Functional characterization of CSAD and its genomic variations modulating taurine synthesis and heat adaptation between two congeneric oyster species

Genome-wide identification and analysis of the PLP_deC genes involved in taurine synthesis in bivalves.

ABSTRACTPreclinical studies suggest that taurine may exert neuroprotective effects. However, its relevance to dementia risk in human populations remains unclear. We investigated the associations between mid‐life dietary taurine intake, circulating taurine concentrations, and the risk of late‐life all‐cause dementia, Alzheimer's disease (AD), and vascular dementia (VaD) in a large prospective cohort. This study utilized data from 27 786 participants of the Malmö Diet and Cancer Study with baseline examination from 1991 to 1996. Dietary taurine intake was estimated from a detailed diet history and adjusted for energy intake. Plasma taurine concentration was measured in a subset of 3693 individuals. Dementia diagnoses were ascertained through the Swedish National Patient Register and validated by memory clinic physicians. Cox proportional hazards models assessed associations with dementia risk, adjusting for potential confounders including APOE ε4 status, lifestyle factors, and comorbidities. Over a median 25‐year follow‐up, 3224 participants developed dementia. No significant associations were found between dietary taurine intake or plasma taurine concentrations and the risk of all‐cause dementia, AD, or VaD. Circulating taurine concentrations were only weakly correlated with dietary intake, suggesting a predominant role of endogenous taurine synthesis and metabolism. Our findings fail to support a protective role for taurine intake against dementia in humans. Further studies are warranted to examine potential effects under specific pathological conditions or with high‐dose supplementation.

Anti-tumor necrosis factor (TNF) therapy for inflammatory bowel disease (IBD) is hampered by issues of nonresponse and resistance, highlighting the urgent need for alternative or complementary treatments. Our study revealed significant upregulation of taurine in the intestinal tissues of IBD patients, which was inversely related to the severity of the disease. A key discovery was that TNF directly induced taurine synthesis in intestinal epithelial cells and increased the production of angiogenin, a nuclease that degrades mitochondrial RNA, which is known to amplify inflammatory responses. By degrading mitochondrial RNA, angiogenin inhibits the inflammatory response in macrophages, suggesting a potent immune-modulatory role for taurine. This mechanism implies that taurine could serve as an adjunct to anti-TNF therapies, enhancing their efficacy and providing a novel strategy for the management of IBD and other chronic inflammatory diseases by harnessing the body's innate immune regulatory mechanisms.

A feeding trial was carried out to investigate the effects of dietary serine on feeding, growth, biochemistry composition, hepatosomatic histological structure and metabolism of taurine synthesis in turbot (Scophthalmus maximus L.) (2.0 ± 0.01 g) fed plant protein-based diets. A fishmeal-based control diet (DietFM) and another two isonitrogenous and isolipidic plant-based diets containing 0.0% (DietPP) and 3.0% (DietS-3%) serine were formulated and fed twice daily (06:30 and 18:30) to fish in triplicate groups for 9 weeks. Feed intake in fish fed DietS-3% was notably higher than that in fish fed DietPP (p < 0.05), and no significant difference was discovered between fish fed DietFM and fish fed DietS-3% (p > 0.05). No significant difference (p > 0.05) was found with the increase of dietary serine in final body weight, specific growth rate, weight gain rate, feed efficiency ratio, protein efficiency ratio and survival rate when a significant increase (p < 0.05) was detected in hepatosomatic index between fish fed DietFM and fish fed DietS-3%. A significant increase was detected from 0.0% to 3.0% serine inclusion in ash content (p < 0.05) when no significant difference was discovered between the DietPP group and the DietS-3% group in moisture, protein and lipid content (p > 0.05). A significant increase (p < 0.05) was found from 0.0% to 3.0% serine supplementation in diets in body tarinre content when hepatosomatic L-cysteinesulphinate decarboxylase activity, cysteamine dioxygenase activity, liver and serum taurine content (p > 0.05) in fish fed DietS-3% showed no obvious difference with those of fish fed DietPP (p > 0.05). The cellular morphology and cell stripes in liver of fish fed diets with 3% serine inclusion were closer to that of fish fed DietFM. Considering the results, 3% serine supplementation in a high plant protein diet significantly increased feeding, mineral accumulation, body taurine content of turbot and obviously improved hepatosomatic histological structure. It is inferred that serine in a taurine-deficient diet can probably convert to taurine to some degree in juvenile turbot, and the transformation differs with tissue distinction.

Studies have shown that 129 mice generate more severe inflammatory responses than C57BL/6 (B6) mice shortly after influenza virus infection. However, the mechanisms for regulation of the magnitudes and kinetics of innate immune responses in different hosts remain to be fully understood. In this study, we found that cysteine sulfinic acid decarboxylase (CSAD), an essential enzyme in the taurine synthesis pathway, inhibits excessive inflammation after viral infection. CSAD KO mice in B6 background initiate stronger inflammatory responses and are more vulnerable to viral infections, exhibiting a phenotype resembling 129 mice. Interestingly, CSAD is differentially expressed in 129 and B6 mice; CSAD is highly expressed in B6 mice than in 129 mice. CSAD inhibits the NF-κB signaling pathway during various virus infections and stimulations. CSAD directly interacts with IKKα at the kinase domain, thus limiting the fast and strong phosphorylation of IKKα and then the downstream signaling pathway. Therefore, CSAD is a novel regulator to fine-tune the intensity of the NF-κB signaling pathway.IMPORTANCEThe mechanisms by which host factors regulate the intensity of innate immune responses are important because excessive inflammatory response can be harmful to the host. CSAD, an enzyme in the taurine synthesis pathway, inhibits excessive inflammatory responses after viral infection or stimulation by interacting with IKKα of the NF-κB signaling pathway, thus limiting the downstream activation of signaling and reducing the cytokine and chemokine gene expression. Our studies reveal for the first time that CSAD plays an important role in regulating innate immune responses, adding novel regulators to the complex networks of the NF-κB signaling pathway. Furthermore, our results also help us further understand the variations in the innate immune responses among individuals and provide a novel perspective for the development of new drugs or therapies for infectious diseases.

Contribution of cysteamine dioxygenase to taurine biosynthesis in the oyster Crassostrea gigas.

BackgroundHepatic fibrosis emerges as a pathological hallmark in the pathogenesis of chronic hepatopathies. Stephania tetrandra S. Moore is a traditional Chinese herb used to treat liver disease. However, the anti-hepatic fibrosis effect of fangchinoline (FAN), an active ingredient of S. tetrandra S. Moore, has not been reported. This study aimed to elucidate the anti-hepatic fibrosis effect of FAN and clarify the underlying molecular mechanisms.MethodsThe DEN-induced hepatic fibrosis mouse model, primary murine hepatic stellate cells (HSCs), and TGF-β-induced activation model of HSCs were used to explore the anti-fibrotic effect of FAN. The proteomics analysis was used to predict the pharmacodynamic mechanisms of FAN, and follow-up validation assays were performed with in vivo and in vitro experiments.ResultsFAN alleviated DEN-induced liver fibrosis in mice, reducing biomarker levels, slowing histopathological changes, and inhibiting collagen deposition. FAN suppressed HSCs activation and the biosynthetic abilities of the extracellular matrix. Proteomics was used to explore the mechanisms of FAN action, which is related to the regulation of taurine metabolism. FAN reversed DEN-induced changes in the levels of taurine and key enzymes that catalyze taurine synthesis. Additional taurine reinforces the regulatory effect of FAN on HSCs activation. Taurine could inhibit oxidative stress. FAN reduced DEN-induced ROS accumulation, which may be associated with Nrf2 pathway activation. Cleaning ROS with N-acetylcysteine enhanced the anti-fibrotic effects of FAN.ConclusionFAN can alleviate hepatic fibrosis by regulating taurine metabolism and oxidative stress, which has an important theoretical value.

This experiment aimed to study the effects of methionine (Met) on growth performance, intestinal structure and transport, Met metabolism, and target of rapamycin (TOR) signaling pathway in golden pompano (Trachinotus ovatus). Fish (9.12 ± 0.03 g) were fed with six diets with 0.79%, 0.90%, 1.01%, 1.12%, 1.23%, and 1.34% DL-Met for 8 weeks. Our study showed that Met supplementation significantly increased fish growth, villus length, crypt depth, and the mRNA levels of intestinal amino acid transporters including asc-type amino acid transporter 1 (asc-1), sodium-dependent neutral amino acid transporter B (asct2), and cationic amino acid transporter1 (cat1) (p < 0.05). Liver histological analysis revealed that Met addition improved cell swelling, nuclear migration, and hepatic vacuolation. Appropriate Met supplementation significantly increased mRNA level of key genes (methionine adenosyl transferase [mat], cystathionine beta-synthase [cbs], cystathionine γ-lyase [cse], and cysteine dioxygenase [cdo]) involved in transmethylation, transsulfuration metabolism, and taurine synthesis pathways. The level of 1.12%–1.23%, 1.12%, and 1.23% Met significantly upregulated the mRNA expression of S-adenosyl methionine/target of rapamycin (samtor), regulatory-associated protein of TOR (raptor), and ribosomal protein s6 (s6), respectively. The protein levels of protein kinase B (AKT), TOR, p-TOR, S6K, p-S6K, and p-S6 increased firstly and then decreased with increasing dietary Met supplementation. In conclusion, Met supplementation may promote growth of golden pompano by improving intestinal structure and amino acid transport, increasing transmethylation and transsulfuration metabolism, and activating TOR signaling pathways through SAMTOR and AKT.

Abstract Taurine is a non-proteinogenic amino acid synthesized from cysteine. Although taurine does not contribute to protein synthesis, it regulates glutathione metabolism, upregulates proliferative and anti-oxidative pathways, downregulates pro-apoptotic pathways, and improves mitochondrial function in normal tissues. However, the role of taurine in tumorigenesis and resistance development in cancer, especially breast cancer, is not widely understood. We aim to study metabolic and cellular changes associated with the taurine metabolism pathway in tamoxifen resistant (TAM-R) MCF-7 breast cancer cell lines. Methods: Three TAM-R MCF-7 models were developed using two strategies. The first was achieved by incrementally increasing the dose until reaching a predetermined dose (TAM-P). The second was achieved by taking cell lines from the first method and continuously treating them with 1μM of tamoxifen (TAM-C). NMR was used to quantify the levels of intracellular metabolites, and HPLC/MS-MS was used to calculate taurine uptake by the cells from media. Gene expression levels of ESR1, PI3KCA and PTEN were measured by RT-PCR. GSCA: Gene Set Cancer Analysis platform was used to check the association of a gene set consisting of taurine metabolism pathway genes (CDO1, ADO, GAD1, GAD2, CSAD) with the regulation of cancer related pathways. Results: Taurine, choline, and glutathione concentrations were significantly higher in TAM-C compared to tamoxifen-sensitive control and TAM-P, while cystine was lower in TAM-C. Taurine uptake from the media in TAM-C and control were slightly higher than TAM-P. ESR1 was 40 folds overexpressed in TAM-C and down regulated in TAM-P, while PI3KCA was overexpressed and PTEN was down regulated in both TAM-C and TAM-P. Moreover, there was a positive correlation between taurine metabolism pathway gene set and activation of ER pathway. Conclusion: The significant increase in taurine and decrease in cysteine in the TAM-C group cannot be explained by the marginal increase in taurine uptake alone, which necessities increased synthesis of the taurine. Overexpression of ESR1 in TAM-C could be caused by upregulation of the taurine synthesis pathway. However, overexpression of PI3KCA and down regulation of PTEN indicates reliance on PI3K/AKT/PTEN pathway instead of estrogen signaling pathway. Moreover, increased glutathione and choline concentrations increased antioxidative capacity, mitochondrial function, and resistance to oxidative stress. Citation Format: Yazan I. Hamadneh, Mohammad Alwahsh, Aya Hasan, Ala A. Alhusban, Osama M. Younis, Roland Hergenröder, Lama Hamadneh. Taurine's potential role in tamoxifen resistant MCF-7 cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 4407.

The razor clam (Sinonovacula constricta) is a key species in marine aquaculture, known for its wide salinity adaptation, and potential for cultivation in saline-alkaline water. Understanding its response mechanisms is crucial for expanding its farming into these regions. This study reveals the response mechanisms of S. constricta in response to low-salinity alkaline stress through a combined analysis of transcriptomics and metabolomics. After 24 h of salt-alkali stress (SA group), 1378 differentially expressed genes (DEGs) were identified, with enriched pathways including glycerophospholipid metabolism, serine, taurine, and hypotaurine metabolism. Additionally, 341 significantly different metabolites (SDMs) were found, primarily involved in taurine and hypotaurine metabolism, purine metabolism, and the FoxO signaling pathway, etc. Both DEGs and SDMs were notably enriched in hypotaurine metabolism, glycerophospholipid metabolism, and the mTOR signaling pathway, showing significant upregulation in the SA group. Correlation analysis found that the integrated regulatory network was involved in the synthesis of taurine, glycerophospholipids, and L-glutamic acid, and the metabolism of 3-mercaptopropionic acid. These results suggest that low salinity and alkalinity induce stress responses in S. constricta by regulating osmotic balance, phospholipid synthesis, and lipid metabolism. This study offers insights into the molecular mechanisms of salt-alkali response in S. constricta.

Background: The mechanisms underlying the progression and metastasis of triple-negative breast cancer (TNBC) in the context of extended morphine exposure remain poorly understood. Morphine consumption has been a pressing issue in many countries. While the physiological impact of extended morphine use is multifaceted, cancer patients with a history of extended morphine usage often have a poor prognosis. Methods: In this study, we investigated the impact of extended morphine treatment on the transcriptional profiles of TNBC. To this end, mice were administered morphine intraperitoneally for 14 days, followed by the implantation of EO771 cells, which are triple-negative breast cancer cells, into their mammary fat pad. After primary tumors were removed on the 38th day, a subset of mice was continuously given saline or morphine until the 68th day. Tumor size, organ metastasis, and tumor RNA expression were analyzed. Results: Our findings showed that extended exposure to morphine led to an increase in lung metastasis in the mouse model of triple-negative breast cancer. We analyzed RNA sequencing on tumors to compare their transcriptional profiles with or without metastasis. Through pathway analysis, we specifically examined the novel impact of morphine on the downregulation of taurine/hypotaurine biosynthesis. Given that morphine, droperidol (a dopamine receptor antagonist), and naloxone (an opioid receptor antagonist) might act through either opioid receptors or dopamine receptors, we further demonstrated that taurine mitigated EO771 cell invasion induced by morphine but not by droperidol or naloxone treatment. Additionally, morphine treatment markedly decreased the expression of GAD1, one of the enzymes essential for taurine biosynthesis, whereas droperidol and naloxone did not. Conclusions: The findings of morphine-induced reduction in GAD1 levels and the inhibition of invasion by taurine treatment suggest that taurine could serve as a potential supplement for triple-negative breast cancer patients who require morphine as part of their treatment regimen or due to their circumstances.

The Pacific oyster Crassostrea gigas is rich in taurine, a conditionally essential amino acid functioning in anti-oxidation, anti-inflammation, anti-aging, osmoregulation, and neuromodulation. Breeding oyster varieties with enhanced taurine content is significant to meet people's demand for high-quality oysters. In the present study, polymorphisms in the oyster cysteamine dioxygenase (CgADO) gene that encodes the central enzyme of the cysteamine pathway for taurine synthesis were investigated, and their association with taurine content was assessed in the Changhai (CH) and Qinhuangdao (QHD) populations. A total of 47 single nucleotide polymorphism (SNP) loci were identified in the exonic region of CgADO through Sanger sequencing, with a synonymous SNP (c.415T>C) showing a significant association with taurine content. Oysters with the CT genotype at c.415T>C exhibited higher taurine content than those with the TT genotype (p < 0.05). Moreover, a significant difference in the CgADO mRNA expression was observed between oysters with different genotypes, with higher expression in the CT genotype compared to the TT genotype (p < 0.001). These findings indicate the potential influence of CgADO polymorphisms on taurine content in C. gigas and provide candidate functional markers for the selective breeding of oyster varieties with improved taurine levels.

Totoaba (Totoaba macdonaldi) aquaculture offers economic and ecological advantages. However, its culture still relies on fishmeal in diets because alternative protein sources show reduced productive performance. The current study assessed the impact of low concentrations of methionine and taurine together with alternative proteins, on the productive performance of T. macdonaldi over a 60-day experimental period. Four diets were formulated for this purpose, a basal diet (D-BD), the basal diet with methionine (D-MET), the basal diet with taurine (D-TAU), and the basal diet with methionine and taurine (D-MET + TAU). The present experiment used a randomized design. One hundred forty-four juveniles (41.0 ± 0.5 g in weight) were randomly distributed in 12 tanks (500 L) in triplicate groups to assess biological indices, cholesterol content, hepatic gene expression, and the synthesis and transport of taurine. The statistical analysis revealed that the dietary treatments D-MET and D-TAU positively affected the growth rate, whereas their interaction resulted in a significantly higher growth (p < 0.05). The expression of the igf-1 gene in the liver increased and showed a positive interaction. When TAU and MET were limited, there was an observed overexpression of csad in hepatic tissue. Diets supplemented with TAU showed a decrease in total cholesterol level, whereas cholesterol level in the liver increased with MET supplemented alone. Total TAU content in fish tissues was significantly higher when both TAU and MET were supplemented. In conclusion, T. macdonaldi exhibits a limited capacity, for TAU synthesis, and MET limitation appears to restrict growth potential.

This present study was conducted to illustrate the effect of dietary cysteamine on feeding, growth, biochemistry composition, hepatosomatic histological structure and metabolism of taurine synthesis in juvenile turbot ( Scophthalmus maximus L.) (2.0 ± 0.01 g) fed high plant protein diets. A fishmeal-based diet (72.5% FM) was designed as the control diet (DietFM). Four isonitrogenous and isolipidic diets consist of 14.0% FM, 23.0% soybean meal and 30.0% wheat gluten meal, which were formulated to substitute FM with 0.0%, 0.05%, 0.1% and 0.15% cysteamine hydrochloride (labeled as DietPP, DietCS-0.05%, DietCS-0.1% and DietCS-0.15% respectively). Fish were stochastically allocated into fifteen 200L tanks and fed twice daily (06:30 and 18:30) to apparent satiation for 9 weeks. Feed intake (FI) in fish-fed DietCS-0.05% was conspicuously higher than that in fish-fed DietPP (p&lt;0.05), and no notable difference was discovered among fish-fed diets with cysteamine inclusion (p&gt;0.05). No conspicuously upward trend was found with the increase of dietary cysteamine in FBW, SGR, WGR, FER, PER, and SR when there was a downward trend in CF, VSI, and HSI (p&gt;0.05). A remarkable increase was discovered from 0.0% to 0.05% cysteamine inclusion in ash content (p&lt;0.05) when no noticeable difference was observed among all the cysteamine inclusion groups in moisture, protein, and lipid content (p&gt;0.05). Only the body taurine content showed a notable increase between fish-fed DietCS-0.05% and fish-fed DPP among the indexes of body taurine, liver taurine, and serum taurine content (p&lt;0.05), whereas no notable difference was observed in hepatosomatic L-cysteine sulfinate decarboxylase (CSD) and cysteamine dioxygenase (CDO) activities among all the cysteamine inclusion groups (p&gt;0.05). The cellular morphology and cell veins in the liver of fish-fed diets with cysteamine inclusion were clearer than those of fish-fed DPP. The results showed that 0.05% cysteamine addition in a high plant protein diet is optimal.

Pancreatic ductal adenocarcinoma (PDAC) exhibits an altered metabolic profile compared to normal pancreatic tissue. However, studies on actual pancreatic tissues are limited. Untargeted metabolomics analysis was conducted on 54 pairs of tumor and matched normal tissues. Taurine levels were validated via immunohistochemistry (IHC) on separate PDAC and normal tissues. Bioinformatics analysis of transcriptomics and proteomics data evaluated genes associated with taurine metabolism. Identified taurine-associated gene was validated through gene modulation. Clinical implications were evaluated using patient data. Metabolomics analysis showed a 2.51-fold increase in taurine in PDAC compared to normal tissues (n=54). IHC confirmed this in independent samples (n=99 PDAC, 19 normal). Bioinformatics identified 2-aminoethanethiol dioxygenase (ADO) as a key gene modulating taurine metabolism. IHC on a tissue microarray (39 PDAC, 10 normal) confirmed elevated ADO in PDAC. The ADO-Taurine axis correlated with PDAC recurrence and disease-free survival. ADO knockdown reduced cancer cell proliferation and tumor growth in a mouse xenograft model. The MEK-related signaling pathway is suggested to be modulated by ADO-Taurine metabolism. Our multi-omics investigation revealed elevated taurine synthesis mediated by ADO upregulation in PDAC. The ADO-Taurine axis may serve as a biomarker for PDAC prognosis and a therapeutic target.

Inflammatory bowel disease (IBD) presents a significant challenge due to its intricate pathogenesis. NSD2, a histone methyltransferase responsible for dimethylating histone 3 at lysine 36, is associated with transcriptional activation. NSD2 expression is decreased in both the intestinal epithelial cells (IECs) of IBD patients and the IBD mouse model. However, the precise role of NSD2 in IBD remains unexplored. Colon tissues from IBD mice, SW620 cells and MC38 cells, were used as research subjects. Clinical databases of IBD patients were analysed to investigate whether NSD2 expression is reduced in the occurrence of IBD. NSD2-knockout mice were generated to further investigate the role of NSD2 in IBD. The IECs were isolated for RNA sequencing and chromatin immunoprecipitation sequencing to identify molecular signalling pathways and key molecules leading to IBD in mice. Molecular and cellular experiments were conducted to analyse and validate the role of NSD2 in the development of IBD. Finally, rescue experiments were performed to confirm the molecular mechanism of NSD2 in the development of IBD. Deficiency of NSD2 in mouse IECs aggravated epithelial barrier disruption and inflammatory response in IBD. Mechanistically, NSD2 loss led to downregulation of H3K36me2 and flavin-containing monooxygenase (FMO) (taurine-synthesis enzyme) mRNA, resulting in decreased taurine biosynthesis in IECs. Significantly, supplementation with taurine markedly alleviated the symptoms of NSD2 deficiency-induced IBD. These data demonstrate that NSD2 plays a pivotal role in maintaining FMO-mediated taurine biosynthesis to prevent intestinal inflammation. Our findings also underscore the importance of NSD2-H3K36me2-mediated taurine biosynthesis in maintaining intestinal mucosal barrier homeostasis. In this study, we investigated the role of the histone methyltransferase NSD2 in preventing intestinal barrier disruption by sustaining taurine biosynthesis. NSD2 levels were reduced in both human specimens and mouse models of IBD. We demonstrate that NSD2 loss hinders the process of taurine synthesis in intestinal cells, leading to increased intestinal inflammation. Supplementation with taurine significantly relieved the symptoms caused by NSD2 deficiency. These data suggest that maintenance of NSD2-mediated taurine biosynthesis is vital for preserving the intestinal barrier and attenuating inflammation.

The CDO1 gene is an important gene in the taurine synthesis pathway and has been observed to have high expression in ovaries of female mammals. This study aims to explore the conservation of CDO1 gene in domestic yaks, as well as to examine the fundamental characteristics of CDO1 gene and its expression in female yaks. Ovarian samples were collected from yaks in the follicular phase, luteal phase and gestation period in this experiment, and their total RNA and protein were extracted. Then Polymerase Chain Reaction (PCR) and bioinformatics online software were used to clone and analyze the CDO1 gene. The relative expression of CDO1 in yak ovaries was detected by Quantitative Real-time PCR (RT-qPCR) and Western blotting. The distribution and localization of CDO1 protein in ovary were detected by immunohistochemistry. We have successfully cloned the coding region of CDO1 gene in yak. The results showed that the CDS region of CDO1 gene was 603 bp, encoding 200 amino acids, and was a relatively stable hydrophilic protein. CDO1 is relatively conservative in species evolution. The protein encoded by CDO1 gene does not have a signaling peptide or a transmembrane structure. It is a protein that is not involved in transmembrane transport and is mainly located in the cytoplasm. The secondary structure of the protein is dominated by the random coil. CDO1 is estimated to interact with 10 proteins. The results of RT-qPCR and Western blotting showed that the CDO1 gene exhibited the highest expression in the ovary during the luteal phase and the lowest expression in the ovary during the follicular phase (P < 0.01). The results of immunohistochemistry showed that CDO1 was mainly expressed in granular cells, theca cells and lutein cells of ovarian tissue. These results suggest that the CDO1 gene has undergone minimal evolutionary changes during the course of animal evolution. The results provide a reference for further investigation of the function of CDO1 gene in reproduction and production in yaks.

Abstract Acrylamide, an endocrine‐disrupting emerging contaminant from both the environment and food processing, has been linked to cardiac developmental toxicity in zebrafish. However, the mechanisms involved in the cardiac developmental toxicity from long‐term exposure to acrylamide remain unclear. This study provides in‐depth evidence on the metabolic regulation of zebrafish embryos with acrylamide exposure. A comprehensive metabolites analysis of four different acrylamide exposures (0, 0.5, 1.0, and 2.0 mM) at different zebrafish developmental stages (6, 24, 48, 72, 96, and 120 h post fertilization, hpf) was performed. Metabolite changes throughout the zebrafish development (6–120 hpf) were closely associated with taurine and hypotaurine metabolism. The pattern of significantly changed metabolites revealed that acrylamide strongly disrupts taurine and hypotaurine metabolism related to a deficient cardiovascular system. Moreover, acrylamide exposure disrupted the de novo synthesis of taurine via cysteine sulfinic acid decarboxylase during early zebrafish embryogenesis. In addition, taurine supplementation (10 mM) effectively alleviates acrylamide‐induced deficient cardiovascular system. Our results demonstrate that acrylamide exposure has a detrimental effect on early heart development in zebrafish due to the inhibition of de novo synthesis of taurine.

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