As the extension of the egg-laying cycle, heightened energy and lipid metabolism cause excessive lipid accumulation, resulting in rapid decline in laying performance during the late laying period. Bile acids (BAs), synthesized from cholesterol in the liver, are potent metabolic and immune signaling molecules involved in lipid metabolism and the regulation of energy homeostasis. However, under different dietary protein levels, the role of BAs on hepatic lipid metabolism of laying hens at the late phase remains unclear. This experiment aimed to evaluate the effects of porcine BAs supplementation on performance, lipid metabolism, antioxidant status and amino acid metabolism in late-phase laying hens fed diets with different protein level. A total of 192 Hy-Line Brown laying hens (62 weeks of age) were randomly assigned to one of four treatment groups, in a 2 × 2 factorial design, with 8 replicates per treatment. The hens were fed diets with either normal protein (16.42 %) or low-protein (15.35 %) levels, with or without BAs supplementation (120 mg/kg for the first 56 days, followed by 200 mg/kg for the next 42 days). The results demonstrated that dietary BAs supplementation significantly enhanced egg production and feed intake (P < 0.05) although it has no notable effect on egg quality. Bile acids supplementation effectively reduced liver total cholesterol (TC), triglyceride (TG), as well as malondialdehyde (MDA) levels, while also ameliorating lipid deposition through the regulation of expression of lipid metabolism-related genes in late laying hens (P < 0.05). Additionally, the low-protein diets downregulated amino acid catabolism, thereby reducing serum uric acid content and enhancing protein utilization. Further analysis revealed that BAs also positively influenced trypsin activity and increased the expression of amino acid transporters, thereby improving amino acid availability (P < 0.05). In conclusion, this study demonstrated that dietary BAs supplementation could enhance the laying performance in late laying hens, primarily by improving hepatic lipid metabolism, antioxidant capacity, and amino acid availability.

The modern livestock industry faces significant challenges due to the extension of production cycles and a growing shortage of feed resources. Low-protein (LP) diets offer potential environmental advantages whereas damage intestinal integrity and increase pro-inflammatory cytokines. Bile acids (BAs), metabolic products of cholesterol in the liver, possess strong antioxidative and immune properties. This study evaluated the effects of dietary porcine BA supplementation at different protein levels on the antioxidant status, immune function, and gut microbiota of late-laying hens. A 2 × 2 factorial design was employed with 198 Hy-Line Brown laying hens (62 weeks old), randomly divided into one of four treatment groups with 8 replicates for each treatment. Diets included normal (16.42%) or low-protein (15.35%) levels, with porcine BAs supplemented at 0 or 120 mg/kg (62-69 weeks) and 0 or 200 mg/kg (70-75 weeks) over 14 weeks. Dietary protein levels and bile acids had no effect on organ development in laying hens. Low-protein diets increased serum anti-inflammatory cytokines IL-4 and IL-10 but elevated pro-inflammatory cytokines IL-1β (p < 0.05), corroborated by higher IL-10 gene expression in the ileum mucosa (p < 0.05). The supplementation of bile acids improved immune function by increasing serum IL-4 and TGF-β while decreasing IL-6 levels (p < 0.05). Moreover, bile acids treatments upregulated IL-10, TGF-β and ZO-1 gene expression in the ileum mucosa (p < 0.05) and alleviated oxidative stress by enhancing serum GSH-Px activity (p < 0.05). Additionally, both low-protein diets and bile acids enriched beneficial cecal bacteria, including Hungatella and Blautia, primarily linked to immune function. These findings demonstrate that porcine bile acids administration improve antioxidant capacity, immune function and gut microbiota dysbiosis. These beneficial effects were associated with Hungatella and Blautia levels, which may be responsible for the porcine bile acids efficacy in poultry nutrition.

Objectives:Obesity leads to severe health issues like cardiovascular disease. Natural substances with anti-obesity properties are gaining attention. This study investigates the impact of taurine on lipid levels in rats fed a high-fat diet. Materials and Methods:The SD rats were fed a high-fat diet and treated with or without taurine for 21 weeks. Taurine was added to their drinking water, and an adipose triglyceride lipase (ATGL) inhibitor was injected for one week. The study evaluated the impact of taurine supplementation on the rats' body weight, Lee index, body fat content, serum levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), fatty acid synthase (FAS), ATGL, and peroxisome proliferator-activated receptor α (PPARα) in the liver. Fat accumulation in the liver and aortic arch was assessed through histopathological observations. Results:The study found that taurine reduced body weight, body fat, serum TG, TC, LDL-C levels, and lipid deposition in the liver and aortic arch while increasing serum HDL-C levels. Taurine intake also increased FAS and ATGL expression in the liver. Interestingly, the ATGL inhibitor atglistatin did not affect FAS and ATGL expression in the presence of taurine. Conclusion:Taurine can reduce fat deposition caused by a high-fat diet in SD rats by decreasing FAS content and increasing ATGL content. However, taurine does not fully regulate FAS and ATGL expression through the ATGL pathway.

[This corrects the article DOI: 10.1016/j.heliyon.2023.e16401.].

IntroductionTaurine has a prominent lipid-lowering effect on hyperlipidemia. However, a comprehensive analysis of the effects of taurine on endogenous metabolites in hyperlipidemia has not been documented. This study aimed to explore the impact of taurine on multiple metabolites associated with hyperlipidemia.MethodsThe hyperlipidemic mouse model was induced by high-fat diet (HFD). Taurine was administered via oral gavage at doses of 700 mg/kg/day for 14 weeks. Evaluation of body weight, serum lipid levels, and histopathology of the liver and adipose tissue was performed to confirm the lipid-lowering effect of taurine. Ultra-high performance liquid chromatography-mass spectrometry (UPLC-MS)-based metabonomics analyses of serum, urine, feces, and liver, coupled with multivariate data analysis, were conducted to assess changes in the endogenous metabolites.Results and discussionBiochemical and histological examinations demonstrated that taurine administration prevented weight gain and dyslipidemia, and alleviated lipid deposition in the liver and adipose tissue in hyperlipidemic mice. A total of 76 differential metabolites were identified by UPLC-MS-based metabolomics approach, mainly involving BAs, GPs, SMs, DGs, TGs, PUFAs and amino acids. Taurine was found to partially prevent HFDinduced abnormalities in the aforementioned metabolites. Using KEGG database and MetaboAnalyst software, it was determined that taurine effectively alleviates metabolic abnormalities caused by HFD, including fatty acid metabolism, sphingolipid metabolism, glycerophospholipid metabolism, diacylglycerol metabolism, amino acid metabolism, bile acid and taurine metabolism, taurine and hypotaurine metabolism. Moreover, DGs, GPs and SMs, and taurine itself may serve as active metabolites in facilitating various anti-hyperlipidemia signal pathways associated with taurine. This study provides new evidence for taurine to prevent hyperlipidemia.

Taurine (2-aminoethanesulfonic acid) could reduce serum and liver cholesterol concentrations via regulating expression and the activity of cholesterol 7 alpha-hydroxylase (CYP7A1). To investigate the possible role of calcineurin in taurine upregulating CYP7A1 expression in HepG2 cells under high cholesterol conditions. High cellular cholesterol conditions were achieved using 0.2 mM cholesterol in HepG2 cells. Calcineurin was decreased by FK506 and was depleted in CnA beta-/- cells. HepG2 cells were cultured in a taurine-containing medium for 24 or 48 h. The levels of total intracellular cholesterol were determined by an enzymatic method, and the expression levels of calcineurin, CYP7A1, and key transcriptional regulatory molecules were detected by western blotting. High-cholesterol resulted in increased CYP7A1 and calcineurin expressions. Taurine exhibited cholesterol-lowering effects regardless of low/high cholesterol conditions or calcineurin status. Taurine induced the expression of CYP7A1, which was abolished by inhibiting or deleting calcineurin. Taurine suppressed MEK1/2, p-c-Jun, and SHP-1, key molecules in one inhibitory pathway of CYP7A1 transcription. In contrast, suppression of MEK1/2 but not p-c-Jun or SHP-1 was reversed after completely knocking down calcineurin. Calcineurin is required for taurine's upregulation of CYP7A1 expression through inhibiting MEK1/2, which was partly responsible for taurine's cholesterol-lowering effect.

Taurine has been proven in many trials to alleviate the symptoms of metabolic associated fatty liver disease. Here its protective effect for hepatic steatosis and modulation of AMP-activated protein kinase and insulin signaling pathway were investigated. Steatotic HepG2 cell established with oleic acid (0.05 mmol/L), treated with taurine (5 mmol/L), dorsomorphin (10 μmol/L) for 24 h. Sprague Dawley rats were divided into regular and high-fat diet (HFD) groups, and their corresponding taurine (70 or 350 mg/kg BW/d) groups, fed for 8 weeks. In steatotic cell, taurine reduced the TG concentration and SREBP-1c, PPARγ, FAS, ACC, SCD1 protein levels, decreased phosphorylation of mTOR, IRS1 (Ser302), increased phosphorylation of AMPKα, LKB1, PI3K, Akt, ACC. While dorsomorphin eliminated taurine's TG-lowering effect. In HFD-fed rats, taurine reduced liver TG, serum TG, ALT, AST, IL-1β, IL-4, TNF-α. The effects of taurine on the main factors of fatty acid synthesis were mostly consistent with cell experiments, and the reduction of microRNAs (451, 33, 291b) was aligned with the improvement in LKB1 and AMPK expression in HFD rats. Taurine alleviated steatosis-induced inhibition of IRS1-PI3K-Akt pathway, but suppressed its positively regulated downstream factor mTOR. In parallel, taurine reduced steatosis by activating LKB1-AMPKα pathway via phosphorylation and no-phosphorylation manner, then inhibiting SREBP-1c directly or by suppressing mTOR phosphorylation.

This article study the influences of fermented wheat germ on rats in terms of the blood glucose, insulin level, serum lipid level, cholesterol metabolism, triglyceride metabolism and enzyme activity on the basis of the high-fat rat model. High fat rats were fed for modeling, and then the serum and liver were collected after sacrifice. Total cholesterol (TC), triglyceride (TG), total superoxide dismutase (SOD), Superoxide dismutase (T-SOD), glutathione peroxidase (GSH-PX), Malonic dialdehyde (MDA), lecithin cholesterol acyltransferase (lecithin cholesterol), Acyltransferase (LCAT), LDL-C, blood glucose and insulin were measured. Fermented wheat germ can significantly increase the levels of insulin and blood glucose in high-fat rats. Fermented wheat germ for 60 days did not affect the levels of serum LDL-C and TG in high-fat rats, but could significantly reduce the level of serum TC. Fermented wheat germ for 60 days did not affect the activities of serum GSH-Px, T-SOD, LCAT and T-SOD, MDA and total lipase in high-fat rats, but it could significantly reduce the activity of serum MDA and increase the activity of GSH-PX in liver. Fermented wheat germ could reduce the protein expression of CYP7A1, induced p-AMPK protein expression, but had no effect on HMGR. Fermented wheat germ can significantly reduce the level of serum cholesterol in high-fat model rats by AMPK signaling pathway, and affect some cholesterol metabolism and triglyceride metabolism related enzyme activities to a certain extent.

牛磺酸(Taurine)是机体内分布广泛且具有众多生理功能的含硫氨基酸,近年来牛磺酸对慢性炎症性疾病具有潜在的防治功能己得到广泛认可.巨噬细胞是参与慢性炎症的重要免疫细胞,其牛磺酸含量细胞内比细胞外高出约100倍.大量研究集中在补充牛磺酸可明显改善"无菌性炎症"疾病引起的巨噬细胞聚集和炎症反应.该文就牛磺酸体内水平及其变化、摄入安全性以及对巨噬细胞免疫功能的调节等方面的研究进行了综述,以期为牛磺酸免疫营养分子机制的深入研究和功能食品领域的开发提供参考.

目的 了解2002-2015年山西农村15岁及以上居民蔬菜和水果摄入及变化情况,为我国北方农村居民膳食指导提供科学依据.方法 在2002年中国居民营养与健康调查的基础上,2015年对山西省5个农村地区的居民进行跟踪调查.选取2002年基线和2015年随访中参与两次调查且具有完整食物频率数据的786名居民为研究对象.2002年和2015年采用相同的调查问卷收集研究对象基本情况、蔬菜和水果摄入量和摄入频次.应用SAS 9.4软件进行x2检验,Kruskal-Wallis检验,Wilcoxon检验和Spearman相关性检验.结果 2002-2015年,研究对象蔬菜摄入量中位数由150.00 g/d上升至200.00 g/d;水果摄入量中位数由21.43g/d上升至100.00 g/d.2002-2015年蔬菜和水果摄入量增加的个体所占比例最高(分别为58.78％和70.74％),蔬菜和水果摄入频次不变的个体所占比例最高(分别为67.94％和42.75％).2002-2015年,15～44岁组与45～59岁组居民蔬菜摄入量变化差异均有统计学意义(P＜0.0167).2002-2015年,15-44岁组与45～59岁组、60岁及以上组居民水果摄入量和摄入频次变化差异均有统计学意义(均P＜0.0167).结论 2002-2015年山西省农村地区15岁及以上居民蔬菜水果摄入量增加的占比最高,但蔬菜和水果摄入频次不变的占比最高.

目的 了解中国西南地区2017年疾控系统慢性病防控人力资源现状,为进一步加强西南地区疾控系统慢性病防控人力资源建设提供参考依据.方法 收集中国疾病预防控制中心2018年7-11月开展的第五次全国慢性病预防控制能力调查中2017年重庆市、四川省、贵州省、云南省和西藏自治区576家疾病预防控制中心2 119名慢性病防控在岗人员的相关信息,分析西南地区疾控系统慢性病防控人员的配置情况及年龄、工作年限、学历、专业、职称分布情况.结果 中国西南地区2017年疾控系统慢性病防控在岗人员占总在岗人员的6.5％,慢性病防控专职在岗人员占总在岗人员的4.6％;慢性病防控人员年龄以25～34岁者所占比例最高(40.7％),工作年限以＜5年者所占比例最高(59.5％),学历以本科及以上者所占比例最高(57.5％),专业以医学专业者所占比例最高(94.9％),职称以初级职称所占比例最高(44.8％).不同地区比较,重庆市、四川省、贵州省、云南省和西藏自治区5个地区慢性病防控在岗人员占总在岗人员比例、专职慢性病防控在岗人员占总在岗人员比例、防控人员年龄、工作年限、副高及以上职称比例差异均有统计学意义(均P＜0.01).慢性病防控在岗人员和专职慢性病防控在岗人员占总在岗人员比例均呈省、地市和县(区)上升趋势(均P＜0.05);慢性病防控人员工作年限、本科及以上学历比例、医学专业比例、副高及以上职称比例均呈省、地市和县(区)下降趋势(均P＜0.05).结论 中国西南地区2017年疾控系统慢性病防控人力资源水平与慢性病巨大的疾病负担水平不匹配,且存在级别差异.

高血糖是多种慢性病的共同危险因素,调节血糖也是慢性病防治的重要手段.单宁作为一种天然活性物质,广泛存在于植物中,具有良好的血糖调节活性.该文简述了植物单宁的分类、提取方法及具有的生物学活性功能,重点梳理了植物单宁的血糖调节活性作用机制.植物单宁血糖调节活性作用机制可分为:抑制α-葡萄糖苷酶和α-淀粉酶的活性,影响食物中碳水化合物分解,延缓碳水化合物的吸收率;促进葡萄糖转运蛋白4的表达,提高体内葡萄糖转运能力,改善胰岛素抵抗;通过激活酪氨酸激酶活性,影响酪氨酸蛋白磷酸化水平,促进细胞对葡萄糖摄取能力等.但目前抑制糖异生、促进糖元酵解方面研究较为匮乏,这可能成为单宁血糖调节活性研究的一个新切入点.

了解2017年西南地区基层机构慢性病防控能力现状,为加强西南地区基层机构慢性病防控能力建设提供依据.本研究选取四川省、重庆市、云南省、贵州省和西藏自治区的调查数据,分析了西南地区基层机构数量、人力和经费配置等情况以及开展重点慢性病患者及高危人群管理、慢性病防控项目等情况.结果 显示,2017年西南地区556家基层机构从事慢性病管理工作的专业人员占卫生技术人员的11.39％.2017年基本公共卫生服务经费标准人均为50.60元,其中国家财政拨款占73.33％.针对高血压与糖尿病患者,开展建档工作的基层机构分别占96.76％、93.99％,开展随访工作的基层机构分别占97.30％、93.46％,随访≥4次人数占总随访人数的比例分别为81.51％、79.26％,开展转诊服务的基层机构分别占77.52％、70.49％,转回人数占转诊到上级医院人数的比例分别为21.10％、27.72％.针对高血压和糖尿病高危人群,开展建档的基层机构分别占50.72％、38.34％,开展随访的基层机构分别占43.11％与33.57％,随访≥4次人数占总随访人数的比例分别为40.92％、23.23％.西南地区有11.51％的基层机构承担了慢性病防控科研项目.调查的西南地区基层机构依然存在慢性病防控专业人员配备和地方经费投入不足、慢性病高危人群管理水平低、双向转诊不通畅、科研能力薄弱的问题.

麦胚是面粉加工的副产物,被誉为"人类天然的营养宝库".麦胚含有多种生物活性物质,将麦胚进行发酵处理可提高其生理活性.本文从麦胚的营养成分、功能活性、以及麦胚发酵所带来的成分、含量、功能活性方面的变化进行系统综述,并对未来麦胚产品的深度开发利用进行展望.

Fatty liver disease (FLD) is mainly characterized by the pathophysiological progression from simple hepatic steatosis to steatohepatitis, which has been increasing in incidence and has attracted much attention due to its risk of hepatocellular carcinoma. It is considered that lipid metabolism disorder, oxidative stress, inflammation etc. are common factors leading to the progression of FLD including alcoholic fatty liver disease (AFLD) and nonalcoholic fatty liver disease (NAFLD). A number of studies provide the evidence that taurine, a small sulfur containing amino acid in food, has the efficient action to FLD. The beneficial effects include lowering lipids level to alleviate hepatic steatosis, increasing the antioxidant enzymes and substances to improve antioxidant defense, regulating the inflammation-related signal pathways to reduce pro-inflammatory factors and inflammatory response, and regulating the enzymes involved in ethanol metabolism etc. This review summarizes the data from in vivo and in vitro studies, and addresses the possible metabolic and molecular mechanisms of taurine in alleviating FLD.

本文探讨牛磺酸对HepG2细胞甘油三酯合成的影响,为牛磺酸预防/改善机体高脂状态的深入研究提供参考.在DMEM培养基中添加0.05 mmol/L油酸建立高甘油三酯细胞模型,分别以终浓度为1、5、10、20 mmol/L的牛磺酸处理细胞24、48、72 h,测定细胞内甘油三酯水平;并检测5 mmol/L牛磺酸作用24h后细胞内固醇调节元件结合蛋白1c(SREBP-1c)及脂肪合成相关酶乙酰辅酶A合成酶(AceCS)、乙酰辅酶A羧化酶(ACC)、脂肪酸合成酶(FAS)、长链酰基辅酶A合成酶1(ACSL1)的蛋白表达水平.1 mmol/L牛磺酸作用72 h,5和10 mmol/L牛磺酸作用24、48、72 h,20 mmol/L牛磺酸作用24和48 h均可使高脂HepG2细胞内甘油三酯水平显著下降(P＜ 0.05);5 mmol/L牛磺酸作用24 h,高脂HepG2细胞的SREBP-1c、FAS、ACC、AceCS1、ACSL1表达明显减少(P＜0.05),磷酸化ACC表达显著增加(P＜0.05).结论:牛磺酸通过调控SREBP-1c及其下游靶基因而抑制高脂HepG2细胞脂肪酸/甘油三酯的合成.

Background Oxidative stress is a key factor that influences piglets’ health. Taurine plays an imperative role in keeping the biological system from damage. This study was conducted to investigate the protective effect of taurine against muscle injury due to the secondary effect of diquat toxicity. Results Our study found that taurine effectively and dose-dependently alleviated the diquat toxicity induced rise of feed/gain, with a concurrent improvement of carcass lean percentage. The plasma content of taurine was considerably increased in a dose-dependent manner. Consequently, dietary taurine efficiently improved the activity of plasma antioxidant enzymes. Furthermore, taurine attenuated muscle damage by restoring mitochondrial micromorphology, suppressing protein degradation and reducing the percentage of apoptotic cells in the skeletal muscle. Taurine supplementation also suppressed the genes expression levels of the antioxidant-, mitochondrial biogenesis-, and muscle atrophy-related genes in the skeletal muscle of piglets with oxidative stress. Conclusions These results showed that the dose of 0.60% taurine supplementation in the diet could attenuate skeletal muscle injury induced by diquat toxicity. It is suggested that taurine could be a potential nutritional intervention strategy to improve growth performance.

Background: Intestinal barrier contributes as an important role in maintaining intestinal homeostasis. Oxidative stress can cause critical damages in intestinal integrity of animals. Objectives: This study was conducted to investigate the alleviated effect of taurine against small intestine (duodenum, jejunum, ileum) injury induced by oxidative stress. Methods: The piglet model of diquat-induced oxidative stress was employed. In addition, analysis of intestinal morphology, reverse transcription PCR (RT-PCR), and Western blot were used in this study. Results: Compared with the control group (CON), diquat-induced oxidative stress triggers immune response; the content of immunoglobulin M (IgM) and immunoglobulin G (IgG) was significantly changed, but 0.60% taurine supplementation could restore the level of serum immunoglobulin. Oxidative stress induces serious damage in intestinal morphology structure and tight junction barrier. Compared with the CON, the villus height of intestine was significantly decreased, the crypt depth and villus height/crypt depth (V/C) were also decreased, and 0.60% taurine supplementation could restore impaired morphology and even improve crypt depth and V/C of the jejunum and ileum. Compared with the CON, oxidative stress markedly increased the messenger RNA (mRNA) expression level of claudin-1 and occludin in the duodenum, and the value of occludin was significantly decreased in the jejunum of the diquat group (DIQ). Relative to the DIQ, 0.60% taurine supplementation increased the mRNA expression level of claudin-1, occludin, and ZO-1 in the ileum. Compared with the CON, the expression of claudin-1 protein was significantly upregulated, and occludin and ZO-1 protein were both downregulated in the small intestine of DIQ. Conclusion: Taurine exerts protective effects by regulating immune response and restores the intestinal tight junction barrier when piglets suffer from oxidative stress.

目的 探讨益生菌/草本提取物复方的清咽作用.方法 大鼠灌胃给予益生菌和/或草本提取物45 d,依据2012修订的保健食品“清咽功能检验方法”进行大鼠棉球植入实验、大鼠足趾肿胀实验及小鼠耳肿胀实验.结果 棉球植入实验中,益生菌高剂量、草本中剂量和高剂量、益生菌低剂量+草本中剂量、益生菌低剂量+草本高剂量、益生菌高剂量+低/中/高剂量草本剂量组,大鼠肉芽肿净量显著低于对照组(P＜0.05),具有干预肉芽肿(慢性炎症)形成的作用;足趾肿胀实验中,致炎1h后,草本高剂量组大鼠足趾肿胀率显著降低(P＜0.05),致炎1、2、6h后,益生菌高剂量+草本高剂量组足趾肿胀率均显著低于对照组(P＜0.05)且低于益生菌高剂量组和草本高剂量组,提示益生菌草本高剂量复方干预致炎剂诱发的足趾肿胀作用效果优于单独给予高剂量益生菌或高剂量草本;小鼠耳廓肿胀实验中,各组耳廓肿胀值及肿胀率均无显著变化.结论 高剂量草本和益生菌草本高剂量复方样品具有清咽作用,且益生菌草本高剂量复方干预致炎剂诱导的急性炎症效果优于高剂量草本.

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