phenotypes, with taurine found to be negatively and positively associated with three and seven phenotypes, respectively. Sensitivity analysis revealed no significant heterogeneity or pleiotropy, suggesting reliable MR findings. CONCLUSION: This study provides insights into the immunological pathways by which taurine contributes to skin anti-aging effects, suggesting that increasing taurine levels could offer a novel strategy for anti-aging skincare.

Insights into the cardiovascular benefits of taurine: a systematic review and meta-analysis.

BACKGROUND: Cardiovascular disease (CVD) remains the foremost cause of mortality globally. Taurine, an amino acid, holds promise for cardiovascular health through mechanisms such as calcium regulation, blood pressure reduction, and antioxidant and anti-inflammatory effects. Despite these potential benefits, previous studies have yielded inconsistent results. This meta-analysis of randomized controlled trials (RCTs) aims to evaluate the existing evidence on the quantitative effects of taurine on hemodynamic parameters and cardiac function grading, which are indicative of overall cardiovascular health and performance. METHODS: We conducted an electronic search across multiple databases, including Embase, PubMed, Web of Science, Cochrane CENTRAL, and ClinicalTrials.gov, from their inception to January 2, 2024. Our analysis focused on key cardiovascular outcomes, such as heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), left ventricular ejection fraction (LVEF), and New York Heart Association (NYHA) Functional Classification. Meta-regression was applied to explore dose-dependent relationships based on the total taurine dose administered during the treatment period. A subgroup analysis, stratified according to the baseline disease status of patients, was also conducted. RESULTS: The analysis included a pooled sample of 808 participants from 20 randomized controlled trials. Taurine demonstrated a significant reduction in HR (weighted mean difference [WMD] = -3.579 bpm, 95% confidence interval [CI] = -6.044 to -1.114, p = 0.004), SBP (WMD = -3.999 mm Hg, 95% CI = -7.293 to -0.706, p = 0.017), DBP (WMD: -1.435 mm Hg, 95% CI: -2.484 to -0.386, p = 0.007), NYHA (WMD: -0.403, 95% CI: -0.522 to -0.283, p < 0.001), and a significant increase in LVEF (WMD: 4.981%, 95% CI: 1.556 to 8.407, p = 0.004). Meta-regression indicated a dose-dependent reduction in HR (coefficient = -0.0150 per g, p = 0.333), SBP (coefficient = -0.0239 per g, p = 0.113), DBP (coefficient = -0.0089 per g, p = 0.110), and NYHA (coefficient = -0.0016 per g, p = 0.111), and a positive correlation with LVEF (coefficient = 0.0285 per g, p = 0.308). No significant adverse effects were observed compared to controls. In subgroup analysis, taurine significantly improved HR in heart failure patients and healthy individuals. Taurine significantly reduced SBP in healthy individuals, heart failure patients, and those with other diseases, while significantly lowered DBP in hypertensive patients It notably increased LVEF in heart failure patients and improved NYHA functional class in both heart failure patients and those with other diseases. CONCLUSIONS: Taurine showed noteworthy effects in preventing hypertension and enhancing cardiac function. Individuals prone to CVDs may find it advantageous to include taurine in their daily regimen.

Taurine rescues intervertebral disc degeneration by activating mitophagy through the PINK1/Parkin pathway.

Intervertebral disc degeneration (IDD) is a common cause of low back pain and disability. Recent studies have highlighted the critical role of mitochondrial dysfunction in the progression of IDD. In this study, we investigated the therapeutic potential of taurine in delaying IDD through the activation of mitophagy via the PINK1/Parkin pathway. Our in vitro and in vivo experiments demonstrate that taurine treatment significantly enhances mitophagy, reduces oxidative stress, delays cell senescence, and promotes the removal of damaged mitochondria in nucleus pulposus cells (NPC). Additionally, taurine-mediated activation of the PINK1/Parkin pathway leads to improved mitochondrial homeostasis and slows the progression of disc degeneration. These findings provide new insights into the protective effects of taurine and highlight its potential as a therapeutic agent for IDD.

Direct Molecular Action of Taurine on Hepatic Gene Expression Associated with the Amelioration of Hypercholesterolemia in Rats.

Taurine can ameliorate hypercholesterolemia by facilitating cholesterol efflux and increasing cytochrome P450 7A1 (CYP7A1) without clear underlying molecular mechanisms. This study aims to elucidate the molecular action of taurine in diet-induced hypercholesterolemia. Male Wistar rats were fed a high cholesterol diet containing 5% taurine for 14 days. Three-dimensional primary hepatocytes from rats were exposed to 10 mM taurine for 24 h. Transcriptome analyses of both the liver and hepatocytes were performed using DNA microarray. Taurine significantly decreased serum cholesterol levels and increased hepatic CYP7A1 mRNA levels and transcription rates in rats. Taurine altered the expression of seventy-seven genes in the liver, involving lipid, drug, amino acid metabolism, and gluconeogenesis pathways. The small heterodimer partner (SHP), a transcription factor regulated by taurine, was suppressed. "Network analysis" revealed a negative correlation between the SHP and induction of CYP7A1 and cytochrome P450 8B1 (CYP8B1). However, CYP7A1 and CYP8B1 levels were not altered by taurine in 3D-primary hepatocytes. Venn diagram analyses of the transcriptomes in both hepatocytes and the liver indicated a consistent upregulation of organic anion transporting polypeptide 2 (OATP2) and betaine homocysteine methyltransferase (BHMT). Taurine ameliorated hypercholesterolemia in rats fed a high cholesterol diet by directly enhancing the hepatic expression of BHMT and OATP2, which modulated the SHP and induced CYP7A1 and CYP8B1, thereby promoting cholesterol catabolism and lowering blood cholesterol levels.

Taurine and Polyphenol Complex Repaired Epidermal Keratinocyte Wounds by Regulating IL8 and TIMP2 Expression.

The healing process after acne lesion extraction provides a miniature model to study skin wound repair mechanisms. In this study, we aimed to identify solutions for acne scars that frequently occur on our faces. We performed acne scar cytokine profiling and found that Interleukin 8 (IL8) and Tissue inhibitor of metalloproteinases 2 (TIMP2) were significant factors at the wounded site. The effect of chlorogenic acid and taurine on human epidermal cells and irritated human skin was investigated. Chlorogenic acid and taurine regulated IL8 and TIMP2 expression and accelerated keratinocyte proliferation. Moreover, tight junction protein expression was upregulated by chlorogenic acid and taurine synergistically. Further, these compounds modulated the expression of several inflammatory cytokines (IL1α, IL1ß, and IL6) and skin hydration related factor (hyaluronan synthase 3; HAS3). Thus, chlorogenic acid and taurine may exert their effects during the late stages of wound healing rather than the initial phase. In vivo experiments using SLS-induced wounds demonstrated the efficacy of chlorogenic acid and taurine treatment compared to natural healing, reduced erythema, and restored barrier function. Skin ultrasound analysis revealed their potential to promote denser skin recovery. Therefore, the wound-restoring effect of chlorogenic acid and taurine was exerted by suppression of inflammatory cytokines, and induction of cell proliferation, tight junction expression, and remodeling factors.

Mitigating diabetes-related complications: Empowering metformin with cholecalciferol and taurine supplementation in type 2 diabetic rats.

BACKGROUND: Type 2 diabetes is one of the most prevalent chronic diseases worldwide, significantly impacting patients' quality of life. Current treatment options like metformin (MET) effectively counteract hyperglycemia but fail to alleviate diabetes-associated complications such as retinopathy, neuropathy, nephropathy, hepatopathy, and cardiovascular diseases. AIM: To propose the supplementation of cholecalciferol (CHO) and taurine (TAU) to enhance MET efficacy in controlling diabetes while minimizing the risk of associated complications. METHODS: The study involved sixty rats, including ten non-diabetic control rats and fifty experimental rats with type 2 diabetes induced by streptozotocin. The experimental rats were further subdivided into positive control and treatment subgroups. The four treatment groups were randomly allocated to a single MET treatment or MET combined with supplements either CHO, TAU, or both. RESULTS: Diabetic rats exhibited elevated levels of glucose, insulin, Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), glycated hemoglobin%, lipid markers, aspartate aminotransferase, and malondialdehyde, along with reduced levels of antioxidant enzymes (catalase and superoxide dismutase). The administration of CHO and TAU supplements alongside MET in diabetic rats led to a noticeable recovery of islet mass. The antioxidative, anti-inflammatory, and anti-apoptotic properties of the proposed combination therapy significantly ameliorated the aforementioned abnormalities. CONCLUSION: The supplementation of CHO and TAU with MET showed the potential to significantly improve metabolic parameters and protect against diabetic complications through its antioxidative, anti-inflammatory, and anti-apoptotic effects.

Gut microbiota, dietary taurine, and fiber shift taurine homeostasis in adipose tissue of calorie-restricted mice to impact fat loss.

Previously, we demonstrated that caloric restriction (CR) stimulates the synthesis, conjugation, secretion, and deconjugation of taurine and bile acids in the intestine, as well as their reuptake. Given taurine's potent antiobesogenic properties, this study aimed to assess whether the CR-induced shift in taurine homeostasis contributes to adipose tissue loss. To verify that, male C57Bl/6 mice were subjected to 20% CR or ad libitum feeding, with variations in cage bedding and gut microbiota conditions. Additional groups received taurine supplementation or were fed a low-taurine diet (LTD). The results showed that in CR animals, taurine derived from the intestine was preferentially trafficked to epididymal white adipose tissue (eWAT) over other tested organs. Besides increased levels of taurine transporter TauT, gene expression of Cysteine dioxygenase (Cdo) involved in taurine synthesis was upregulated in CR eWAT. Taurine concentration in adipocytes was inversely correlated with fat pad weight of CR mice. Different types of cage bedding did not impact eWAT taurine levels; however, the lack of bedding and consumption of a diet high in soluble fiber did. Depleting gut microbiota with antibiotics or inhibiting bile salt hydrolase (BSH) activity reduced WAT taurine concentration in CR mice. Taurine supplementation increased taurine levels in WAT and brown adipose tissue (BAT), promoting fat loss in CR animals. LTD consumption blunted WAT loss in CR animals, with negligible impact on BAT. This study provides multiple insights into taurine's role in CR-triggered fat loss and describes a novel communication path between the liver, gut, microbiota, and WAT, with taurine acting as a messenger.

The association between taurine concentrations and dog characteristics, clinical variables, and diet in English cocker spaniels: The Canine taURinE (CURE) project.

BACKGROUND: Occurrence of low blood taurine concentrations (B-TauC) and predisposing factors to taurine deficiency in English Cocker Spaniels (ECS) are incompletely understood. OBJECTIVES: Investigate the occurrence of low B-TauC in a Swedish population of ECS and evaluate the association between B-TauC and dog characteristics, clinical variables, and diet composition. ANIMALS: One-hundred eighty privately owned ECS. METHODS: Dogs were prospectively recruited and underwent physical examination, blood analyses, and echocardiographic and ophthalmic examinations. Dogs with clinical signs of congestive heart failure (CHF) also underwent thoracic radiography. Taurine concentrations were analyzed in plasma (EDTA and heparin) and whole blood. Diets consumed by the dogs at the time of the examination were analyzed for dietary taurine- (D-TauC), cysteine- (D-CysC), and methionine concentrations (D-MetC). RESULTS: Fifty-three of 180 dogs (29%) had low B-TauC, of which 13 (25%) dogs had clinical and radiographic signs of CHF, increased echocardiographic left ventricular (LV) dimensions and volumes, and impaired LV systolic function. Five (9%) dogs with low B-TauC had retinal abnormalities. Dietary MetC, dietary animal protein source (red/white meat), and age were associated with B-TauC in the final multivariable regression model (P < .001, R2 adj = .39). CONCLUSIONS AND CLINICAL IMPORTANCE: Low B-TauC suggests that taurine deficiency may play a role in the development of myocardial failure and CHF in ECS. Low D-MetC and diets with red meat as the animal protein source were associated with low B-TauC. Dogs with B-TauC below the normal reference range were older than dogs with normal concentrations.

Modulation of Ionizing Radiation-Induced Apoptosis by Taurine in Human Peripheral Blood Lymphocytes: Flow Cytometry-based Quantification.

Background: Radiotherapy, a highly effective method of radiation-based treating cancers, can reduce the size of tumors and affect healthy tissues. Radiation-induced lymphopenia as a side effect of radiation therapy can reduce the effectiveness of the treatment. Objective: This study aimed to examine how taurine can protect peripheral blood lymphocytes from radiation-based apoptosis. Material and Methods: In this experimental study, the effects of the taurine on lymphocytes were studied, and blood samples were divided into three groups: a negative control group that was not treated, a positive control group that was treated with cysteine (100 µg/ml), and a group that was treated with taurine (100 µg. mL-1) in three different doses (4, 8 & 12 Gy) before irradiation. The percentage of apoptotic and necrotic lymphocytes was measured using flow cytometry 48 and 72 hours after the irradiation, respectively. Results: According to the groups treated with taurine, the number of lymphocytes undergoing apoptosis was lower and higher compared to the negative and positive control groups, respectively. The decrease in this value was more pronounced 48 hours after radiation compared to 72 hours. Furthermore, there was a slight increase in the number of apoptotic lymphocytes with increasing radiation dose. Conclusion: Taurine effectively protects human peripheral blood lymphocytes from radiation-based apoptosis.

The role of cytidine 5'-triphosphate synthetase 1 in metabolic rewiring during epithelial-to-mesenchymal transition in non-small-cell lung cancer.

Epithelial-to-mesenchymal transition (EMT) contributes to the poor prognosis of patients with cancer by promoting distant metastasis and anti-cancer drug resistance. Several distinct metabolic alterations have been identified as key EMT phenotypes. In the present study, we further characterize the role of transforming growth factor-ß (TGF-ß)-induced EMT in non-small-cell lung cancer. Our study revealed that TGF-ß plays a role in EMT functions by upregulation of cytidine 5'-triphosphate synthetase 1 (CTPS), a vital enzyme for CTP biosynthesis in the pyrimidine metabolic pathway. Both knockdown and enzymatic inhibition of CTPS reduced TGF-ß-induced changes in EMT marker expression, chemoresistance and migration in vitro. Moreover, CTPS knockdown counteracted the TGF-ß-mediated downregulation of UDP-glucuronate, glutarate, creatine, taurine and nicotinamide. These findings indicate that CTPS plays a multifaceted role in EMT metabolism, which is crucial for the malignant transformation of cancer through EMT, and underline its potential as a promising therapeutic target for preventing drug resistance and metastasis in non-small-cell lung cancer.