short-chain fatty acids (SCFAs)

短链脂肪酸 (SCFA)
  • 文章类型: Journal Article
    全球每天都会产生大量的废活性污泥,带来重大的环境挑战。厌氧发酵是一种很有前途的污泥处置方法,但是它有两个技术瓶颈:产生短链脂肪酸(SCFA)的底物的可用性和甲烷生成所消耗的SCFA。本研究提出了一种结合过碳酸钠(SPC)和磁铁矿(Fe3O4)的预处理策略来解决这些问题。在优化条件下(20mgFe3O4/gTSS和15mgSPC/gTSS),SCFAs产量增加到3244.10±216.31mgCOD/L,约为对照的3.06倍(1057.29±35.06mgCOD/L),超过了报道的处理方法。联合预处理增强了细胞外聚合物的破坏,增加了可生物降解物质的释放,改善产酸酶活性,并抑制甲烷生成。此外,它增加了NH4-N的释放,有利于从污泥残渣中回收磷。这项研究证明了从WAS中进行高SCFA生产和资源回收的有效预处理。
    Large amounts of waste activated sludge are generated daily worldwide, posing significant environmental challenges. Anaerobic fermentation is a promising method for sludge disposal, but it has two technical bottlenecks: the availability of short-chain fatty acids (SCFAs)-producing substrates and SCFAs consumption by methanogenesis. This study proposes a pretreatment strategy combining sodium percarbonate (SPC) and magnetite (Fe3O4) to address these issues. Under optimized conditions (20 mg Fe3O4/g TSS and 15 mg SPC/g TSS), SCFAs production increased to 3244.10 ± 216.31 mg COD/L, about 3.06 times the control (1057.29 ± 35.06 mg COD/L) and surpassing reported treatments. The combined pretreatment enhanced the disruption of extracellular polymeric substances, increased the release of biodegradable matters, improved acidogenesis enzyme activities, and inhibited methanogenesis. Additionally, it increased NH4+-N release in favor of the recovery of phosphorus from sludge residual. This study demonstrates an efficient pretreatment for high SCFAs production and resource recovery from WAS.
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  • 文章类型: Journal Article
    阿尔茨海默病(AD)是一种神经退行性疾病,已知其积累淀粉样β(Aβ)和tau蛋白。临床研究尚未确定发病机制或产生AD的有效治愈。Aβ单克隆抗体lecanemab可减少Aβ斑块形成,用于治疗AD,但是需要更多的研究来提高药物的有效性,以减少认知能力下降。在过去的10年中,缺乏AD治疗靶标以及与一些细菌和病毒引起的急性神经炎症反应相关的证据导致了感染假说的建立。病原体如何穿过血脑屏障是高度局部的,被认为是证明这一假设的关键。本文综述了肠道菌群在AD发病机制中的可能作用、可行的治疗方法和目前研究的局限性。
    Alzheimer\'s disease (AD) is a neurodegenerative disease that is known to accumulate amyloid-β (Aβ) and tau protein. Clinical studies have not identified pathogenesis mechanisms or produced an effective cure for AD. The Aβ monoclonal antibody lecanemab reduces Aβ plaque formation for the treatment of AD, but more studies are required to increase the effectiveness of drugs to reduce cognitive decline. The lack of AD therapy targets and evidence of an association with an acute neuroinflammatory response caused by several bacteria and viruses in some individuals has led to the establishment of the infection hypothesis during the last 10 years. How pathogens cross the blood-brain barrier is highly topical and is seen to be pivotal in proving the hypothesis. This review summarizes the possible role of the gut microbiome in the pathogenesis of AD and feasible therapeutic approaches and current research limitations.
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  • 文章类型: Journal Article
    益生菌对改善代谢紊乱的有益作用已被深入研究;然而,这些效应在益生菌菌株特异性和疾病特异性方式中是明显的。因此,评估每种菌株对目标疾病的功效仍然至关重要。这里,我们提出了一种抗肥胖和抗糖尿病的益生菌菌株,植物乳杆菌APsulloc331261(GTB1™),它是从绿茶中分离出来的,之前进行了安全性测试。在高脂饮食诱导的肥胖小鼠中,GTB1™发挥了多种有益效果,包括肥胖的显著减少,葡萄糖不耐受,和血脂异常,循环激素和脂肪因子水平的改善进一步支持了这一点。通过GTB1™治疗,通过激活PPAR/PGC1α信号恢复脂肪组织中的脂质代谢,肠道微生物组成变化和短链脂肪酸产生促进了这一点。我们的发现提供了证据,表明GTB1™是益生菌补充剂的潜在候选者,可全面改善代谢紊乱。
    The beneficial effects of probiotics for the improvement of metabolic disorders have been studied intensively; however, these effects are evident in a probiotic strain-specific and disease-specific manner. Thus, it is still essential to evaluate the efficacy of each strain against a target disease. Here, we present an anti-obese and anti-diabetic probiotic strain, Lactiplantibacillus plantarum APsulloc331261 (GTB1™), which was isolated from green tea and tested for safety previously. In high-fat-diet-induced obese mice, GTB1™ exerted multiple beneficial effects, including significant reductions in adiposity, glucose intolerance, and dyslipidemia, which were further supported by improvements in levels of circulating hormones and adipokines. Lipid metabolism in adipose tissues was restored through the activation of PPAR/PGC1α signaling by GTB1™ treatment, which was facilitated by intestinal microbiota composition changes and short-chain fatty acid production. Our findings provide evidence to suggest that GTB1™ is a potential candidate for probiotic supplementation for comprehensive improvement in metabolic disorders.
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  • 文章类型: Journal Article
    作为一种可以通过胃肠道系统快速吸收的食物污染物,呋喃已被证明会破坏肠道菌群和屏障。研究呋喃的肠道毒性机制对健康具有重要意义。我们先前确定了红景天苷(SAL)对呋喃引起的肠道损伤的调节作用,本工作进一步探讨了SAL对呋喃引起的肠损伤的缓解作用是否基于肠道菌群;三种模型,正常,伪无菌,和粪便微生物移植(FMT),建立,以及肠道形态的变化,屏障,并观察到炎症。此外,16SrDNA测序观察到与炎症和短链脂肪酸(SCFA)相关的粪便菌群的变化。从LC-MS/MS获得的结果表明,SAL增加了呋喃抑制的SCFA水平,激活SCFA受体(GPR41,GPR43和GPR109A)的mRNA表达,并抑制呋喃激活的TLR4/MyD88/NF-κB信号传导。蛋白质-蛋白质相互作用的分析进一步证实了SAL的上述作用,抑制呋喃诱导的屏障损伤和肠道炎症。
    As a food contaminant that can be quickly absorbed through the gastrointestinal system, furan has been shown to disrupt the intestinal flora and barrier. Investigation of the intestinal toxicity mechanism of furan is of great significance to health. We previously identified the regulatory impact of salidroside (SAL) against furan-provoked intestinal damage, and the present work further explored whether the alleviating effect of SAL against furan-caused intestinal injury was based on the intestinal flora; three models, normal, pseudo-germ-free, and fecal microbiota transplantation (FMT), were established, and the changes in intestinal morphology, barrier, and inflammation were observed. Moreover, 16S rDNA sequencing observed the variation of the fecal flora associated with inflammation and short-chain fatty acids (SCFAs). Results obtained from the LC-MS/MS suggested that SAL increased furan-inhibited SCFA levels, activated the mRNA expressions of SCFA receptors (GPR41, GPR43, and GPR109A), and inhibited the furan-activated TLR4/MyD88/NF-κB signaling. Analysis of protein-protein interaction further confirmed the aforementioned effects of SAL, which inhibited furan-induced barrier damage and intestinal inflammation.
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  • 文章类型: Journal Article
    短链脂肪酸(SCFA)如醋酸盐,丙酸盐,还有丁酸盐,调节免疫细胞功能,特别是巨噬细胞。这篇综述探讨了SCFA在肺部真菌感染中的潜在治疗应用。由于它们的高死亡率和抗真菌耐药性,这是一个至关重要的问题。SCFA通过促进吞噬体-溶酶体融合增强巨噬细胞功能,增加活性氧的产生,和平衡细胞因子反应。肺部真菌感染,由烟曲霉等病原体引起,在免疫功能低下的患者中普遍存在,包括糖尿病患者,慢性阻塞性肺疾病,和那些大剂量皮质类固醇。在这些情况下,SCFA在改善巨噬细胞功能方面显示出希望。然而,SCFA的应用必须与潜在的副作用保持平衡,包括肠道微生物群破坏和代谢紊乱。需要进一步的研究来优化SCFA治疗以管理肺部真菌感染。
    Short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, modulate immune cell functions, particularly macrophages. This review explores the potential therapeutic applications of SCFAs in pulmonary fungal infections, a critical concern due to their high mortality rates and antifungal resistance. SCFAs enhance macrophage functions by promoting phagosome-lysosome fusion, increasing reactive oxygen species production, and balancing cytokine responses. Pulmonary fungal infections, caused by pathogens like Aspergillus fumigatus, are prevalent in immunocompromised patients, including those with diabetes, chronic obstructive pulmonary disease, and those on high-dose corticosteroids. SCFAs have shown promise in improving macrophage function in these contexts. However, the application of SCFAs must be balanced against potential side effects, including gut microbiota disruption and metabolic disorders. Further research is needed to optimize SCFA therapy for managing pulmonary fungal infections.
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  • 文章类型: Journal Article
    溃疡性结肠炎(UC)是一种自身免疫性疾病,其中免疫系统攻击结肠,导致溃疡发展,结肠功能丧失,和血性腹泻。人类肠道生态系统由近2000种不同的细菌组成,形成以膳食微量营养素为燃料的生物反应器,以产生生物活性化合物,它们被我们的身体吸收并向远处的器官发出信号。研究表明,西方饮食,短链脂肪酸(SCFA)较少,可以改变肠道微生物组组成并引起宿主的表观遗传重编程。此外,由于饮食模式的改变,肠道微生物组的H2S过量产生可以进一步激活UC的促炎信号通路。这篇综述讨论了西方饮食如何影响微生物组的功能并改变宿主的生理稳态和对UC的易感性。这篇文章还涵盖了流行病学,预后,病理生理学,以及目前UC的治疗策略,以及它们与结直肠癌的联系。
    Ulcerative colitis (UC) is an autoimmune disease in which the immune system attacks the colon, leading to ulcer development, loss of colon function, and bloody diarrhea. The human gut ecosystem consists of almost 2000 different species of bacteria, forming a bioreactor fueled by dietary micronutrients to produce bioreactive compounds, which are absorbed by our body and signal to distant organs. Studies have shown that the Western diet, with fewer short-chain fatty acids (SCFAs), can alter the gut microbiome composition and cause the host\'s epigenetic reprogramming. Additionally, overproduction of H2S from the gut microbiome due to changes in diet patterns can further activate pro-inflammatory signaling pathways in UC. This review discusses how the Western diet affects the microbiome\'s function and alters the host\'s physiological homeostasis and susceptibility to UC. This article also covers the epidemiology, prognosis, pathophysiology, and current treatment strategies for UC, and how they are linked to colorectal cancer.
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  • 文章类型: Journal Article
    OBJECTIVE: To observe the effects of acupuncture on blood pressure, fecal short-chain fatty acids (SCFAs) and toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway in spontaneously hypertensive rats (SHR), and to explore the mechanism of acupuncture for anti-hypertension.
    METHODS: Twenty-four male SHR of SPF grade were randomly divided into a model group, a western medication group, an acupuncture group and a sham acupuncture group, with 6 rats in each group, and 6 male Wistar-Kyoto rats were selected as the blank group additionally. Hydrochlorothiazide solution was given by gavage in the western medication group; acupuncture was applied at bilateral \"Renying\" (ST 9) and \"Zusanli\" (ST 36) in the acupuncture group, 20 min a time; acupuncture was applied at the non-meridian and non-acupoint points close to bilateral \"Renying\" (ST 9) and \"Zusanli\" (ST 36) in the sham acupuncture group, 20 min a time. The intervention was adopted once a day for 4 weeks continuously in each group. The systolic blood pressure (SBP) of the caudal artery was measured before intervention and after 1, 2, 3 and 4 weeks of intervention. After intervention, the morphology of colonic tissue was observed by HE staining; the fecal level of SCFAs was detected by gas chromatography; the serum levels of interleukin (IL)-6, IL-1βand tumor necrosis factor-α (TNF-α) were detected by ELISA; the protein expression of TLR4, MyD88 and NF-κB p65 in the mesenteric artery was detected by Western blot.
    RESULTS: Compared with the blank group, in the model group, the SBP was increased (P<0.05), significant pathological changes could be found in the colonic tissue, the fecal SCFAs level was decreased (P<0.05), the serum levels of IL-6, IL-1β and TNF-α were increased (P<0.05), the protein expression of TLR4, MyD88 and NF-κB p65 in the mesenteric artery was increased (P<0.05). Compared with the model group, the SBP after 2, 3 and 4 weeks of intervention was decreased (P<0.05), the serum levels of IL-6, IL-1β and TNF-α were decreased (P<0.05) in the acupuncture group and the western medication group; the mucosal epithelium of colonic tissue was intact, the number of intestinal glands was abundant, the fecal SCFAs level was increased (P<0.05), and the protein expression of TLR4, MyD88 and NF-κB p65 in the mesenteric artery was decreased (P<0.05) in the acupuncture group. Compared with the sham acupuncture group, the SBP after 2, 3 and 4 weeks of intervention was decreased (P<0.05), the fecal SCFAs level was increased (P<0.05), the serum levels of IL-6, IL-1β and TNF-α were decreased (P<0.05), the protein expression of TLR4, MyD88 and NF-κB p65 in the mesenteric artery was decreased (P<0.05) in the acupuncture group.
    CONCLUSIONS: Acupuncture at bilateral \"Renying\" (ST 9) and \"Zusanli\" (ST 36) can effectively play an anti-hypertensive role in SHR. Its mechanism may be related to regulating fecal SCFAs level and inhibiting the TLR4/MyD88/NF-κB signaling pathway.
    目的:观察针刺对自发性高血压大鼠(SHR)血压、粪便短链脂肪酸(SCFAs)及toll样受体4(TLR4)/髓样分化因子88(MyD88)/核因子κB(NF-κB)信号通路的影响,探讨针刺降压的作用机制。方法:将24只SPF级雄性SHR随机分为模型组、西药组、针刺组和假针组,每组6只;另设6只Wistar-Kyoto(WKY)大鼠为空白组。西药组予氢氯噻嗪溶液灌胃;针刺组针刺双侧“人迎”“足三里”,每次20 min;假针组针刺双侧“人迎”“足三里”附近的非经非穴点,每次20 min。均每日1次,持续4周。干预前及干预第1、2、3、4周后测量各组大鼠尾动脉收缩压(SBP);HE染色观察大鼠结肠组织形态;气相色谱-质谱联用仪检测大鼠粪便SCFAs含量;ELISA法检测大鼠血清白细胞介素(IL)-6、IL-1β和肿瘤坏死因子-α(TNF-α)含量;Western Blot法检测大鼠肠系膜动脉中TLR4、MyD88和NF-κB p65蛋白表达。结果:与空白组比较,模型组大鼠SBP升高(P<0.05),结肠组织有明显病理变化,粪便SCFAs含量降低(P<0.05),血清IL-1β、IL-6和TNF-α含量升高(P<0.05),肠系膜动脉中TLR4、MyD88、NF-κB p65蛋白表达升高(P<0.05)。与模型组比较,针刺组和西药组大鼠干预2、3、4周后SBP降低(P<0.05),血清IL-1β、IL-6和TNF-α含量降低(P<0.05);针刺组大鼠结肠组织黏膜上皮完整,肠腺数量丰富,粪便SCFAs含量升高(P<0.05),肠系膜动脉中TLR4、MyD88、NF-κB p65蛋白表达降低(P<0.05)。与假针组比较,针刺组干预2、3、4周后SBP降低(P<0.05),粪便SCFAs含量升高(P<0.05),血清IL-1β、IL-6和TNF-α含量降低 (P<0.05),肠系膜动脉中TLR4、MyD88、NF-κB p65蛋白表达降低(P<0.05)。结论:针刺双侧“人迎”“足三里”可有效降低SHR血压,其机制可能与调节粪便SCFAs含量、抑制TLR4/MyD88/NF-κB信号通路有关。.
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  • 文章类型: Journal Article
    腹泻性大肠杆菌(DEC)是五岁以下儿童腹泻的主要原因。DEC的毒力受到肠道微生物群及其代谢物影响的环境信号的严格调节。短链脂肪酸(SCFAs)是肠道厌氧发酵的主要代谢产物,但它们在DEC腹泻中的作用尚未确定。在这项研究中,我们确定了醋酸盐的含量,丙酸盐,DEC引起的腹泻儿童粪便样本中的丁酸盐,我们从粪便肠道菌群中鉴定出与SCFA产生相关的细菌。通过16SrRNA基因测序和HPLC测定了40例腹泻儿童和43例健康儿童粪便样本中的微生物群和SCFAs水平,分别。此外,鸟枪宏基因组学用于鉴定样品亚组中的宏基因组组装基因组(MAG).结果显示,在腹泻样品中测试的所有SCFA的水平明显高于健康对照。链球菌的丰度。,Limosilactacillus,Blautia,埃希氏菌,拟杆菌,Megamonas,DEC组的Roseburia高于健康个体。细菌及其主要代谢途径的功能分析使鉴定可能导致DEC阳性腹泻中检测到的SCFA水平的MAG物种成为可能。总之,根据我们的结果和公布的数据,我们认为SCFA在肠道微生物群和DEC病原体之间的串扰中可能很重要。
    Diarrheagenic Escherichia coli (DEC) is the main cause of diarrhea in children under five years old. The virulence of DEC is tightly regulated by environmental signals influenced by the gut microbiota and its metabolites. Short-chain fatty acids (SCFAs) are the main metabolic product of anaerobic fermentation in the gut, but their role in DEC diarrhea has not yet been established. In this study, we determine the levels of acetate, propionate, and butyrate in stool samples from children with diarrhea caused by DEC, and we identify bacteria from the fecal gut microbiota associated with the production of SCFAs. The microbiota and SCFAs levels in stool samples obtained from 40 children with diarrhea and 43 healthy children were determined by 16S rRNA gene sequencing and HPLC, respectively. Additionally, shotgun metagenomics was used to identify metagenome-assembled genomes (MAGs) in a subgroup of samples. The results showed significantly higher levels of all SCFAs tested in diarrheal samples than in healthy controls. The abundance of Streptococcus sp., Limosilactobacillus, Blautia, Escherichia, Bacteroides, Megamonas, and Roseburia was higher in the DEC group than in healthy individuals. Functional analysis of bacteria and their main metabolic pathways made it possible to identify species MAGs that could be responsible for the detected SCFAs levels in DEC-positive diarrhea. In conclusion, based on our results and published data, we suggest that SCFAs may be important in the crosstalk between the microbiota and DEC pathogens in the gut.
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  • 文章类型: Journal Article
    胃肠道是数万亿不同微生物的家园,统称为肠道微生物群,它们在分解未消化的食物中起着关键作用,如膳食纤维。通过这些食物成分的发酵,短链脂肪酸(SCFA),如乙酸盐,丙酸盐,产生丁酸,为宿主提供许多健康益处。这些SCFA的产生和吸收通过人体肠道内的各种机制发生,取决于到达肠道的膳食纤维的类型和参与发酵的特定微生物。医学文献广泛记录了SCFA的补充,特别是丁酸,在胃肠道的治疗中,新陈代谢,心血管,和肠道大脑相关疾病。这篇综述旨在概述乙酸盐的生产和吸收所涉及的动力学,丙酸盐,和人体肠道内的丁酸盐。此外,它将集中在这些SCFA在促进胃肠道和代谢健康方面发挥的关键作用,以及它们目前的治疗意义。
    The gastrointestinal tract is home to trillions of diverse microorganisms collectively known as the gut microbiota, which play a pivotal role in breaking down undigested foods, such as dietary fibers. Through the fermentation of these food components, short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate are produced, offering numerous health benefits to the host. The production and absorption of these SCFAs occur through various mechanisms within the human intestine, contingent upon the types of dietary fibers reaching the gut and the specific microorganisms engaged in fermentation. Medical literature extensively documents the supplementation of SCFAs, particularly butyrate, in the treatment of gastrointestinal, metabolic, cardiovascular, and gut-brain-related disorders. This review seeks to provide an overview of the dynamics involved in the production and absorption of acetate, propionate, and butyrate within the human gut. Additionally, it will focus on the pivotal roles these SCFAs play in promoting gastrointestinal and metabolic health, as well as their current therapeutic implications.
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  • 文章类型: Journal Article
    硝酸盐光解已成为一种高效、低成本和有前途的新兴污染物去除技术,而其对废活性污泥(WAS)处理的性能和机理尚不清楚。本研究创新性地引入硝酸盐光解用于WAS崩解,并研究了厌氧发酵(AF)过程中添加硝酸盐(150-375mgN/L)对短链脂肪酸(SCFA)产生的影响。结果表明,硝酸盐光解显著促进了WAS产生SCFA,和峰值在280.7mg/gVSS与7-d发酵与150mgN/L添加(150N-UV),与其他光解基团和唯一的硝酸盐基团相比,分别增加了8.8-35.0%和10.7-23.3%。在AF期间,在硝酸盐光解基团中观察到可溶性有机物的有效释放,特别是可溶性蛋白质,150N-UV组在9d时达到1505.4mgCOD/L,比硝酸盐/硝酸盐光解组提高7.0~15.7%。模型化合物模拟实验进一步证明了硝酸盐光解对有机物水解和SCFAs积累的积极影响。自由基捕获和猝灭的结果证实了与活性氮物种相比,活性氧物种的贡献更大。官能团分析证实了发酵过程中大分子有机物的有效生物转化。此外,硝酸盐光解增强了功能聚生体的富集,包括厌氧发酵细菌(AFB),例如,Fnoteella,Romboutsia,Gacilibacter和Sedimentialbacter,和硝酸盐还原细菌(NRB),例如,不动杆菌属和Ahniella。宏观遗传学分析进一步揭示了糖酵解,氨基酸代谢,乙酸代谢和氮代谢是发酵过程中的主要代谢途径,150N-UV组相关基因丰度增强。
    Nitrate photolysis has become an efficient, low-cost and promising technology for emerging contaminants removal, while its performance and mechanism for waste activated sludge (WAS) treatment is still unknown. This study innovatively introduced nitrate photolysis for WAS disintegration, and investigated the effect of nitrate addition (150-375 mg N/L) for short-chain fatty acids (SCFAs) production during anaerobic fermentation (AF). The results showed that nitrate photolysis significantly promoted the SCFAs production from WAS, and peaked at 280.7 mg/g VSS with 7-d fermentation with 150 mg N/L addition (150N-UV), which increased by 8.8-35.0 % and 10.7-23.3 % compared with other photolysis groups and sole nitrate groups. Effective release of the soluble organics was observed in the nitrate photolysis groups during AF, especially soluble proteins, reaching 1505.4 mg COD/L at 9 d in 150N-UV group, promoted by 7.0∼15.7 % than nitrate/nitrate photolysis groups. The model compounds simulation experiment further demonstrated the positive effect of nitrate photolysis on organics hydrolysis and SCFAs accumulation. The result of the radical capture and quenching verified the reactive oxygen species contributed more compared with reactive nitrogen species. Functional group analysis confirmed the effective bioconversion of the macromolecular organics during the fermentation. Moreover, the nitrate photolysis enhanced the enrichment of the functional consortia, including anaerobic fermentation bacteria (AFB), e.g., Fnoticella, Romboutsia, Gracilibacter and Sedimentibacter, and nitrate reducing bacteria (NRB), e.g., Acinerobacter and Ahniella. The macrogenetic analysis further revealed that glycolysis, amino acid metabolism, acetate metabolism and nitrogen metabolism were the dominating metabolic pathways during fermentation, and the abundance of the relevant genes were enhanced in 150N-UV group.
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