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.

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.

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.

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.

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.