首页 > 最新文献

Journal of Nutritional Biochemistry最新文献

英文 中文
Artemisinin and its derivatives modulate glucose homeostasis and gut microbiota remodeling in a nutritional context 青蒿素及其衍生物在营养背景下调节葡萄糖稳态和肠道微生物群重塑。
IF 4.8 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-10 DOI: 10.1016/j.jnutbio.2024.109687
Yajie Guo , Ying Chen , Dan Wang , Guangnan Liu , Yuhua Chen , Changfeng Peng , Tingting Cao , Yuewei Liu , Xiaoxiao Hu , Xinyue Xu , Yuebin Ke , Suli Huang , Tong Wang , Ziquan Lv

Glucose metabolic disorders, prevalent in numerous metabolic diseases, have become a pressing global public health concern. Artemisinin (ART) and its derivatives, including artesunate (ARTs) and artemether (ARTe), have shown potential as metabolic regulators. However, the specific effects of ART and its derivatives on glucose metabolism under varying nutritional conditions and the associated molecular mechanisms remain largely unexplored. In this study, we examined the impact of ART, ARTs, and ARTe on glucose homeostasis using a mouse model subjected to different dietary regimens. Our findings revealed that ART, ARTs, and ARTe increased blood glucose levels in mice on a normal-chow diet (ND) while mitigating glucose imbalances in high-fat diet (HFD) mice. Notably, treatment with ART, ARTs, and ARTe had contrasting effects on in vivo insulin signaling, impairing it in ND mice and enhancing it in HFD mice. Moreover, the composition of gut microbiota underwent significant alterations following administration of ART and its derivatives. In ND mice, these treatments reduced the populations of bacteria beneficial for improving glucose homeostasis, including Parasutterella, Alloprevotella, Bifidobacterium, Ileibacterium, and Alistipes. In HFD mice, there was an increase in the abundance of beneficial bacteria (Alistipes, Akkermanisia) and a decrease in bacteria known to negatively impact glucose metabolism (Coprobacillus, Helicobacter, Mucispirillum, Enterorhabdus). Altogether, ART, ARTs, and ARTe exhibited distinct effects on the regulation of glucose metabolism, depending on the nutritional context, and these effects were closely associated with modifications in gut microbiota composition.

葡萄糖代谢紊乱在多种代谢性疾病中十分常见,已成为全球公共卫生领域的一个紧迫问题。青蒿素(ART)及其衍生物,包括青蒿琥酯(ARTs)和蒿甲醚(ARTe),已显示出作为代谢调节剂的潜力。然而,青蒿素及其衍生物在不同营养条件下对葡萄糖代谢的具体影响以及相关的分子机制在很大程度上仍未得到探索。在本研究中,我们利用小鼠模型,采用不同的饮食方案,研究了 ART、ARTs 和 ARTe 对葡萄糖稳态的影响。我们的研究结果表明,ART、ARTs 和 ARTe 会增加正常低脂饮食(ND)小鼠的血糖水平,同时缓解高脂饮食(HFD)小鼠的血糖失衡。值得注意的是,ART、ARTs 和 ARTe 对体内胰岛素信号转导的影响截然不同,在 ND 小鼠中会损害胰岛素信号转导,而在 HFD 小鼠中则会增强胰岛素信号转导。此外,服用 ART 及其衍生物后,肠道微生物群的组成发生了显著变化。在 ND 小鼠中,这些处理减少了有益于改善葡萄糖稳态的细菌数量,包括副伞菌、异型伞菌、双歧杆菌、Ileibacterium 和 Alistipes。在高氟低脂小鼠中,有益细菌(Alistipes、Akkermanisia)的数量有所增加,而已知对糖代谢有负面影响的细菌(Coprobacillus、Helicobacter、Mucispirillum、Enterorhabdus)则有所减少。总之,ART、ARTs 和 ARTe 对葡萄糖代谢的调节有不同的影响,这取决于营养环境,而这些影响与肠道微生物群组成的改变密切相关。
{"title":"Artemisinin and its derivatives modulate glucose homeostasis and gut microbiota remodeling in a nutritional context","authors":"Yajie Guo ,&nbsp;Ying Chen ,&nbsp;Dan Wang ,&nbsp;Guangnan Liu ,&nbsp;Yuhua Chen ,&nbsp;Changfeng Peng ,&nbsp;Tingting Cao ,&nbsp;Yuewei Liu ,&nbsp;Xiaoxiao Hu ,&nbsp;Xinyue Xu ,&nbsp;Yuebin Ke ,&nbsp;Suli Huang ,&nbsp;Tong Wang ,&nbsp;Ziquan Lv","doi":"10.1016/j.jnutbio.2024.109687","DOIUrl":"10.1016/j.jnutbio.2024.109687","url":null,"abstract":"<div><p>Glucose metabolic disorders, prevalent in numerous metabolic diseases, have become a pressing global public health concern. Artemisinin (ART) and its derivatives, including artesunate (ARTs) and artemether (ARTe), have shown potential as metabolic regulators. However, the specific effects of ART and its derivatives on glucose metabolism under varying nutritional conditions and the associated molecular mechanisms remain largely unexplored. In this study, we examined the impact of ART, ARTs, and ARTe on glucose homeostasis using a mouse model subjected to different dietary regimens. Our findings revealed that ART, ARTs, and ARTe increased blood glucose levels in mice on a normal-chow diet (ND) while mitigating glucose imbalances in high-fat diet (HFD) mice. Notably, treatment with ART, ARTs, and ARTe had contrasting effects on in vivo insulin signaling, impairing it in ND mice and enhancing it in HFD mice. Moreover, the composition of gut microbiota underwent significant alterations following administration of ART and its derivatives. In ND mice, these treatments reduced the populations of bacteria beneficial for improving glucose homeostasis, including <em>Parasutterella, Alloprevotella, Bifidobacterium, Ileibacterium</em>, and <em>Alistipes</em>. In HFD mice, there was an increase in the abundance of beneficial bacteria (<em>Alistipes, Akkermanisia</em>) and a decrease in bacteria known to negatively impact glucose metabolism (<em>Coprobacillus, Helicobacter, Mucispirillum, Enterorhabdus</em>). Altogether, ART, ARTs, and ARTe exhibited distinct effects on the regulation of glucose metabolism, depending on the nutritional context, and these effects were closely associated with modifications in gut microbiota composition.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109687"},"PeriodicalIF":4.8,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324001207/pdfft?md5=391a79e38eb01cf5aa1e6520d6b93139&pid=1-s2.0-S0955286324001207-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141310882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Association between flavonoid intake and rheumatoid arthritis among US adults 美国成年人类黄酮摄入量与类风湿关节炎之间的关系。
IF 4.8 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-10 DOI: 10.1016/j.jnutbio.2024.109673
Yan Chen , Haoxian Tang , Nan Luo , Xiaoqing Liang , Penchao Yang , Xuan Zhang , Jingtao Huang , Qinglong Yang , Shuxin Huang , Ling Lin

Basic research shows that flavonoids have anti-inflammatory effects that influence rheumatoid arthritis (RA) in rats. Investigating potential dietary interventions for RA helps prevent the onset and progression of the disease. Clinical evidence on the association of flavonoid and subclass intake with RA is lacking. Using three survey cycles of 2007–2008, 2009–2010, and 2017–2018 from the National Health and Nutrition Survey and the United States Department of Agriculture's Food and Nutrient Database for Dietary Studies (FNDDS), we analyzed 7,419 American adults (≥20 years old). The values of flavonoid and subclass intake were calculated using FNDDS. The status questions for self-reported RA were from the NHANES codebook. Weighted analyses, revealed that among the 7,419 participants included in this study (mean age of 44.69 years [standard error, 0.40] and 3,584 [48.31%] were female), 408 met the classification criteria for RA. According to the multivariable logistic regression model, compared with the risk of RA in the first quartile (Q1), the risks of RA in the second quartile (Q2), the third quartile (Q3) and the fourth quartile (Q4) were lower (Q2: OR=0.55, 95% CI: 0.38–0.80; Q3: OR=0.66, 95% CI: 0.44–0.97; Q4: OR=0.64, 95% CI: 0.46–0.89; trend: P=.03). The association between total flavonoids and RA remained significant after full consideration of confounding factors. With regard to the subclasses of flavonoids, high flavanones intake was associated with low RA prevalence in Model 3 (Q3: OR= 0.60, 95% CI:0.39–0.92; Q4: OR = 0.56, 95% CI: 0.32–0.99, trend: P=.02), but no such association was found in the other subclasses. Total flavonoids intake protected against RA, and the risk of developing RA decreased significantly with increasing intake of total flavonoids. Total flavonoids and flavanones were significantly associated with reduced RA risk for the American adult population. We highlighted the importance of employing diverse methodologies to assess the health effects of flavonoids.

背景:基础研究表明,类黄酮具有抗炎作用,可影响大鼠的类风湿性关节炎(RA)。研究潜在的类风湿关节炎饮食干预措施有助于预防疾病的发生和发展。目前还缺乏类黄酮和亚类黄酮摄入量与类风湿性关节炎关系的临床证据:利用2007-2008年、2009-2010年和2017-2018年三个调查周期的美国国家健康与营养调查以及美国农业部的膳食研究食品与营养数据库(FNDDS),我们对7419名美国成年人(≥20岁)进行了分析。类黄酮和亚类摄入量的数值是通过 FNDDS 计算得出的。自我报告的RA状况问题来自NHANES编码手册:加权分析显示,在7419名参与研究的人员中(平均年龄44.69岁[标准误差0.40],女性3584人[48.31%]),有408人符合RA的分类标准。根据多变量逻辑回归模型,与第一四分位数(Q1)的 RA 风险相比,第二四分位数(Q2)、第三四分位数(Q3)和第四四分位数(Q4)的 RA 风险较低(Q2: OR=0.55, 95% CI: 0.38-0.80; Q3: OR=0.66, 95% CI: 0.44-0.97; Q4:OR=0.64,95% CI:0.46-0.89;趋势:P=0.03).在充分考虑混杂因素后,总黄酮与RA之间的关系仍然显著。在模型 3 中,黄酮亚类摄入量高与 RA 患病率低相关(Q3:OR= 0.60,95% CI:0.39-0.92;Q4:OR= 0.56,95% CI:0.46-0.89;趋势:P=0.03):OR=0.56,95% CI:0.32-0.99,趋势:P=0.02),但在其他亚类中没有发现这种关联。总黄酮类化合物的摄入量可预防RA,随着总黄酮类化合物摄入量的增加,患RA的风险显著降低:总黄酮和黄烷酮与降低美国成年人群患RA的风险有显著关系。我们强调了采用不同方法评估类黄酮对健康影响的重要性。
{"title":"Association between flavonoid intake and rheumatoid arthritis among US adults","authors":"Yan Chen ,&nbsp;Haoxian Tang ,&nbsp;Nan Luo ,&nbsp;Xiaoqing Liang ,&nbsp;Penchao Yang ,&nbsp;Xuan Zhang ,&nbsp;Jingtao Huang ,&nbsp;Qinglong Yang ,&nbsp;Shuxin Huang ,&nbsp;Ling Lin","doi":"10.1016/j.jnutbio.2024.109673","DOIUrl":"10.1016/j.jnutbio.2024.109673","url":null,"abstract":"<div><p>Basic research shows that flavonoids have anti-inflammatory effects that influence rheumatoid arthritis (RA) in rats. Investigating potential dietary interventions for RA helps prevent the onset and progression of the disease. Clinical evidence on the association of flavonoid and subclass intake with RA is lacking. Using three survey cycles of 2007–2008, 2009–2010, and 2017–2018 from the National Health and Nutrition Survey and the United States Department of Agriculture's Food and Nutrient Database for Dietary Studies (FNDDS), we analyzed 7,419 American adults (≥20 years old). The values of flavonoid and subclass intake were calculated using FNDDS. The status questions for self-reported RA were from the NHANES codebook. Weighted analyses, revealed that among the 7,419 participants included in this study (mean age of 44.69 years [standard error, 0.40] and 3,584 [48.31%] were female), 408 met the classification criteria for RA. According to the multivariable logistic regression model, compared with the risk of RA in the first quartile (Q1), the risks of RA in the second quartile (Q2), the third quartile (Q3) and the fourth quartile (Q4) were lower (Q2: OR=0.55, 95% CI: 0.38–0.80; Q3: OR=0.66, 95% CI: 0.44–0.97; Q4: OR=0.64, 95% CI: 0.46–0.89; trend: <em>P</em>=.03). The association between total flavonoids and RA remained significant after full consideration of confounding factors. With regard to the subclasses of flavonoids, high flavanones intake was associated with low RA prevalence in Model 3 (Q3: OR= 0.60, 95% CI:0.39–0.92; Q4: OR = 0.56, 95% CI: 0.32–0.99, trend: <em>P</em>=.02), but no such association was found in the other subclasses. Total flavonoids intake protected against RA, and the risk of developing RA decreased significantly with increasing intake of total flavonoids. Total flavonoids and flavanones were significantly associated with reduced RA risk for the American adult population. We highlighted the importance of employing diverse methodologies to assess the health effects of flavonoids.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109673"},"PeriodicalIF":4.8,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141310883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects and mechanisms of sciadonic acid on colonic transit function through regulating 5-HT4/cAMP/PKA/AQP4 signaling pathway in STC model mice 通过调节5-HT4/cAMP/PKA/AQP4信号通路促进STC模型小鼠结肠转运功能的作用和机制
IF 4.8 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-06 DOI: 10.1016/j.jnutbio.2024.109676
Zhuoli Yu , Lalai Zikela , Dingli Wang , Xuezhu Wang , Huilin Zhu , Songtao Li , Qiang Han

Torreya grandis (T. grandis) oil has been reported to alleviate symptoms of slow transit constipation (STC). However, the impact of sciadonic acid (SA), a distinctive fatty acid found in T. grandis oil, on the pathological progression of STC remains unclear. This study aimed to evaluate the effect of SA on STC and uncover the underlying mechanisms. The STC model was established by feeding Balb/c mice with loperamide. After 2 weeks of intervention, SA significantly improved weight loss and intestinal motility decline induced by STC, along with enhancing plasma indices and reducing colon pathological damage. SA effectively reversed the STC-induced decrease in the 5-HT4/cAMP/PKA/AQP4 signaling pathway genes and expression. Furthermore, 16S rRNA analysis demonstrated that SA mitigated the imbalance of the intestinal microbiota induced by STC, by reducing the ratio of Firmicutes to Bacteroidetes (F/B) and increasing the abundance of beneficial bacteria such as Akkermansia. In conclusion, SA intervention alleviated colonic dysfunction in STC mice. The activation of the SA-mediated 5-HT4/cAMP/PKA/AQP4 signaling pathway may serve as a potential target for STC treatment. These findings suggest that SA holds promise as a treatment option for STC and could potentially be extended to other related gut diseases for further investigation.

据报道,大叶香榧油(Torreya grandis,T. grandis)可减轻慢传输性便秘(STC)的症状。然而,大叶香榧油中的一种独特脂肪酸--香榧酸(SA)对STC病理进展的影响仍不清楚。本研究旨在评估SA对STC的影响并揭示其潜在机制。通过给 Balb/c 小鼠喂食洛哌丁胺,建立了 STC 模型。干预2周后,SA明显改善了STC引起的体重下降和肠蠕动减弱,同时提高了血浆指数,减少了结肠病理损伤。SA能有效逆转STC诱导的5-HT4/cAMP/PKA/AQP4信号通路基因的减少和表达。此外,16S rRNA 分析表明,SA 可降低固缩菌与类杆菌(F/B)的比例,增加有益菌(如 Akkermansia)的数量,从而缓解 STC 引起的肠道微生物群失衡。总之,SA干预缓解了STC小鼠的结肠功能障碍。激活 SA 介导的 5-HT4/cAMP/PKA/AQP4 信号通路可能是 STC 治疗的潜在靶点。这些研究结果表明,SA有望成为治疗STC的一种选择,并有可能扩展到其他相关的肠道疾病,以供进一步研究。
{"title":"Effects and mechanisms of sciadonic acid on colonic transit function through regulating 5-HT4/cAMP/PKA/AQP4 signaling pathway in STC model mice","authors":"Zhuoli Yu ,&nbsp;Lalai Zikela ,&nbsp;Dingli Wang ,&nbsp;Xuezhu Wang ,&nbsp;Huilin Zhu ,&nbsp;Songtao Li ,&nbsp;Qiang Han","doi":"10.1016/j.jnutbio.2024.109676","DOIUrl":"10.1016/j.jnutbio.2024.109676","url":null,"abstract":"<div><p><em>Torreya grandis</em> (<em>T. grandis</em>) oil has been reported to alleviate symptoms of slow transit constipation (STC). However, the impact of sciadonic acid (SA), a distinctive fatty acid found in <em>T. grandis</em> oil, on the pathological progression of STC remains unclear. This study aimed to evaluate the effect of SA on STC and uncover the underlying mechanisms. The STC model was established by feeding Balb/c mice with loperamide. After 2 weeks of intervention, SA significantly improved weight loss and intestinal motility decline induced by STC, along with enhancing plasma indices and reducing colon pathological damage. SA effectively reversed the STC-induced decrease in the 5-HT4/cAMP/PKA/AQP4 signaling pathway genes and expression. Furthermore, 16S rRNA analysis demonstrated that SA mitigated the imbalance of the intestinal microbiota induced by STC, by reducing the ratio of <em>Firmicutes</em> to <em>Bacteroidetes</em> (F/B) and increasing the abundance of beneficial bacteria such as <em>Akkermansia</em>. In conclusion, SA intervention alleviated colonic dysfunction in STC mice. The activation of the SA-mediated 5-HT4/cAMP/PKA/AQP4 signaling pathway may serve as a potential target for STC treatment. These findings suggest that SA holds promise as a treatment option for STC and could potentially be extended to other related gut diseases for further investigation.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109676"},"PeriodicalIF":4.8,"publicationDate":"2024-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141293495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inhibiting mitochondrial citrate shuttling induces hepatic triglyceride deposition in Nile tilapia (Oreochromis niloticus) through lipid anabolic remodeling 抑制线粒体柠檬酸盐穿梭可通过脂质合成代谢重塑诱导尼罗罗非鱼(Oreochromis niloticus)肝脏甘油三酯沉积。
IF 4.8 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-05 DOI: 10.1016/j.jnutbio.2024.109678
Jun-Xian Wang , Yuan Luo , Samwel Mchele Limbu , Yu-Cheng Qian , Yan-Yu Zhang , Rui-Xin Li , Wen-Hao Zhou , Fang Qiao , Li-Qiao Chen , Mei-Ling Zhang , Zhen-Yu Du

The solute carrier family 25 member 1 (Slc25a1)-dependent mitochondrial citrate shuttle is responsible for exporting citrate from the mitochondria to the cytoplasm for supporting lipid biosynthesis and protein acetylation. Previous studies on Slc25a1 concentrated on pathological models. However, the importance of Slc25a1 in maintaining metabolic homeostasis under normal nutritional conditions remains poorly understood. Here, we investigated the mechanism of mitochondrial citrate shuttle in maintaining lipid metabolism homeostasis in male Nile tilapia (Oreochromis niloticus). To achieve the objective, we blocked the mitochondrial citrate shuttle by inhibiting Slc25a1 under normal nutritional conditions. Slc25a1 inhibition was established by feeding Nile tilapia with 250 mg/kg 1,2,3-benzenetricarboxylic acid hydrate for 6 weeks or intraperitoneal injecting them with dsRNA to knockdown slc25a1b for 7 days. The Nile tilapia with Slc25a1 inhibition exhibited an obesity-like phenotype accompanied by fat deposition, liver damage and hyperglycemia. Moreover, Slc25a1 inhibition decreased hepatic citrate-derived acetyl-CoA, but increased hepatic triglyceride levels. Furthermore, Slc25a1 inhibition replenished cytoplasmic acetyl-CoA through enhanced acetate pathway, which led to hepatic triglycerides accumulation. However, acetate-derived acetyl-CoA caused by hepatic Slc25a1 inhibition did not activate de novo lipogenesis, but rather modified protein acetylation. In addition, hepatic Slc25a1 inhibition enhanced fatty acids esterification through acetate-derived acetyl-CoA, which increased Lipin1 acetylation and its protein stability. Collectively, our results illustrate that inhibiting mitochondrial citrate shuttle triggers lipid anabolic remodeling and results in lipid accumulation, indicating the importance of mitochondrial citrate shuttle in maintaining lipid metabolism homeostasis.

溶质运载家族 25 成员 1(Slc25a1)依赖的线粒体柠檬酸穿梭器负责将柠檬酸从线粒体输出到细胞质,以支持脂质生物合成和蛋白质乙酰化。以前对 Slc25a1 的研究主要集中在病理模型上。然而,人们对 Slc25a1 在正常营养条件下维持代谢平衡的重要性仍然知之甚少。在此,我们研究了线粒体柠檬酸穿梭在维持雄性尼罗罗非鱼(Oreochromis niloticus)脂代谢平衡中的机制。为了实现这一目标,我们在正常营养条件下通过抑制 Slc25a1 来阻断线粒体柠檬酸穿梭。用 250 毫克/千克的 1,2,3-苯三羧酸水合物喂养尼罗罗非鱼六周,或腹腔注射dsRNA 以敲除 slc25a1b 七天,从而建立 Slc25a1 抑制机制。抑制了 Slc25a1 的尼罗罗非鱼表现出类似肥胖的表型,并伴有脂肪沉积、肝损伤和高血糖。此外,抑制 Slc25a1 会降低肝脏柠檬酸衍生乙酰-CoA,但会增加肝脏甘油三酯水平。此外,抑制 Slc25a1 可通过增强乙酸途径补充细胞质乙酰-CoA,从而导致肝脏甘油三酯积累。然而,肝脏 Slc25a1 抑制所导致的乙酸衍生乙酰-CoA 并未激活新的脂肪生成,而是改变了蛋白质的乙酰化。此外,肝脏 Slc25a1 抑制通过乙酸衍生的乙酰-CoA 增强了脂肪酸的酯化,从而增加了 Lipin1 的乙酰化及其蛋白质的稳定性。总之,我们的研究结果表明,抑制线粒体柠檬酸穿梭会引发脂质合成代谢重塑并导致脂质积累,这表明线粒体柠檬酸穿梭在维持脂质代谢平衡中的重要性。
{"title":"Inhibiting mitochondrial citrate shuttling induces hepatic triglyceride deposition in Nile tilapia (Oreochromis niloticus) through lipid anabolic remodeling","authors":"Jun-Xian Wang ,&nbsp;Yuan Luo ,&nbsp;Samwel Mchele Limbu ,&nbsp;Yu-Cheng Qian ,&nbsp;Yan-Yu Zhang ,&nbsp;Rui-Xin Li ,&nbsp;Wen-Hao Zhou ,&nbsp;Fang Qiao ,&nbsp;Li-Qiao Chen ,&nbsp;Mei-Ling Zhang ,&nbsp;Zhen-Yu Du","doi":"10.1016/j.jnutbio.2024.109678","DOIUrl":"10.1016/j.jnutbio.2024.109678","url":null,"abstract":"<div><p>The solute carrier family 25 member 1 (Slc25a1)-dependent mitochondrial citrate shuttle is responsible for exporting citrate from the mitochondria to the cytoplasm for supporting lipid biosynthesis and protein acetylation. Previous studies on Slc25a1 concentrated on pathological models. However, the importance of Slc25a1 in maintaining metabolic homeostasis under normal nutritional conditions remains poorly understood. Here, we investigated the mechanism of mitochondrial citrate shuttle in maintaining lipid metabolism homeostasis in male Nile tilapia (<em>Oreochromis niloticus</em>). To achieve the objective, we blocked the mitochondrial citrate shuttle by inhibiting Slc25a1 under normal nutritional conditions. Slc25a1 inhibition was established by feeding Nile tilapia with 250 mg/kg 1,2,3-benzenetricarboxylic acid hydrate for 6 weeks or intraperitoneal injecting them with dsRNA to knockdown <em>slc25a1b</em> for 7 days. The Nile tilapia with Slc25a1 inhibition exhibited an obesity-like phenotype accompanied by fat deposition, liver damage and hyperglycemia. Moreover, Slc25a1 inhibition decreased hepatic citrate-derived acetyl-CoA, but increased hepatic triglyceride levels. Furthermore, Slc25a1 inhibition replenished cytoplasmic acetyl-CoA through enhanced acetate pathway, which led to hepatic triglycerides accumulation. However, acetate-derived acetyl-CoA caused by hepatic Slc25a1 inhibition did not activate <em>de novo</em> lipogenesis, but rather modified protein acetylation. In addition, hepatic Slc25a1 inhibition enhanced fatty acids esterification through acetate-derived acetyl-CoA, which increased Lipin1 acetylation and its protein stability. Collectively, our results illustrate that inhibiting mitochondrial citrate shuttle triggers lipid anabolic remodeling and results in lipid accumulation, indicating the importance of mitochondrial citrate shuttle in maintaining lipid metabolism homeostasis.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109678"},"PeriodicalIF":4.8,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Gallic acid attenuates murine ulcerative colitis by promoting group 3 innate lymphocytes, affecting gut microbiota, and bile acid metabolism 没食子酸通过促进第 3 组先天性淋巴细胞、影响肠道微生物群和胆汁酸代谢来减轻小鼠溃疡性结肠炎。
IF 4.8 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-05 DOI: 10.1016/j.jnutbio.2024.109677
Yun Leng , Xiao Zhang , Qian Zhang, Jiaxuan Xia, Yuefeng Zhang, Chong Ma, Kun Liu, Hao Li, Yanjun Hong, Zhiyong Xie

Gallic acid (GA), a plant phenol that is widely distributed in fruits and vegetables, and exhibits a protective role against ulcerative colitis (UC). UC is an inflammatory disease characterized by immune response disorders. However, the role and mechanism of action of GA in gut immunity remain unknown. Here, we observed that GA treatment improved enteritis symptoms, decreased the concentrations of cytokines TNF-α, IFN-γ, IL-6, IL-17A, and IL-23, increased the concentrations of cytokines IL-10, TGF-β and IL-22, and increased the proportion of group 3 innate lymphoid cells (ILC3) in mesenteric lymph nodes and lamina propria. However, GA did not upregulate ILC3 or impair UC in antibody-treated sterile mice. Notably, transplantation of fecal bacteria derived from GA-treated UC mice, instead of UC mice, increased ILC3 levels. Therefore, we analyzed the gut microbiota and related metabolites to elucidate the mechanism promoting ILC3. We determined that GA treatment altered the diversity of the gut microbiota and activated the bile acid (BA) metabolic pathway. We evaluated three BAs, namely, UDCA, isoalloLCA, and 3-oxoLCA that were significantly upregulated after GA treatment, improved UC symptoms, and elevated the proportion of ILC3 in vivo and in vitro. Collectively, these data indicate that GA attenuates UC by elevating ILC3 proportion, regulating the gut microbiota, and impacting BA metabolism. Additionally, we highlight the modulatory effects of BAs on ILC3 for the first time. Our findings provide novel insights into the multiple roles of GA in alleviating UC and provide a mechanistic explanation that supports the dietary nutrition in UC therapy.

没食子酸(GA)是一种植物酚,广泛分布于水果和蔬菜中,对溃疡性结肠炎(UC)具有保护作用。溃疡性结肠炎是一种以免疫反应紊乱为特征的炎症性疾病。然而,GA 在肠道免疫中的作用和作用机制仍然未知。在这里,我们观察到 GA 治疗可改善肠炎症状,降低细胞因子 TNF-α、IFN-γ、IL-6、IL-17A 和 IL-23 的浓度,增加细胞因子 IL-10、TGF-β 和 IL-22 的浓度,并增加肠系膜淋巴结和固有膜中第 3 组先天性淋巴细胞(ILC3)的比例。然而,GA 不会上调 ILC3,也不会损害抗体处理的不育小鼠的 UC。值得注意的是,移植来自经 GA 处理的 UC 小鼠而非 UC 小鼠的粪便细菌会增加 ILC3 的水平。因此,我们分析了肠道微生物群和相关代谢物,以阐明促进 ILC3 的机制。我们确定,GA 治疗改变了肠道微生物群的多样性,并激活了胆汁酸(BA)代谢途径。我们评估了三种胆汁酸,即 UDCA、isoalloLCA 和 3-oxoLCA,它们在 GA 治疗后显著上调,改善了 UC 症状,并提高了体内和体外 ILC3 的比例。总之,这些数据表明,GA 可通过提高 ILC3 比例、调节肠道微生物群和影响 BA 代谢来减轻 UC。此外,我们还首次强调了 BA 对 ILC3 的调节作用。我们的研究结果为了解 GA 在缓解 UC 中的多重作用提供了新的视角,并为支持 UC 治疗中的膳食营养提供了机理解释。
{"title":"Gallic acid attenuates murine ulcerative colitis by promoting group 3 innate lymphocytes, affecting gut microbiota, and bile acid metabolism","authors":"Yun Leng ,&nbsp;Xiao Zhang ,&nbsp;Qian Zhang,&nbsp;Jiaxuan Xia,&nbsp;Yuefeng Zhang,&nbsp;Chong Ma,&nbsp;Kun Liu,&nbsp;Hao Li,&nbsp;Yanjun Hong,&nbsp;Zhiyong Xie","doi":"10.1016/j.jnutbio.2024.109677","DOIUrl":"10.1016/j.jnutbio.2024.109677","url":null,"abstract":"<div><p>Gallic acid (GA), a plant phenol that is widely distributed in fruits and vegetables, and exhibits a protective role against ulcerative colitis (UC). UC is an inflammatory disease characterized by immune response disorders. However, the role and mechanism of action of GA in gut immunity remain unknown. Here, we observed that GA treatment improved enteritis symptoms, decreased the concentrations of cytokines TNF-α, IFN-γ, IL-6, IL-17A, and IL-23, increased the concentrations of cytokines IL-10, TGF-β and IL-22, and increased the proportion of group 3 innate lymphoid cells (ILC3) in mesenteric lymph nodes and lamina propria. However, GA did not upregulate ILC3 or impair UC in antibody-treated sterile mice. Notably, transplantation of fecal bacteria derived from GA-treated UC mice, instead of UC mice, increased ILC3 levels. Therefore, we analyzed the gut microbiota and related metabolites to elucidate the mechanism promoting ILC3. We determined that GA treatment altered the diversity of the gut microbiota and activated the bile acid (BA) metabolic pathway. We evaluated three BAs, namely, UDCA, isoalloLCA, and 3-oxoLCA that were significantly upregulated after GA treatment, improved UC symptoms, and elevated the proportion of ILC3 <em>in vivo</em> and <em>in vitro</em>. Collectively, these data indicate that GA attenuates UC by elevating ILC3 proportion, regulating the gut microbiota, and impacting BA metabolism. Additionally, we highlight the modulatory effects of BAs on ILC3 for the first time. Our findings provide novel insights into the multiple roles of GA in alleviating UC and provide a mechanistic explanation that supports the dietary nutrition in UC therapy.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109677"},"PeriodicalIF":4.8,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
LncRNA MALAT1-miR-339-5p-NIS axis is involved in the increased level of thyroid stimulating hormone (TSH) induced by combined exposure of high iodine and hyperlipidemia LncRNA MALAT1-miR-339-5p-NIS轴参与了高碘和高脂血症联合暴露诱导的促甲状腺激素(TSH)水平的升高。
IF 5.6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-31 DOI: 10.1016/j.jnutbio.2024.109672
Jinyin Yao , Chunpeng Lv , Peng Liu , Lijun Fan , Zhiwei Zhang , Yi Chen , Xianglan Chen , Xiaodan Zhang , Chunyu Zhang , Jinyu Li , Xuesong Wang , Wen Jiang , Jianxin Niu , Feng Song , Wei Zhang , Dianjun Sun

Hypothyroidism and subclinical hypothyroidism were both characterized by elevated levels of thyroid stimulating hormone (TSH). Previous studies had found that high iodine or hyperlipidemia alone was associated with increased TSH level. However, their combined effects on TSH have not been elucidated. In this study, combination of high iodine and hyperlipidemia was established through the combined exposure of high-water iodine and high fat diet in Wistar rats. The results showed that combined exposure of high iodine and high fat can induce higher TSH level. The mRNA and protein levels of sodium iodide transporters (NIS) and type 1 deiodinase (D1) in thyroid tissues, which were crucial genes in the synthesis of thyroid hormones, decreased remarkably in combined exposure group. Mechanistically, down-regulated long non-coding RNA (lncRNA) metastasis associated in lung denocarcinoma transcript 1 (MALAT1) may regulate the expression of NIS by increasing miR-339-5p, and regulating D1 by increasing miR-224-5p. Then, the above findings were explored in subjects exposed to high water iodine and hyperlipidemia. The results indicated that in population combined with high iodine and hyperlipidemia, TSH level increased to higher level and lncRNA MALAT1-miR-339-5p-NIS axis was obviously activated. Collectively, this study found that combined exposure of high iodine and hyperlipidemia induced a higher level of TSH, and lncRNA MALAT1-miR-339-5p-NIS axis may play important role.

甲状腺功能减退症和亚临床甲状腺功能减退症都以促甲状腺激素(TSH)水平升高为特征,以往的研究发现,单独的高碘或高脂血症与 TSH 水平有关。然而,它们对促甲状腺激素的联合影响尚未阐明。本研究通过对 Wistar 大鼠进行高碘水溶液和高脂饮食的联合暴露,确定了高碘和高脂血症的联合作用。结果表明,高碘和高脂的联合暴露可诱导促甲状腺激素水平升高。甲状腺组织中碘化钠转运体(NIS)和1型脱碘酶(D1)是合成甲状腺激素的关键基因,其mRNA和蛋白水平在联合暴露组明显下降。从机制上看,下调的lncRNA MALAT1可能通过增加miR-339-5p来调控NIS的表达,通过增加miR-224-5p来调控D1的表达。随后,研究人员在暴露于高碘水和高脂血症的受试者中对上述发现进行了探讨。结果表明,在合并高碘和高脂血症的人群中,TSH水平升高,lncRNA MALAT1-miR-339-5p-NIS轴明显被激活。综上所述,本研究发现,高碘和高脂血症联合暴露会诱导促甲状腺激素水平升高,而lncRNA MALAT1-miR-339-5p-NIS轴可能发挥了重要作用。
{"title":"LncRNA MALAT1-miR-339-5p-NIS axis is involved in the increased level of thyroid stimulating hormone (TSH) induced by combined exposure of high iodine and hyperlipidemia","authors":"Jinyin Yao ,&nbsp;Chunpeng Lv ,&nbsp;Peng Liu ,&nbsp;Lijun Fan ,&nbsp;Zhiwei Zhang ,&nbsp;Yi Chen ,&nbsp;Xianglan Chen ,&nbsp;Xiaodan Zhang ,&nbsp;Chunyu Zhang ,&nbsp;Jinyu Li ,&nbsp;Xuesong Wang ,&nbsp;Wen Jiang ,&nbsp;Jianxin Niu ,&nbsp;Feng Song ,&nbsp;Wei Zhang ,&nbsp;Dianjun Sun","doi":"10.1016/j.jnutbio.2024.109672","DOIUrl":"10.1016/j.jnutbio.2024.109672","url":null,"abstract":"<div><p>Hypothyroidism and subclinical hypothyroidism were both characterized by elevated levels of thyroid stimulating hormone (TSH). Previous studies had found that high iodine or hyperlipidemia alone was associated with increased TSH level. However, their combined effects on TSH have not been elucidated. In this study, combination of high iodine and hyperlipidemia was established through the combined exposure of high-water iodine and high fat diet in Wistar rats. The results showed that combined exposure of high iodine and high fat can induce higher TSH level. The mRNA and protein levels of sodium iodide transporters (NIS) and type 1 deiodinase (D1) in thyroid tissues, which were crucial genes in the synthesis of thyroid hormones, decreased remarkably in combined exposure group. Mechanistically, down-regulated long non-coding RNA (lncRNA) metastasis associated in lung denocarcinoma transcript 1 (MALAT1) may regulate the expression of NIS by increasing miR-339-5p, and regulating D1 by increasing miR-224-5p. Then, the above findings were explored in subjects exposed to high water iodine and hyperlipidemia. The results indicated that in population combined with high iodine and hyperlipidemia, TSH level increased to higher level and lncRNA MALAT1-miR-339-5p-NIS axis was obviously activated. Collectively, this study found that combined exposure of high iodine and hyperlipidemia induced a higher level of TSH, and lncRNA MALAT1-miR-339-5p-NIS axis may play important role.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109672"},"PeriodicalIF":5.6,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Citrulline supplementation exacerbates sepsis severity in infected preterm piglets via early induced immunosuppression 通过早期诱导免疫抑制,补充瓜氨酸会加剧感染早产仔猪败血症的严重程度。
IF 5.6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-31 DOI: 10.1016/j.jnutbio.2024.109674
Jingren Zhong , Sebastian Høj Johansen , Ole Bæk , Duc Ninh Nguyen

Arginine (ARG)/Citrulline (CIT) deficiency is associated with increased sepsis severity after infection. Supplementation of CIT to susceptible patients with ARG/CIT deficiency such as preterm newborns with suspected infection might prevent sepsis, via maintaining immune and vascular function. Caesarean-delivered, parenterally nourished preterm pigs were treated with CIT (1g/kg bodyweight) via oral or continuous intravenous supplementation, then inoculated with live Staphylococcus epidermidis and clinically monitored for 14 h. Blood, liver, and spleen samples were collected for analysis. In vitro cord blood stimulation was performed to explore how CIT and ARG affect premature blood cell responses. After infection, oral CIT supplementation led to higher mortality, increased blood bacterial load, and systemic and hepatic inflammation. Intravenous CIT administration showed increased inflammation and bacterial burdens without significantly affecting mortality. Liver transcriptomics and data from in vitro blood stimulation indicated that CIT induces systemic immunosuppression in preterm newborns, which may impair resistance response to bacteria at the early stage of infection, subsequently causing later uncontrollable inflammation and tissue damage. The early stage of CIT supplementation exacerbates sepsis severity in infected preterm pigs, likely via inducing systemic immunosuppression.

背景:精氨酸(ARG)/瓜氨酸(CIT)缺乏与感染后败血症严重程度增加有关。向缺乏 ARG/CIT 的易感人群(如疑似感染的早产新生儿)补充 CIT 可通过维持免疫和血管功能来预防败血症:方法:通过口服或持续静脉注射 CIT(1 克/千克),对剖腹产的亲喂早产猪进行治疗,然后接种活的表皮葡萄球菌,并进行 14 小时的临床监测。收集血液、肝脏和脾脏样本进行分析。对脐带血进行体外刺激,以探索 CIT 和 ARG 如何影响早老性血细胞反应:结果:感染后,口服 CIT 会导致死亡率升高、血液细菌负荷增加以及全身和肝脏炎症。静脉注射 CIT 会增加炎症和细菌负荷,但不会显著影响死亡率。肝脏转录组学和体外血液刺激的数据表明,CIT会诱导早产新生儿的全身免疫抑制,这可能会在感染早期损害对细菌的抵抗反应,随后导致无法控制的炎症和组织损伤:结论:补充 CIT 的早期阶段会加剧感染早产猪的败血症严重程度,这可能是通过诱导全身免疫抑制造成的。
{"title":"Citrulline supplementation exacerbates sepsis severity in infected preterm piglets via early induced immunosuppression","authors":"Jingren Zhong ,&nbsp;Sebastian Høj Johansen ,&nbsp;Ole Bæk ,&nbsp;Duc Ninh Nguyen","doi":"10.1016/j.jnutbio.2024.109674","DOIUrl":"10.1016/j.jnutbio.2024.109674","url":null,"abstract":"<div><p>Arginine (ARG)/Citrulline (CIT) deficiency is associated with increased sepsis severity after infection. Supplementation of CIT to susceptible patients with ARG/CIT deficiency such as preterm newborns with suspected infection might prevent sepsis, via maintaining immune and vascular function. Caesarean-delivered, parenterally nourished preterm pigs were treated with CIT (1g/kg bodyweight) via oral or continuous intravenous supplementation, then inoculated with live <em>Staphylococcus epidermidis</em> and clinically monitored for 14 h. Blood, liver, and spleen samples were collected for analysis. <em>In vitro</em> cord blood stimulation was performed to explore how CIT and ARG affect premature blood cell responses. After infection, oral CIT supplementation led to higher mortality, increased blood bacterial load, and systemic and hepatic inflammation. Intravenous CIT administration showed increased inflammation and bacterial burdens without significantly affecting mortality. Liver transcriptomics and data from <em>in vitro</em> blood stimulation indicated that CIT induces systemic immunosuppression in preterm newborns, which may impair resistance response to bacteria at the early stage of infection, subsequently causing later uncontrollable inflammation and tissue damage. The early stage of CIT supplementation exacerbates sepsis severity in infected preterm pigs, likely via inducing systemic immunosuppression.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109674"},"PeriodicalIF":5.6,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324001074/pdfft?md5=621ed60d5683bfa85e879fe7ff215c28&pid=1-s2.0-S0955286324001074-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Pomegranate (Punica granatum L.) phytochemicals target the components of metabolic syndrome 石榴(Punica granatum L.)植物化学物质针对代谢综合征的成分。
IF 5.6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-19 DOI: 10.1016/j.jnutbio.2024.109670
Lucas Fornari Laurindo , Victória Dogani Rodrigues , Giulia Minniti , Antonelly Cassio Alves de Carvalho , Tereza Laís Menegucci Zutin , Lindsay K. DeLiberto , Anupam Bishayee , Sandra Maria Barbalho

Pomegranate (Punica granatum L.) is a multipurpose dietary and medicinal plant known for its ability to promote various health benefits. Metabolic syndrome (MetS) is a complex metabolic disorder driving health and socioeconomic challenges worldwide. It may be characterized by insulin resistance, abdominal obesity, hypertension, and dyslipidemia. This study aims to conduct a review of pomegranate's effects on MetS parameters using a mechanistic approach relying on pre-clinical studies. The peel, juice, roots, bark, seeds, flowers, and leaves of the fruit present several bioactive compounds that are related mainly to anti-inflammatory and antioxidant activities as well as cardioprotective, antidiabetic, and antiobesity effects. The use of the juice extract can work as a potent inhibitor of angiotensin-converting enzyme activities, consequently regulating blood pressure. The major bioactive compounds found within the fruit are phenolic compounds (hydrolysable tannins and flavonoids) and fatty acids. Alkaloids, punicalagin, ellagitannins, ellagic acid, anthocyanins, tannins, flavonoids, luteolin, and punicic acid are also present. The antihyperglycemia, antihyperlipidemia, and weight loss promoting effects are likely related to the anti-inflammatory and antioxidant effects. When considering clinical application, pomegranate extracts are found to be frequently well-tolerated, further supporting its efficacy as a treatment modality. We suggest that pomegranate fruit, extract, or processed products can be used to counteract MetS-related risk factors. This review represents an important step towards exploring potential avenues for further research in this area.

石榴(Punica granatum L.)是一种多用途膳食和药用植物,因其能够促进各种健康益处而闻名。代谢综合征(MetS)是一种复杂的代谢紊乱,在全球范围内对健康和社会经济造成挑战。其特征可能是胰岛素抵抗、腹部肥胖、高血压和血脂异常。本研究旨在以临床前研究为基础,采用机理研究的方法对石榴对代谢综合征参数的影响进行综述。石榴的果皮、果汁、根、树皮、种子、花和叶中含有多种生物活性化合物,主要与抗炎和抗氧化活性以及心脏保护、抗糖尿病和抗肥胖作用有关。使用果汁提取物可以有效抑制血管紧张素转换酶的活性,从而调节血压。水果中的主要生物活性化合物是酚类化合物(可水解单宁酸和类黄酮)和脂肪酸。此外,还含有生物碱、punicalagin、鞣花丹宁、鞣花酸、花青素、单宁、类黄酮、木犀草素和布匿酸。石榴的抗高血糖、抗高血脂和减肥功效可能与抗炎和抗氧化作用有关。在考虑临床应用时,我们发现石榴提取物通常具有良好的耐受性,这进一步支持了其作为一种治疗方式的功效。我们建议,石榴果实、提取物或加工产品可用于对抗 MetS 相关风险因素。本综述是探索该领域进一步研究潜在途径的重要一步。
{"title":"Pomegranate (Punica granatum L.) phytochemicals target the components of metabolic syndrome","authors":"Lucas Fornari Laurindo ,&nbsp;Victória Dogani Rodrigues ,&nbsp;Giulia Minniti ,&nbsp;Antonelly Cassio Alves de Carvalho ,&nbsp;Tereza Laís Menegucci Zutin ,&nbsp;Lindsay K. DeLiberto ,&nbsp;Anupam Bishayee ,&nbsp;Sandra Maria Barbalho","doi":"10.1016/j.jnutbio.2024.109670","DOIUrl":"10.1016/j.jnutbio.2024.109670","url":null,"abstract":"<div><p>Pomegranate <em>(Punica granatum</em> L.) is a multipurpose dietary and medicinal plant known for its ability to promote various health benefits. Metabolic syndrome (MetS) is a complex metabolic disorder driving health and socioeconomic challenges worldwide. It may be characterized by insulin resistance, abdominal obesity, hypertension, and dyslipidemia. This study aims to conduct a review of pomegranate's effects on MetS parameters using a mechanistic approach relying on pre-clinical studies. The peel, juice, roots, bark, seeds, flowers, and leaves of the fruit present several bioactive compounds that are related mainly to anti-inflammatory and antioxidant activities as well as cardioprotective, antidiabetic, and antiobesity effects. The use of the juice extract can work as a potent inhibitor of angiotensin-converting enzyme activities, consequently regulating blood pressure. The major bioactive compounds found within the fruit are phenolic compounds (hydrolysable tannins and flavonoids) and fatty acids. Alkaloids, punicalagin, ellagitannins, ellagic acid, anthocyanins, tannins, flavonoids, luteolin, and punicic acid are also present. The antihyperglycemia, antihyperlipidemia, and weight loss promoting effects are likely related to the anti-inflammatory and antioxidant effects. When considering clinical application, pomegranate extracts are found to be frequently well-tolerated, further supporting its efficacy as a treatment modality. We suggest that pomegranate fruit, extract, or processed products can be used to counteract MetS-related risk factors. This review represents an important step towards exploring potential avenues for further research in this area.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109670"},"PeriodicalIF":5.6,"publicationDate":"2024-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Approaches to nutritional research using organoids; fructose treatment induces epigenetic changes in liver organoids 利用器官组织进行营养研究的方法;果糖处理诱导肝脏器官组织发生表观遗传学变化。
IF 5.6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-18 DOI: 10.1016/j.jnutbio.2024.109671
Mirai Yamazaki , Hiroya Yamada , Eiji Munetsuna , Yoshitaka Ando , Genki Mizuno , Atsushi Teshigawara , Hayato Ichikawa , Yuki Nouchi , Itsuki Kageyama , Takuya Wakasugi , Hiroaki Ishikawa , Nobutaka Ohgami , Koji Suzuki , Koji Ohashi

Nutritional researches have successfully used animal models to gain new insights into nutrient action. However, comprehensive descriptions of their molecular mechanisms of action remain elusive as appropriate in vitro evaluation systems are lacking. Organoid models can mimic physiological structures and reproduce in vivo functions, making them increasingly utilized in biomedical research for a better understand physiological and pathological phenomena. Therefore, organoid modeling can be a powerful approach for to understand the molecular mechanisms of nutrient action. The present study aims to demonstrate the utility of organoids in nutritional research by further investigating the molecular mechanisms responsible for the negative effects of fructose intake using liver organoids. Here, we treated liver organoids with fructose and analyzed their gene expression profiles and DNA methylation levels. Microarray analysis demonstrated that fructose-treated organoids exhibited increased selenoprotein p (Sepp1) gene expression, whereas pyrosequencing assays revealed reduced DNA methylation levels in the Sepp1 region. These results were consistent with observations using hepatic tissues from fructose-fed rats. Conversely, no differences in Sepp1 mRNA and DNA methylation levels were observed in two-dimensional cells. These results suggest that organoids serve as an ideal in vitro model to recapitulate in vivo tissue responses and help to validate the molecular mechanisms of nutrient action compared to conventional cellular models.

营养研究成功地利用动物模型获得了营养作用的新见解。然而,由于缺乏适当的体外评估系统,对其分子作用机制的全面描述仍然难以实现。类器官模型可模仿生理结构并再现体内功能,因此越来越多地被用于生物医学研究,以更好地了解生理和病理现象。因此,类器官模型可以成为了解营养素作用分子机制的有力方法。本研究旨在利用肝脏类器官进一步研究果糖摄入负面影响的分子机制,从而证明类器官在营养学研究中的作用。在这里,我们用果糖处理了肝脏器官组织,并分析了它们的基因表达谱和DNA甲基化水平。微阵列分析表明,果糖处理过的器官组织显示硒蛋白p(Sepp1)基因表达增加,而热释光测序分析则显示Sepp1区域的DNA甲基化水平降低。这些结果与使用果糖喂养大鼠的肝组织观察到的结果一致。相反,在二维细胞中没有观察到 Sepp1 mRNA 和 DNA 甲基化水平的差异。这些结果表明,与传统的细胞模型相比,器官组织是再现体内组织反应的理想体外模型,有助于验证营养素作用的分子机制。
{"title":"Approaches to nutritional research using organoids; fructose treatment induces epigenetic changes in liver organoids","authors":"Mirai Yamazaki ,&nbsp;Hiroya Yamada ,&nbsp;Eiji Munetsuna ,&nbsp;Yoshitaka Ando ,&nbsp;Genki Mizuno ,&nbsp;Atsushi Teshigawara ,&nbsp;Hayato Ichikawa ,&nbsp;Yuki Nouchi ,&nbsp;Itsuki Kageyama ,&nbsp;Takuya Wakasugi ,&nbsp;Hiroaki Ishikawa ,&nbsp;Nobutaka Ohgami ,&nbsp;Koji Suzuki ,&nbsp;Koji Ohashi","doi":"10.1016/j.jnutbio.2024.109671","DOIUrl":"10.1016/j.jnutbio.2024.109671","url":null,"abstract":"<div><p>Nutritional researches have successfully used animal models to gain new insights into nutrient action. However, comprehensive descriptions of their molecular mechanisms of action remain elusive as appropriate <em>in vitro</em> evaluation systems are lacking. Organoid models can mimic physiological structures and reproduce <em>in vivo</em> functions, making them increasingly utilized in biomedical research for a better understand physiological and pathological phenomena. Therefore, organoid modeling can be a powerful approach for to understand the molecular mechanisms of nutrient action. The present study aims to demonstrate the utility of organoids in nutritional research by further investigating the molecular mechanisms responsible for the negative effects of fructose intake using liver organoids. Here, we treated liver organoids with fructose and analyzed their gene expression profiles and DNA methylation levels. Microarray analysis demonstrated that fructose-treated organoids exhibited increased selenoprotein p (<em>Sepp1</em>) gene expression, whereas pyrosequencing assays revealed reduced DNA methylation levels in the <em>Sepp1</em> region. These results were consistent with observations using hepatic tissues from fructose-fed rats. Conversely, no differences in <em>Sepp1</em> mRNA and DNA methylation levels were observed in two-dimensional cells. These results suggest that organoids serve as an ideal <em>in vitro</em> model to recapitulate <em>in vivo</em> tissue responses and help to validate the molecular mechanisms of nutrient action compared to conventional cellular models.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109671"},"PeriodicalIF":5.6,"publicationDate":"2024-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Transgenerational impact of maternal zinc deficiency on offspring metabolic outcomes in Drosophila melanogaster 母体缺锌对黑腹果蝇后代代谢结果的跨代影响
IF 5.6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-15 DOI: 10.1016/j.jnutbio.2024.109669
Kamaldeen Olalekan Sanusi , Murtala Bello Abubakar , Kasimu Ghandi Ibrahim , Mustapha Umar Imam

Maternal zinc deficiency significantly influences fetal development and long-term health outcomes, yet its transgenerational effects remain poorly understood. This study aims to investigate the transgenerational effects of maternal zinc deficiency on metabolic outcomes in Drosophila melanogaster. Zinc deficiency was induced in Drosophila by incorporating TPEN (N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine) into their diet. Offspring (F1 to F3) were maintained on a standard diet for subsequent analyses. Various metabolic markers, including glucose, trehalose, glycogen, and triglyceride levels, were assessed, and gene expression analyses were conducted to examine the molecular responses across generations. Significant reductions in locomotor performance in female F1 flies and increased body weight in the F2 generation were observed. Maternal zinc deficiency exhibited gender- and generation-specific impacts on metabolic markers. Notably, an adaptive response in the F3 generation included increased catalase activity and total antioxidant capacity, along with decreased malondialdehyde levels. Gene expression analyses revealed upregulation of DILP2 mRNA across generations and significant variations in PEPCK, SOD1, CAT, EGR, and UPD2 mRNA levels, demonstrating intricate responses to maternal zinc deficiency. This study provides a holistic understanding of the consequences of maternal zinc deficiency, emphasizing the complex interplay between zinc status and metabolic outcomes across generations in Drosophila. These findings lay the foundation for future research elucidating the underlying molecular mechanisms, with potential implications for humans. The insights gained contribute to informing targeted interventions aimed at optimizing offspring health in the context of maternal zinc deficiency.

母体缺锌会严重影响胎儿的发育和长期的健康结果,但对其跨代影响的了解仍然很少。本研究旨在探讨母体缺锌对黑腹果蝇代谢结果的跨代影响。通过在果蝇食物中添加 TPEN(N,N,N',N'-四(2-吡啶基甲基)乙二胺)诱导果蝇缺锌。后代(F1 至 F3)以标准食物饲养,以进行后续分析。评估了各种代谢指标,包括葡萄糖、三卤糖、糖原和甘油三酯水平,并进行了基因表达分析,以研究各代的分子反应。结果表明,F1 代雌蝇的运动能力显著下降,F2 代体重增加。母体缺锌对代谢指标的影响具有性别和世代特异性。值得注意的是,F3 代的适应性反应包括过氧化氢酶活性和总抗氧化能力的提高,以及丙二醛水平的降低。基因表达分析表明,DILP2 mRNA在各代之间上调,PEPCK、SOD1、CAT、EGR和UPD2 mRNA水平也有显著变化,这显示了对母体锌缺乏的复杂反应。这项研究提供了对母体缺锌后果的整体认识,强调了锌状态与果蝇跨代代谢结果之间复杂的相互作用。这些发现为今后阐明潜在分子机制的研究奠定了基础,并可能对人类产生影响。所获得的见解有助于在母体缺锌的情况下,为旨在优化后代健康的针对性干预措施提供信息。
{"title":"Transgenerational impact of maternal zinc deficiency on offspring metabolic outcomes in Drosophila melanogaster","authors":"Kamaldeen Olalekan Sanusi ,&nbsp;Murtala Bello Abubakar ,&nbsp;Kasimu Ghandi Ibrahim ,&nbsp;Mustapha Umar Imam","doi":"10.1016/j.jnutbio.2024.109669","DOIUrl":"10.1016/j.jnutbio.2024.109669","url":null,"abstract":"<div><p>Maternal zinc deficiency significantly influences fetal development and long-term health outcomes, yet its transgenerational effects remain poorly understood. This study aims to investigate the transgenerational effects of maternal zinc deficiency on metabolic outcomes in <em>Drosophila melanogaster</em>. Zinc deficiency was induced in Drosophila by incorporating TPEN (N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine) into their diet. Offspring (F1 to F3) were maintained on a standard diet for subsequent analyses. Various metabolic markers, including glucose, trehalose, glycogen, and triglyceride levels, were assessed, and gene expression analyses were conducted to examine the molecular responses across generations. Significant reductions in locomotor performance in female F1 flies and increased body weight in the F2 generation were observed. Maternal zinc deficiency exhibited gender- and generation-specific impacts on metabolic markers. Notably, an adaptive response in the F3 generation included increased catalase activity and total antioxidant capacity, along with decreased malondialdehyde levels. Gene expression analyses revealed upregulation of <em>DILP2</em> mRNA across generations and significant variations in <em>PEPCK, SOD1, CAT, EGR</em>, and <em>UPD2</em> mRNA levels, demonstrating intricate responses to maternal zinc deficiency. This study provides a holistic understanding of the consequences of maternal zinc deficiency, emphasizing the complex interplay between zinc status and metabolic outcomes across generations in Drosophila. These findings lay the foundation for future research elucidating the underlying molecular mechanisms, with potential implications for humans. The insights gained contribute to informing targeted interventions aimed at optimizing offspring health in the context of maternal zinc deficiency.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"130 ","pages":"Article 109669"},"PeriodicalIF":5.6,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140957415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Journal of Nutritional Biochemistry
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1