Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is now the most prevalent chronic liver disease worldwide, imposing a severe public health burden. Its core pathological hallmark is excessive hepatic lipid accumulation driven by systemic metabolic dysregulation. Concomitant hepatocellular injury impairs hepatic lactate clearance, leading to aberrant lactate buildup in the liver microenvironment. However, the causal role of lactate in exacerbating liver lipid metabolism dysfunction and driving the progression of MASLD remains unclear. Methods: First, we performed a comprehensive bioinformatic analysis of publicly available transcriptomic datasets. Mining of the Gene Expression Omnibus (GEO) database showed that lactate dehydrogenase (LDH) expression was significantly upregulated in liver tissues from both metabolic dysfunction-associated fatty liver disease (MASLD) patients and MASLD mouse models. Next, network pharmacology approaches were employed to predict putative molecular targets that could mediate lactate’s biological effects. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that these candidate targets were predominantly enriched in pathways governing fatty acid metabolism and long-chain fatty acid transport. Molecular docking and molecular dynamics simulations further suggested possible interactions and supported the prioritization of cluster of differentiation 36 (CD36) as candidate lipid metabolism regulators potentially involved in lactate-mediated effects. Finally, liver-specific Ldha knockdown mice (AAV8-TBG-shRNA) and free fatty acid-induced steatotic AML12 hepatocytes were used to investigate the functional relevance of these findings in vivo and in vitro. Results: Network pharmacology analyses preliminarily identified the PPAR signaling pathway as a candidate pathway potentially linking lactate to MASLD. Experimental results showed that exogenous lactate administration was associated with significantly increased lipid accumulation in steatotic AML12 hepatocytes and the livers of MASLD mice, manifested as elevated triglyceride levels and enhanced lipid droplet formation, accompanied by upregulated expression of PPARγ and CD36. Conversely, inhibiting endogenous lactate production or silencing PPARγ or CD36 attenuated this lipid-accumulation phenotype and significantly reduced intracellular triglyceride levels. Conclusions: In conclusion, these findings indicate that lactate exposure is associated with hepatic lipid accumulation and upregulation of the PPARγ/CD36 axis. Pharmacological inhibition or silencing of PPARγ or CD36 attenuates this phenotype, suggesting that this pathway may contribute to lactate-associated hepatic steatosis and potentially accelerate MASLD progression.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a globally prevalent hepatic disorder, characterized by hepatic lipid accumulation and extrahepatic complications, notably intestinal barrier injury, which further exacerbates MASLD progression. The "gut-liver axis" has been identified as a critical contributor to MASLD development, with insulin-like growth factor 1 (IGF-1) serving as a pivotal coupling factor of this axis. However, the specific role and molecular mechanism by which IGF-1 modulates intestinal barrier function in the context of MASLD remains unclear. Methods: This study analyzed the correlations between the GH/IGF-1 axis and intestinal barrier function in MASLD rats, and explored the effects of IGF-1 intervention both in vivo and in vitro. Results: Our results showed that MASLD rats exhibited intestinal barrier impairment, characterized by elevated serum Diamine oxidase (DAO) and D-Lactate (D-LAC) levels, villus damage, and downregulation of tight junction proteins and Mucin (MUC2). These changes were accompanied by suppression of the GH/IGF-1 axis. Correlation analysis uncovered a negative association between IGF-1 levels and markers of barrier dysfunction. IGF-1 intervention effectively repaired the intestinal barrier structure of MASLD rats and significantly upregulated the expressions of IGF-1R, PI3K, and AKT. In vitro, IGF-1 treatment improved transepithelial electrical resistance (TEER), enhanced barrier-related gene expression, promoted cell proliferation, and inhibited apoptosis. Conclusions: These findings suggested that GH/IGF-1 axis suppression, intestinal barrier dysfunction, and IGF-1R/PI3K/AKT signaling were interconnected within the gut-liver axis in MASLD. IGF-1 may contribute to barrier regulation through associated signaling changes, highlighting the GH/IGF-1 axis as a potential complementary target.

Aflatoxin B1 (AFB1) is a potent mycotoxin that poses significant risks to food safety, public health, and livestock production. Taurochenodeoxycholic acid (TCDCA), a bioactive bile acid, exhibits hepatoprotective and intestinal barrier-modulating potential; however, its role in mitigating AFB1 toxicity remains unclear. This study employed a broiler model to evaluate the protective effects of TCDCA against AFB1-induced hepatic and intestinal injury. The results demonstrated that TCDCA treatment significantly improved growth performance impaired by AFB1 exposure. TCDCA alleviated hepatic lesions, decreased serum hepatic enzyme activities, and suppressed hepatocyte apoptosis and oxidative stress. Mechanistically, TCDCA modulated AFB1 detoxification by downregulating hepatic cytochrome P450 enzymes (CYP1A2 and CYP3A4), thereby reducing the formation of AFB1-DNA adducts. Furthermore, TCDCA attenuated pyroptosis and inflammation by lowering serum inflammatory cytokine contents and inhibiting activation of the hepatic NLRP3/Caspase-1/GSDMD signaling pathway. In the intestine, TCDCA improved the villus morphology, upregulated the expression of tight junction proteins including zonula occludens-1 (ZO-1), claudin-1 (CLDN1), occludin (Occludin), and mucin-2 (MUC2), reduced serum diamine oxidase (DAO) activity and D-lactate level, and restored secretory immunoglobulin A (sIgA) content, thereby strengthening intestinal barrier integrity. Additionally, 16S rRNA sequencing revealed that TCDCA mitigated AFB1-induced gut microbiota dysbiosis by increasing the abundance of Akkermansia and decreasing harmful genera such as Megamonas. Collectively, TCDCA mitigates AFB1-induced growth suppression and hepatotoxicity through mechanisms involving metabolic regulation, antioxidation, inhibition of pyroptosis and inflammation, reinforcement of intestinal barrier function, and modulation of gut microbiota.

Fatty liver hemorrhagic syndrome (FLHS), a common metabolism-associated fatty liver disease (MAFLD) in modern intensive laying hens, affects not only liver function but also other organs, including the lungs, causing lung impairment and susceptibility to respiratory ailments. Clinical investigations have revealed an independent association between MAFLD and diminished lung function. Previous studies have demonstrated that taurine enhances the body's antioxidant capacity and exerts a significant inhibitory effect on both acute and chronic inflammation. Additionally, taurine exhibits promising preventive and therapeutic efficacy in the occurrence and development of FLHS, significantly ameliorating liver damage in laying hens. However, whether taurine can mitigate FLHS-induced lung injury remains unexplored. This study investigated the effects of taurine on lung injury in FLHS laying hens induced by a high-energy and low-protein diet, and macrophage inflammation model stimulated by Lipopolysaccharide (LPS). The results showed that taurine treatment significantly reduced inflammatory cell infiltration in lung tissue and improved alveolar structure. Furthermore, antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), as well as the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and its downstream factors expression levels of quinone oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1), were significantly increased in the lungs and macrophages of laying hens following taurine administration. Taurine also effectively suppressed M1 macrophage polarization, reduced levels of proinflammatory cytokines, including inducible nitric oxide synthase (iNOS), nitric oxide (NO), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α), inhibited the activation of the LPS/TLR4/NF-κB signaling pathway, JAK2-STAT1 signaling pathway, and NLRP3 inflammasome. The results suggested that taurine can alleviate lung injury in FLHS laying hens by enhancing antioxidant capacity and inhibiting inflammatory response mediated by macrophage M1 polarization.

Fatty liver hemorrhagic syndrome (FLHS) in laying hens is a nutritional and metabolic disease involving liver enlargement, hepatic steatosis, and hepatic hemorrhage as the primary symptoms. The syndrome is prone to occur during the peak laying period of laying hens, which has resulted in significant economic losses in the laying hen breeding industry; however, the specific pathogenesis of FLHS remains unclear. Our group and previous studies have shown that bile acid levels are significantly decreased during the development of fatty liver and that targeted activation of bile acid–related signaling pathways is beneficial for preventing and treating fatty liver. In this study, we generated a FLHS laying hen model by feeding hens a high-energy, low-protein diet, with goose deoxycholic acid (CDCA) given as an intervention. HE staining, fluorescence quantitative PCR, and ELISA were used to evaluate the effects of CDCA on pathological changes and inflammatory responses in the liver. The results showed that hepatic hemorrhage in FLHS laying hens was reduced after CDCA treatment. Furthermore, fat vacuoles and transaminase levels decreased significantly. In addition, expression levels of M1-type macrophage markers and polarization products were significantly reduced, and the expression of pro-inflammatory regulatory factors related to the JAK-STAT signaling pathway, LPS-TLR4-Myd88–NF-kB signaling pathway, and NLRP3 inflammasomes decreased significantly as well. Expression levels of M2-type macrophage markers and polarization products increased significantly, as did the expression of anti-inflammatory regulators related to the JAK-STAT signaling pathway. These results suggest that CDCA ameliorates liver injury in laying hens with FLHS by inhibiting macrophage M1-type polarization and the resulting pro-inflammatory response, thereby promoting M2-type macrophage polarization and an anti-inflammatory response.

Type 2 diabetes mellitus (T2DM) is a serious metabolic disease characterized by insulin resistance and reduced insulin production, which causes abnormally elevated blood glucose. It has been reported that T2DM can enhance oxidative stress and inflammatory responses, and stimulate a variety of complications including liver injury. Studies have shown that taurine has antioxidant and anti-inflammatory effects that can not only ameliorate diabetes but also alleviate liver injury caused by various diseases. However, its effect on liver injury in T2DM is not clear. In our study, a high-fat diet and intraperitoneal injection of streptozotocin (STZ) was used to induce liver injury in T2DM rats, and taurine was given as a treatment. Through the use of HE staining on paraffin sections, ELISA, and qRT-PCR, the effects of taurine on liver pathological alterations, antioxidant capacity, and inflammatory response were investigated. We found that: hepatic transaminase levels of rats were reduced significantly following taurine administration; histopathological observations revealed that the morphology of rat hepatocytes was close to normal, and the number of inflammatory cells around liver vessels was significantly reduced; antioxidant-related indicators were significantly increased, including SOD, CAT, GSH-Px and T-AOC, while related factors of the Nrf2 signalling pathway and its downstream HO-1, NQO1 and γ-GCS were significantly increased; the expression of the JAK2-STAT1 signalling pathway, TLR4/NF-κB signalling pathway and NLRP3 inflammatory vesicle-related factors were significantly reduced. Our results suggest taurine can alleviate T2DM-induced liver injury by improving the antioxidant capacity of the liver and inhibiting macrophage M1-type polarization and the inflammatory response mediated thereby.

Diarrhea in piglets is one of the most important diseases and a significant cause of death in piglets. Preliminary studies have confirmed that taurine reduces the rate and index of diarrhea in piglets induced by LPS. However, there is still a lack of relevant information on the specific target and mechanism of action of taurine. Therefore, we investigated the effects of taurine on the growth and barrier functions of the intestine, microbiota composition, and metabolite composition of piglets induced by LPS. Eighteen male weaned piglets were randomly divided into the CON group (basal diet + standard saline injection), LPS group (basal diet + LPS-intraperitoneal injection), and TAU + LPS group (basal diet + 0.3% taurine + LPS-intraperitoneal injection). The results show that taurine significantly increased the ADG and decreased the F/G (p < 0.05) compared with the group of CON. The group of TAU + LPS significantly improved colonic villous damage (p < 0.05). The expression of ZO-1, Occludin and Claudin-1 genes and proteins were markedly up-regulated (p < 0.05). Based on 16s rRNA sequencing analysis, the relative abundance of Lactobacilluscae and Firmicutes in the colon was significantly higher in the LPS + TAU group compared to the LPS group (p < 0.05). Four metabolites were significantly higher and one metabolite was significantly lower in the TAU + LPS group compared to the LPS group (p < 0.01). The above results show that LPS disrupts intestinal microorganisms and metabolites in weaned piglets and affects intestinal barrier function. Preventive addition of taurine enhances beneficial microbiota, modulates intestinal metabolites, and strengthens the intestinal mechanical barrier. Therefore, taurine can be used as a feed additive to prevent intestinal damage by regulating intestinal microorganisms and metabolites.

Metabolic-associated fatty liver disease (MAFLD) is a chronic liver disease caused by fat deposition in the liver of humans and mammals, while fatty liver hemorrhagic syndrome (FLHS) is a fatty liver disease in laying hens which can increase the mortality and cause severe economic losses to the laying industry. Increasing evidence has shown a close relationship between the occurrence of fatty liver disease and the disruption of mitochondrial homeostasis. Studies have proven that taurine can regulate hepatic fat metabolism, reduce hepatic fatty deposition, inhibit oxidative stress, and alleviate mitochondrial dysfunction. However, the mechanisms by which taurine regulates mitochondrial homeostasis in hepatocytes need to be further studied. In this study, we determined the effects and mechanisms of taurine on high-energy low-protein diet-induced FLHS in laying hens and in cultured hepatocytes in free fatty acid (FFA)-induced steatosis. The liver function, lipid metabolism, antioxidant capacity, mitochondrial function, mitochondrial dynamics, autophagy, and biosynthesis were detected. The results showed impaired liver structure and function, mitochondrial damage and dysfunction, lipid accumulation, and imbalance between mitochondrial fusion and fission, mitochondrial autophagy, and biosynthesis in both FLHS hens and steatosis hepatocytes. Taurine administration can significantly inhibit the occurrence of FLHS, protect mitochondria in hepatocytes from disease induced by lipid accumulation and FFA, up-regulate the expression levels of Mfn1, Mfn2, Opa1, LC3I, LC3II, PINK1, PGC-1α, Nrf1, Nrf2, and Tfam, and down-regulate the expression levels of Fis1, Drp1, and p62. In conclusion, taurine can protect laying hens from FLHS through the regulation of mitochondrial homeostasis, including the regulation of mitochondrial dynamics, autophagy, and biosynthesis.

Aflatoxin B1 (AFB1), which widely exists in soil and crops, is the most toxic aflatoxin and a carcinogen to humans and animals. The liver is the main organ that processes AFB1 and other mycotoxins and is also the main target of AFB1 toxicity. Taurine is known to exhibit a variety of physiological and pharmacological functions. In the present study, taurine was administered to detect the protective effect and mechanism of taurine in AFB1induced liver injury in rats. The results showed that taurine inhibited the increase in hepatic injury indices, hepatic apoptosis and hepatic malondialdehyde (MDA) contents while significantly enhanced the hepatic activities of antioxidant enzymes and mitochondrial function-related indices in AFB1-poisoned rats. Meanwhile, the expression levels of key factors in the Nrf2 signalling pathway were upregulated while the expression levels of key proteins in the mitochondria-mediated apoptotic pathway were downregulated after taurine administration. The results showed that taurine can reverse AFB1-induced liver injury and abnormal apoptosis through activation of the Nrf2 signalling pathway and its downstream antioxidant enzymes, which further protects mitochondria from oxidative stress and the subsequent apoptotic pathway.

本试验旨在研究低敏宠物核心料的抗过敏效果并初步探讨其可能机制.试验以5周龄雌性BALB/c小鼠为实验动物,通过OVA诱导食源性过敏小鼠模型.同时给予低敏宠物核心料,检测其对食源性过敏小鼠肠道组织结构以及过敏反应的影响,并通过检测小鼠免疫球蛋白、细胞因子、组胺水平,脾、胸腺器官指数,初步探讨其抗过敏的可能机理.结果显示:与对照组相比,食源性过敏小鼠体重增长缓慢,平均日增重极显著降低(P＜0.01),绒毛高度、隐窝深度、二者比值(V/C)均显著降低(P＜0.05或P＜0.01),腹泻率极显著升高(P＜0.01),达到86％,直肠温度极显著降低(P＜0.01),过敏反应评分极显著增加(P＜0.01),血清IgE、IgG、His、IL-4水平均极显著上升(P＜0.01),IL-10水平极显著下降(P＜0.01),肥大细胞脱颗粒比率显著增加(P＜0.05),胸腺及脾指数则均极显著降低(P＜0.01);给予低敏宠物核心料的小鼠上述指标较过敏小鼠均显著改善.本试验采用的低敏宠物核心料可通过抑制肥大细胞脱颗粒,减少组织胺的释放,抑制OVA诱导的食源性小鼠过敏反应的发生,减轻过敏反应症状,同时可改善过敏小鼠肠道组织结构,促进营养物质的吸收.

The promotion of neurogenesis from neural stem cells (NSCs) in the hippocampus was found to be the most fundamental and effective therapy for depression. Our previous studies proved an antidepressive effect of taurine on rats, but the exact mechanism remains unclear. In this study, CUMS model was established in rats, and NSCs were cultured in vitro to investigate the protective effect and mechanisms of taurine on neurogenesis and apoptosis in CUMS rats and glutamate-injured NSCs. The results showed that ki67-positive cells were significantly increased by taurine, while apoptosis in the DG of CUMS rats was significantly inhibited by taurine. In vitro study, cell viability, Brdu+, β-tubulin III+, and GFAP+ cells in taurine-treated cells were significantly higher, while apoptosis rate was lower than the glutamate-treated cells. The protein expression of BDNF and its downstream pathway was upregulated by taurine administration. The results demonstrated that taurine can increase the survival, proliferation, and differentiation of NSCs; this protective effect of taurine may be due to the upregulation of BDNF/ERK/CREB signaling pathway. On the other hand, taurine can also inhibit abnormal apoptosis induced by CUMS or glutamate, the mechanism of which may be due to its antioxidative ability.

Hypoxia caused by low ambient temperature leads to hypoxemia in broilers, which aggravates the metabolic burden of the liver. Liver damage is closely related to oxidative stress and apoptosis. It has been proved that taurine can reduce oxygen free radicals, exert antioxidant properties, and inhibit mitochondria-dependent apoptosis. This experiment aimed to determine whether taurine could prevent liver damage by inhibiting oxidative stress and the cytochrome c-mediated apoptotic pathway in broilers under low ambient temperature. Broilers were given 1% taurine in drinking water, and the temperature was raised at 10 °C ~ 12 °C from 21 to 42 days. At 28 and 42 days, the hepatic tissues were collected. The antioxidant capacity of liver tissues and mRNA expression levels of the factors related with cytochrome c-medicated apoptosis pathway were measured. The results showed taurine significantly increased the total antioxidant capacity (T-AOC) at 28 days. Furthermore, taurine also increased the activities of glutathione peroxidase (GSH-PX) while reducing malondialdehyde (MDA) concentration at 28 days and 42 days. Our results also revealed that taurine significantly increased the mRNA expression levels of Hsp 27 and Hsp 90 while decreasing caspase-3 mRNA expression in broiler hepatocytes at 28 days. In addition, taurine also upregulated the expression level of Bcl-2 at 42 days. In summary, the present study found that taurine enhances the antioxidant ability and alleviates cytochrome c-mediated apoptosis in hepatic tissue of broilers under low temperature.

Aflatoxin B1 (AFB1) is one of the most toxic mycotoxins, which can cause serious kidney damage after ingestion. Taurine protects the kidney, an effect related to its antioxidation and anti-apoptotic actions. In the present study, taurine was administered to detect the protective effect and mechanism of taurine on AFB1-induced renal injury in rats. The results show that taurine ameliorated the increase in serum blood urea nitrogen (BUN), blood creatinine (CRE), blood uric acid (UA), cystatin c (Cys-c), and urinary protein and AKP levels. Taurine also inhibits the content of superoxide dismutase (SOD), total antioxidant capacity (T-AOC), catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-Px), succinate dehydrogenase (SDH), and the mRNA expression of SOD, nicotinamide adenine dinucleotide phosphate-quinine oxidoreductase 1 (NQO1), γ-glutamylcysteine synthetase (γ-GCS), heme oxygenase-1 (HO-1), and glutamate cysteine ligase catalytic (GCLC) in rat kidney tissue. The apoptotic rate of renal cells was decreased by taurine through inhibition of a mitochondrial mechanism. In summary, we found that taurine prevents AFB1-induced renal injury via enhanced antioxidant ability and mitochondrial-dependent apoptosis.

This study employed taurine as a feed additive to explore the prophylactic effect of taurine on LPS-induced hepatic injury in piglets. The pathological shifts within hepatic tissue were observed by HE staining. Serum levels of ALT and AST together with SOD, CAT, GSH-PX activity, and MDA serum and liver levels were detected. TUNEL was used to detect apoptosis, while qPCR was employed to detect HO-1, Nrf-2, Bcl2, BAX, Caspase-3, and NF- κB p65 transcriptomic expression levels. TRL4, Caspase-3, Nrf-2, and NF- κB p-p65/NF- κB p65 were detected by Western blot. The results revealed that taurine reduces LPS-induced pathological damage of hepatic tissue and reduces the levels of ALT and AST in pig serum. The transcriptomic expression levels of HO-1 and Nrf-2 were upregulated, and proteomic expression of Nrf-2 was increased. SOD, CAT, and GSH-PX activity was elevated, while MDA content was reduced in serum and liver. The levels of mRNA of BAX and Caspase-3 were downregulated, but mRNA content of Bcl2 was increased, and the protein levels of TRL4, NF-κB p-p65/NF-κB p65, and Caspase-3 were diminished. Overall, the degree of hepatocyte apoptosis was also significantly reduced. In conclusion, taurine reduces LPS-induced injury of piglet liver, while reducing hepatocyte apoptotic levels. These data provide a scientific basis for the selection of animal feed additives and lay a foundation for the healthy and sustainable development of the porcine industry.

Taurine has the advantages of being safe, highly efficient, chemically stabile, and biologically active, together with having versatile functions. Presently, it is employed as a veterinary feed additive in animal research. The tight junctions that constitute the intestinal epithelial cells are the most critical structures for ensuring regular and uninterrupted digestion and absorption of food by the intestinal mucosa, while at the same time resisting invasions by toxins. The purpose of this study was to investigate the protective effect and mechanism of taurine action on intestinal mechanical barrier function of piglets that were infected with LPS. The results showed that 0.3% taurine inhibits LPS-driven increase in intestinal permeability and intestinal mucosal injury, the rise in the ratio of villus length to crypt depth within the duodenum, jejunum, and ileum, and the significant enhancement in the expression of tight junction protein-related genes. In summary, dietary taurine significantly reduces intestinal mucosal structural damage and intestinal mucosal permeability while increasing gene expression of tight junction proteins of the intestinal mucosa of piglets induced by LPS, thereby enhancing the effect of intestinal mucosal mechanical barriers.

Ca and P metabolic disorders during the egg-laying period can reduce egg production, impair eggshell quality, and even cause bone problems in hens; however, little is known regarding the capacity of duodenal and nephritic Ca and P absorption. Here, the levels of serum Ca and P metabolic indices and the expression of duodenal and renal Ca and P transporter genes were measured in hens at different egg-laying stages. The Ca, 25-(OH)-VD3, and 1,25-(OH)2-VD3 content increased during the peak (43 weeks of age) and late (72 weeks of age) egg-laying periods compared to that during the early (23 weeks of age) egg-laying period; however, there were no differences in Pi levels among the three egg-laying periods. Moreover, duodenal VDR and CaBP-D28k mRNA expression was markedly higher but NPt2b mRNA expression was markedly lower during the peak and late egg-laying periods than during the early egg-laying period. Furthermore, nephritic CaBP-D28k, PMCA1b, and FGFR1 mRNA expression was markedly higher but NPt2a and Cyp24a1 mRNA expression was markedly lower during the peak and late egg-laying periods than during the early egg-laying period. In conclusion, the present study indicated that the increased duodenal and nephritic Ca absorption during the peak and late egg-laying periods may be associated with the VD–VDR pathway, while the decreased P absorption despite relatively stable serum P levels in all three egg-laying stages may associated with osteolysis.

Meat quality characteristics, including juiciness, flavor, and tenderness, can be mostly attributed to the total muscle fat content, intramuscular fat (IMF), and the composition of its fatty acids, which are regulated by the balance between lipid uptake, transport, synthesis, and subsequent metabolism, involving many genes and pathways. However, the detailed molecular mechanisms remain unclear. The purpose of this study was to identify the key signaling pathways related to chicken meat quality, and to provide help for improving chicken meat quality. The present study reports the RNA-sequencing analysis of pectorales and crureus of the Zhuanghe dagu chicken and the Arbor Acres Broiler chicken (AA chicken). We identified certain differentially expressed genes that affect IMF deposition, such as EHHADH, TECRL, NDUFAB1, PCCB, and HIBCH, which were upregulated in Zhuanghe dagu chicken , and GCDH, TPI1, ABHD13, PSMC1, MYST2, and FBXO11, which were upregulated in AA chickens. Pathway analysis using the Kyoto Encyclopedia of Genes and Genomes indicated that the extracellular matrix (ECM)–receptor interaction pathway is co-enriched in both tissues, and forms a sub-pathway of other enriched pathways. Intriguingly, the ECM–receptor interaction pathway genes are regulated differently in different gene pools. Collagens, which are main ECM constituents, and laminin and integrin β1 transmembrane receptors were significantly downregulated in both tissues of the AA chicken. The results showed that the ECM-receptor interaction pathway affect the quality of chicken meat by affecting the metabolism of intramuscular adipocytes. Further investigation of this signaling pathway will be helpful to the improvement of chicken meat quality.

Pathological cardiac hypertrophy is ultimately accompanied by cardiomyocyte apoptosis. Apoptosis mainly related to calpain-1-mediated apoptotic pathways. Studies had proved that taurine can maintain heart health through antioxidation and antiapoptotic functions, but the effect of taurine on cardiac hypertrophy is still unclear. This study aimed to determine whether taurine could inhibit calpain-1-mediated mitochondria-dependent apoptotic pathways in isoproterenol (ISO)-induced hypertrophic cardiomyocytes. We found that taurine could inhibit the increase in cell surface area and reduce the protein expression levels of the hypertrophic markers atrial natriuretic peptide, brain natriuretic polypeptide, and β-myosin heavy chain. Taurine also reduced ROS, intracellular Ca2+ overload and mitochondrial membrane potential. Moreover, taurine inhibited cardiomyocyte apoptosis by decreasing the protein expression of calpain-1, Bax, t-Bid, cytosolic cytochrome c, Apaf-1, cleaved caspase-9 and cleaved caspase-3 and by enhancing calpastatin and Bcl-2 protein expression. Calpain-1 small interfering RNA transfection results showed similar antiapoptotic effects as the taurine prevention group. However, compared with the two treatments, taurine inhibited the expression of cleaved caspase-9 more significantly. Therefore, we believe that taurine prevents ISO-induced H9c2 cardiomyocyte hypertrophy by inhibiting oxidative stress, intracellular Ca2+ overload, the calpain-1-mediated mitochondria-dependent apoptotic pathway and cleaved caspase-9 levels.

The calpain-1-activated apoptotic pathway plays a key role in right ventricular hypertrophy (RVH). Taurine has been shown to attenuate apoptosis by inhibiting calpain activity. This experiment aimed to determine whether taurine could prevent RVH by inhibiting the calpain-1/cytochrome c apoptotic pathway. The broilers were given 1% taurine dissolved in drinking water and were raised at 10 °C ~ 12 °C from day 21 to day 42. At 21 d, 28 d, 35 d and 42 d, the right ventricular (RV) tissues were collected. Increased RVH index, angiotensin II, norepinephrine and atrial natriuretic peptide mRNA expression were reduced by taurine in the broiler RVs. Taurine obviously inhibited cardiomyocyte apoptosis via maintaining the mitochondrial membrane potential and decreased the activation of caspase-9 and caspase-3 in the broiler RVs. The antioxidant assay demonstrated that taurine enhanced the activities of superoxide dismutase, total antioxidant capacity and glutathione peroxidase and the glutathione/glutathione disulfide ratio. Western blot results revealed that taurine also downregulated the expression of calpain-1 and cytosolic cytochrome c while upregulating the expression of Bcl-2/Bax and mitochondrial cytochrome c in broiler cardiomyocytes during RVH. In summary, we found that taurine could enhance cardiomyocyte antioxidant ability and further prevented cardiomyocyte apoptosis by inhibiting the calpain-1/cytochrome c pathway during RVH in broilers.

It has been confirmed by our laboratory that taurine could decrease uric acid levels in hyperuricemic rats and regulate the expressions of some urate transporters. The present study aims to investigate the effects of taurine on uric acid uptake in human renal proximal tubular epithelial cells (HK-2). The cell growth inhibition rate was measured by MTS assay, which was up to 50% after treatment with 1.5 mmol/L uric acid. After administration of 15 mmol/L taurine, the inhibition rate and uric acid uptake were both significantly decreased. Then the HK-2 cells were grouped as follows: control group (C); model group (M), in which 1.5 mmol/L uric acid was added to the medium; taurine group (MT), in which 1.5 mmol/L uric acid and 15 mmol/L taurine were added to the medium; and taurine control group (T), in which 15 mmol/L taurine was added to the medium. The mRNA and protein expression levels of URAT1 and GLUT9 were measured by real-time PCR and western-blot. The results showed that URAT1 and GLUT9 mRNA/protein expression levels in group M were significantly increased compared with group C, and they were both down-regulated in MT group. In addition, the expression levels of these two transporters in group T were significantly lower than group C. The results indicated that taurine could inhibit uric acid uptake and down-regulate the expressions of URAT1 and GLUT9 in HK-2 cells.