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Effects of riboflavin deficiency and high dietary fat on hepatic lipid accumulation: a synergetic action in the development of non-alcoholic fatty liver disease 核黄素缺乏和高膳食脂肪对肝脏脂质积累的影响:非酒精性脂肪肝发病过程中的协同作用
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2024-01-02 DOI: 10.1186/s12986-023-00775-8
Yanxian Wang, Xiangyu Bian, Min Wan, Weiyun Dong, Weina Gao, Zhanxin Yao, Changjiang Guo
Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. Riboflavin, one of water soluble vitamins, plays a role in lipid metabolism and antioxidant function. However, the effects of riboflavin deficiency on NAFLD development have not yet to be fully explored. In the present study, an animal model of NAFLD was induced by high fat diet feeding in mice and a cellular model of NAFLD was developed in HepG2 cells by palmitic acid (PA) exposure. The effects of riboflavin deficiency on lipid metabolism and antioxidant function were investigated both in vivo and in vitro. In addition, the possible role of peroxisome proliferator-activated receptor gamma (PPARγ) was studied in HepG2 cells using gene silencing technique. The results showed that riboflavin deficiency led to hepatic lipid accumulation in mice fed high fat diet. The expressions of fatty acid synthase (FAS) and carnitine palmitoyltransferase 1 (CPT1) were up-regulated, whereas that of adipose triglyceride lipase (ATGL) down-regulated. Similar changes in response to riboflavin deficiency were demonstrated in HepG2 cells treated with PA. Factorial analysis revealed a significant interaction between riboflavin deficiency and high dietary fat or PA load in the development of NAFLD. Hepatic PPARγ expression was significantly upregulated in mice fed riboflavin deficient and high fat diet or in HepG2 cells treated with riboflavin deficiency and PA load. Knockdown of PPARγ gene resulted in a significant reduction of lipid accumulation in HepG2 cells exposed to riboflavin deficiency and PA load. There is a synergetic action between riboflavin deficiency and high dietary fat on the development of NAFLD, in which PPARγ may play an important role.
非酒精性脂肪肝(NAFLD)的特点是肝脏中脂质过度积累。核黄素是水溶性维生素之一,在脂质代谢和抗氧化功能中发挥作用。然而,核黄素缺乏对非酒精性脂肪肝发展的影响尚未得到充分探讨。在本研究中,通过高脂饮食喂养小鼠诱导了非酒精性脂肪肝的动物模型,并通过棕榈酸(PA)暴露在 HepG2 细胞中建立了非酒精性脂肪肝的细胞模型。在体内和体外研究了核黄素缺乏对脂质代谢和抗氧化功能的影响。此外,还利用基因沉默技术研究了过氧化物酶体增殖激活受体γ(PPARγ)在 HepG2 细胞中可能发挥的作用。结果表明,核黄素缺乏会导致以高脂肪饮食喂养的小鼠肝脏脂质积累。脂肪酸合成酶(FAS)和肉碱棕榈酰基转移酶1(CPT1)的表达上调,而脂肪甘油三酯脂酶(ATGL)的表达下调。用 PA 处理的 HepG2 细胞对核黄素缺乏的反应也发生了类似的变化。因子分析显示,核黄素缺乏与高膳食脂肪或 PA 负荷在非酒精性脂肪肝的发生中存在明显的交互作用。在缺乏核黄素和高脂肪饮食喂养的小鼠中,或在缺乏核黄素和 PA 负荷处理的 HepG2 细胞中,肝脏 PPARγ 表达明显上调。敲除 PPARγ 基因可显著减少暴露于核黄素缺乏和 PA 负荷的 HepG2 细胞中的脂质积累。核黄素缺乏和高膳食脂肪对非酒精性脂肪肝的发生有协同作用,PPARγ可能在其中发挥了重要作用。
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引用次数: 0
Deficiency of Trex1 leads to spontaneous development of type 1 diabetes 缺乏 Trex1 会导致自发罹患 1 型糖尿病
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2024-01-02 DOI: 10.1186/s12986-023-00777-6
Jiang-Man Zhao, Zhi-Hui Su, Qiu-Ying Han, Miao Wang, Xin Liu, Jing Li, Shao-Yi Huang, Jing Chen, Xiao-Wei Li, Xia-Ying Chen, Zeng-Lin Guo, Shuai Jiang, Jie Pan, Tao Li, Wen Xue, Tao Zhou
Type 1 diabetes is believed to be an autoimmune condition, characterized by destruction of insulin-producing cells, due to the detrimental inflammation in pancreas. Growing evidences have indicated the important role of type I interferon in the development of type 1 diabetes. Trex1-deficient rats were generated by using CRISPR-Cas9. The fasting blood glucose level of rat was measured by a Roche Accuchek blood glucose monitor. The levels of insulin, islet autoantibodies, and interferon-β were measured using enzyme-linked immunosorbent assay. The inflammatory genes were detected by quantitative PCR and RNA-seq. Hematein-eosin staining was used to detect the pathological changes in pancreas, eye and kidney. The pathological features of kidney were also detected by Masson trichrome and periodic acid-Schiff staining. The distribution of islet cells, immune cells or ssDNA in pancreas was analyzed by immunofluorescent staining. In this study, we established a Trex1-deletion Sprague Dawley rat model, and unexpectedly, we found that the Trex1−/− rats spontaneously develop type 1 diabetes. Similar to human diabetes, the hyperglycemia in rats is accompanied by diabetic complications such as diabetic nephropathy and cataract. Mechanistical investigation revealed the accumulation of ssDNA and the excessive production of proinflammatory cytokines, including IFN-β, in Trex1 null pancreas. These are likely contributing to the inflammation in pancreas and eventually leading to the decline of pancreatic β cells. Our study links the DNA-induced chronic inflammation to the pathogenesis of type 1 diabetes, and also provides an animal model for type 1 diabetes studies.
1 型糖尿病被认为是一种自身免疫性疾病,其特点是由于胰腺中的有害炎症导致胰岛素分泌细胞遭到破坏。越来越多的证据表明,I型干扰素在1型糖尿病的发病过程中起着重要作用。利用 CRISPR-Cas9 技术生成了 Trex1 基因缺陷大鼠。用罗氏 Accuchek 血糖监测仪测量大鼠的空腹血糖水平。用酶联免疫吸附法测定胰岛素、胰岛自身抗体和干扰素-β的水平。炎症基因通过定量 PCR 和 RNA-seq 进行检测。血红素-伊红染色用于检测胰腺、眼睛和肾脏的病理变化。肾脏的病理特征也通过马森三色染色法和周期性酸-希夫染色法进行检测。免疫荧光染色法分析了胰腺中胰岛细胞、免疫细胞或 ssDNA 的分布。在这项研究中,我们建立了Trex1缺失的Sprague Dawley大鼠模型,并意外地发现Trex1-/-大鼠会自发患上1型糖尿病。与人类糖尿病相似,大鼠的高血糖也伴随着糖尿病并发症,如糖尿病肾病和白内障。机理研究发现,Trex1 基因缺失的大鼠胰腺中积累了 ssDNA,并产生了过多的促炎细胞因子,包括 IFN-β。这些都可能导致胰腺发炎,并最终导致胰腺β细胞衰退。我们的研究将DNA诱导的慢性炎症与1型糖尿病的发病机制联系起来,同时也为1型糖尿病的研究提供了一个动物模型。
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引用次数: 0
Effect of probiotic supplementation on lipoprotein-associated phospholipase A2 in type 2 diabetic patients: a randomized double blind clinical controlled trial 补充益生菌对 2 型糖尿病患者脂蛋白相关磷脂酶 A2 的影响:随机双盲临床对照试验
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2024-01-02 DOI: 10.1186/s12986-023-00778-5
Salman Jaff, Mohammed Gubari, Sakineh Shab-Bidar, Kurosh Djafarian
It has been recently reported that lipoprotein-associated phospholipase A2 (Lp-PLA2) may predict the risk of cardiovascular disease. The effect of multi-strain probiotics on Lp-PLA2 in patients with type 2 diabetes is still not clear. This study aimed to determine the effect of multi-strain probiotic supplementation on lipoprotein-associated phospholipase A2, and glycemic status, lipid profile, and body composition in patients with type 2 diabetes. In this randomized double-blind placebo-controlled clinical trial, 68 participants with type 2 diabetes, in the age group of 50–65 years, were recruited and randomly allocated to take either probiotic (n = 34) or placebo (n = 34) for 12 weeks. The primary outcome was lipoprotein-associated phospholipase A2, and secondary outcomes were glycemic parameters, lipid profile, anthropometric characters, and body composition (fat mass and fat-free mass). There was a significant reduction in serum lipoprotein-associated phospholipase A2, in the probiotic group, it dropped by 6.4 units at the end of the study (p < 0.001) compared to the placebo group. Probiotic supplementation also resulted in a significant improvement in the hemoglobin A1c and high-density lipoprotein cholesterol 1.5% (p < 0.001) and 6 mg/dl (p 0.005), respectively. There were no significant changes in other outcomes. Probiotic supplementation was beneficial for reducing Lp-PLA2 and hemoglobin-A1c and improving high-density lipoprotein cholesterol, which may suggest an improvement in the prognosis in patients with type 2 diabetes.
最近有报道称,脂蛋白相关磷脂酶 A2(Lp-PLA2)可预测心血管疾病的风险。多菌株益生菌对 2 型糖尿病患者 Lp-PLA2 的影响尚不明确。本研究旨在确定补充多菌株益生菌对脂蛋白相关磷脂酶 A2 以及 2 型糖尿病患者血糖状况、血脂谱和身体成分的影响。在这项随机双盲安慰剂对照临床试验中,共招募了 68 名年龄在 50-65 岁之间的 2 型糖尿病患者,并随机分配他们服用益生菌(34 人)或安慰剂(34 人),为期 12 周。主要结果是脂蛋白相关磷脂酶 A2,次要结果是血糖参数、血脂概况、人体测量特征和身体成分(脂肪量和无脂肪量)。与安慰剂组相比,益生菌组的血清脂蛋白相关磷脂酶 A2 明显下降,研究结束时下降了 6.4 个单位(p < 0.001)。补充益生菌还能显著改善血红蛋白 A1c 和高密度脂蛋白胆固醇,分别为 1.5% (p < 0.001) 和 6 mg/dl (p 0.005)。其他结果没有明显变化。补充益生菌有利于降低脂蛋白磷酸二酯和血红蛋白-A1c,改善高密度脂蛋白胆固醇,这可能表明2型糖尿病患者的预后有所改善。
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引用次数: 0
D-mannose promotes the degradation of IDH2 through upregulation of RNF185 and suppresses breast cancer D-mannose 通过上调 RNF185 促进 IDH2 的降解并抑制乳腺癌的发生
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2024-01-02 DOI: 10.1186/s12986-023-00774-9
Ruonan Zhang, Ziyin Tian, Yanping Xu, Lei Lv
D-mannose, an epimer of glucose, which is abundant in some fruits, such as cranberry, has been previously reported to inhibit urinary tract infection. In recent years, the potential function of D-mannose has been broadened into the regulation of other inflammation diseases and cancer. It was reported that D-mannose can increase reactive oxygen species (ROS) production, while IDH2 is important for the generation of NADPH, the crucial reducing factor. These findings prompted us to determine whether D-mannose can regulate IDH2 and IDH2-mediated NADPH production in tumor. The breast cancer cell line MDA-MB-231 was cultured and treated with 100mM D-mannose. IDH2 expression was detected by Western Blot and qRT-PCR. RNA-seq was conducted to identify the differentially expressed genes. BioGRID database was used to find the IDH2 interactors. Tumor cells were collected to measure the NADPH production using the NADP+/NADPH detection Kit. Colony formation assay and CCK-8 assay were conducted to evaluate the proliferation of cells. D-mannose can promote IDH2 protein degradation through ubiquitination-proteasome pathway. Mechanistically, D-mannose treatment upregulated the expression of an E3 ligase - RNF185, which can interact with IDH2 and promotes its proteasomal degradation. Consequently, IDH2-mediated NADPH production was inhibited by D-mannose, the proliferation of breast cancer cells was retarded, and the sensitivity to pro-oxidant of breast cancer cells was elevated. Our study demonstrated that D-mannose can degrade IDH2 and inhibit the production of NADPH to suppress the proliferation of breast cancer cells and render the breast cancer cells more sensitive to pro-oxidant treatment. Furthermore, we illustrated the E3 ligase RNF185 plays an important role in D-mannose-mediated proteasomal degradation of IDH2.
D-mannose 是葡萄糖的一种表聚体,在蔓越莓等一些水果中含量丰富,以前曾有报道称它能抑制尿路感染。近年来,D-甘露糖的潜在功能已扩展到调节其他炎症疾病和癌症。据报道,D-甘露糖能增加活性氧(ROS)的产生,而 IDH2 对产生 NADPH(重要的还原因子)非常重要。这些发现促使我们研究 D-甘露糖是否能调节 IDH2 和 IDH2 介导的 NADPH 在肿瘤中的产生。我们培养了乳腺癌细胞株 MDA-MB-231,并用 100mM D-甘露糖进行处理。通过 Western 印迹和 qRT-PCR 检测 IDH2 的表达。通过 RNA-seq 鉴定差异表达基因。利用 BioGRID 数据库查找 IDH2 的相互作用因子。收集肿瘤细胞,使用 NADP+/NADPH 检测试剂盒检测 NADPH 的产生。集落形成试验和 CCK-8 试验用于评估细胞的增殖情况。D-mannose 可通过泛素化-蛋白酶体途径促进 IDH2 蛋白降解。从机理上讲,D-甘露糖能上调E3连接酶RNF185的表达,而RNF185能与IDH2相互作用并促进其蛋白酶体降解。因此,D-甘露糖抑制了 IDH2 介导的 NADPH 生成,延缓了乳腺癌细胞的增殖,并提高了乳腺癌细胞对促氧化剂的敏感性。我们的研究表明,D-甘露糖能降解 IDH2 并抑制 NADPH 的产生,从而抑制乳腺癌细胞的增殖,并使乳腺癌细胞对促氧化剂更敏感。此外,我们还发现E3连接酶RNF185在D-甘露糖介导的IDH2蛋白酶体降解过程中发挥了重要作用。
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引用次数: 0
Amelioration of Atherosclerosis by lycopene is linked to the modulation of gut microbiota dysbiosis and related gut-heart axis activation in high-fat diet-fed ApoE-/- mice. 在高脂肪饮食喂养的ApoE-/-小鼠中,番茄红素对动脉粥样硬化的改善与肠道微生物群失调和相关的肠-心轴激活的调节有关。
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2023-12-01 DOI: 10.1186/s12986-023-00772-x
Tengcan Tu, Hao Liu, Zhenhao Liu, Yunyi Liang, Chujun Tan, Dan Feng, Jun Zou

Background: Interplay between gut microbiota and heart, termed "gut-heart" axis, has a crucial role in the pathogenesis of atherosclerosis. Our previous study showed that lycopene possesses anti-inflammatory and anti-atherosclerotic effects, but its link to the gut microbiota is poorly understood. Herein, we surmised that lycopene could regulate the gut microbiota, exert anti-atherosclerotic effect by regulating the "gut-heart" axis.

Methods: Male ApoE-/- mice were fed a high-fat diet (HFD) with or without lycopene (0.1% w/w) for 19 weeks. Gut microbiota was analyzed by 16 S rRNA sequencing, the protein levels of zonula occludens-1 (ZO-1), occludin, toll-like receptor 4 (TLR4) and phospho-nuclear factor-κB (NF-κB) p65 were measured by Western blotting, the levels of serum inflammatory factors including monocyte chemotactic protein 1 (MCP-1), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 were assayed using ELISA kits. Also, the concentrations of serum lipopolysaccharide (LPS), D-lactic acid (D-LA) and diamine peroxidase (DAO) were measured through ELISA method.

Results: The aortic sinus sections revealed that lycopene supplementation significantly reduced the extent of atherosclerotic lesions and inhibited atherosclerosis development caused by HFD. The analysis of gut microbiota showed that lycopene reduced the ratio of Firmicutes/Bacteroides and increased the relative abundance of Verrucomicrobia, Akkermansia and Alloprevotella, which were related to elevated intestinal barrier function and reduced inflammation. Moreover, lycopene up-regulated the expression of intestinal ZO-1 and occludin and decreased serum LPS, D-LA and DAO levels. In addition, lycopene inhibited the expression of TLR4 and phospho-NF-κB p65 in aortic sinus plaque, serum MCP-1, TNF-α, IL-1β, and IL-6 levels were also lowered by lycopene treatment.

Conclusions: Our results indicated the protective effect of lycopene against atherosclerosis induced by HFD and further revealed that its mechanism might be its prebiotic effect on maintaining gut microbiota homeostasis and improving intestinal barrier function, consequently reducing serum LPS-triggered inflammatory response in the heart.

背景:肠道微生物群和心脏之间的相互作用,被称为“肠-心”轴,在动脉粥样硬化的发病机制中起着至关重要的作用。我们之前的研究表明,番茄红素具有抗炎和抗动脉粥样硬化的作用,但其与肠道微生物群的联系尚不清楚。因此,我们推测番茄红素可能通过调节“肠-心”轴来调节肠道微生物群,发挥抗动脉粥样硬化的作用。方法:雄性ApoE-/-小鼠分别饲喂含或不含番茄红素(0.1% w/w)的高脂饲料(HFD) 19周。采用16s rRNA测序法分析肠道菌群,采用Western blotting法检测封闭带-1 (ZO-1)、occludin、toll样受体4 (TLR4)和磷酸化核因子-κB (NF-κB) p65蛋白水平,采用ELISA试剂盒检测血清炎症因子单核细胞趋化蛋白1 (MCP-1)、肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β)、IL-6水平。采用ELISA法测定血清脂多糖(LPS)、d -乳酸(D-LA)和二胺过氧化物酶(DAO)的浓度。结果:主动脉窦切片显示,补充番茄红素可显著降低动脉粥样硬化病变程度,抑制HFD引起的动脉粥样硬化发展。肠道菌群分析显示,番茄红素降低了厚壁菌门/Bacteroides的比例,增加了Verrucomicrobia、Akkermansia和Alloprevotella的相对丰度,这与提高肠道屏障功能和减轻炎症有关。番茄红素上调肠道ZO-1和occludin的表达,降低血清LPS、D-LA和DAO水平。此外,番茄红素可抑制主动脉窦斑块中TLR4和磷酸化nf -κB p65的表达,降低血清MCP-1、TNF-α、IL-1β和IL-6水平。结论:我们的研究结果表明番茄红素对HFD诱导的动脉粥样硬化具有保护作用,其机制可能是通过其益生元作用维持肠道菌群稳态,改善肠道屏障功能,从而减少血清脂多糖引发的心脏炎症反应。
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引用次数: 0
Correction: The association between dietary quality scores with C-reactive protein and novel biomarkers of inflammation platelet-activating factor and lipoprotein-associated phospholipase A2: a cross-sectional study. 更正:饮食质量评分与c反应蛋白和炎症血小板活化因子和脂蛋白相关磷脂酶A2的新生物标志物之间的关系:一项横断面研究。
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2023-11-27 DOI: 10.1186/s12986-023-00771-y
Carolyn J English, Anna E Lohning, Hannah L Mayr, Mark Jones, Helen MacLaughlin, Dianne P Reidlinger
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引用次数: 0
Exploring the underlying mechanisms of fisetin in the treatment of hepatic insulin resistance via network pharmacology and in vitro validation. 通过网络药理学和体外验证探索非瑟酮治疗肝脏胰岛素抵抗的潜在机制。
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2023-11-23 DOI: 10.1186/s12986-023-00770-z
Tian Li, Junjun Ling, Xingrong Du, Siyu Zhang, Yan Yang, Liang Zhang

Objective: To characterize potential mechanisms of fisetin on hepatic insulin resistance (IR) using network pharmacology and in vitro validation.

Methods: Putative targets of fisetin were retrieved from the Traditional Chinese Medicine Systems Pharmacology database, whereas the potential genes of hepatic IR were obtained from GeneCards database. A protein-protein interaction (PPI) network was constructed according to the intersection targets of fisetin and hepatic IR using the Venn diagram. The biological functions and potential pathways related to genes were determined using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Cell experiments were also conducted to further verify the mechanism of fisetin on hepatic IR.

Results: A total of 118 potential targets from fisetin were associated with hepatic IR. The areas of nodes and corresponding degree values of TP53, AKT1, TNF, IL6, CASP3, CTNNB1, JUN, SRC, epidermal growth factor receptor (EGFR), and HSP90AA1 were larger and could be easily found in the PPI network. Furthermore, GO analysis revealed that these key targets were significantly involved in multiple biological processes that participated in oxidative stress and serine/threonine kinase activity. KEGG enrichment analysis showed that the PI3K/AKT signaling pathway was a significant pathway involved in hepatic IR. Our in vitro results demonstrated that fisetin treatment increased the expressions of EGFR and IRS in HepG2 and L02 cells under normal or IR conditions. Western blot results revealed that p-AKT/AKT levels were significantly up-regulated, suggesting that fisetin was involved in the PI3K/AKT signaling pathway to regulate insulin signaling.

Conclusion: We explored the pharmacological actions and the potential molecular mechanism of fisetin in treating hepatic IR from a holistic perspective. Our study lays a theoretical foundation for the development of fisetin for type 2 diabetes.

目的:利用网络药理学和体外验证方法探讨非瑟酮对肝脏胰岛素抵抗(IR)的作用机制。方法:从中药系统药理学数据库中检索非瑟酮的推定靶点,从GeneCards数据库中检索肝脏IR的潜在基因。根据非瑟酮与肝脏IR的交叉靶点,利用维恩图构建了蛋白质-蛋白质相互作用(PPI)网络。利用基因本体(GO)和京都基因与基因组百科全书(KEGG)分析确定基因相关的生物学功能和潜在途径。通过细胞实验进一步验证非瑟酮对肝脏IR的作用机制。结果:非瑟酮共有118个潜在靶点与肝脏IR相关。TP53、AKT1、TNF、IL6、CASP3、CTNNB1、JUN、SRC、表皮生长因子受体(EGFR)、HSP90AA1的淋巴结面积及对应度值较大,在PPI网络中容易发现。此外,氧化石墨烯分析显示,这些关键靶点显著参与了参与氧化应激和丝氨酸/苏氨酸激酶活性的多种生物过程。KEGG富集分析表明,PI3K/AKT信号通路是参与肝脏IR的重要通路。我们的体外实验结果表明,在正常或IR条件下,非西汀处理增加了HepG2和L02细胞中EGFR和IRS的表达。Western blot结果显示,p-AKT/AKT水平显著上调,提示非瑟酮参与PI3K/AKT信号通路调节胰岛素信号。结论:从整体上探讨了非瑟汀治疗肝脏IR的药理作用及其可能的分子机制。本研究为非瑟酮治疗2型糖尿病的发展奠定了理论基础。
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引用次数: 0
Intrauterine growth restriction alters kidney metabolism at the end of nephrogenesis. 在肾脏发生末期,宫内生长限制改变肾脏代谢。
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2023-11-21 DOI: 10.1186/s12986-023-00769-6
Sheng-Yuan Ho, Merryl Esther Yuliana, Hsiu-Chu Chou, Chung-Ming Chen

Background: This study investigated the effect of uteroplacental insufficiency (UPI) on renal development by detecting metabolic alterations in the kidneys of rats with intrauterine growth restriction (IUGR).

Methods: On gestational day 17, pregnant Sprague Dawley rats were selected and allocated randomly to either the IUGR group or the control group. The IUGR group received a protocol involving the closure of bilateral uterine vessels, while the control group underwent a sham surgery. The rat pups were delivered on gestational day 22 by natural means. Pups were randomly recruited from both the control and IUGR groups on the seventh day after birth. The kidneys were surgically removed to conduct Western blot and metabolomic analyses.

Results: IUGR was produced by UPI, as evidenced by the significantly lower body weights of the pups with IUGR compared to the control pups on postnatal day 7. UPI significantly increased the levels of cleaved caspase-3 (p < 0.05) and BAX/Bcl-2 (p < 0.01) in the pups with IUGR. Ten metabolites exhibited statistically significant differences between the groups (q < 0.05). Metabolic pathway enrichment analysis demonstrated statistically significant variations between the groups in the metabolism related to fructose and mannose, amino and nucleotide sugars, and inositol phosphate.

Conclusions: UPI alters kidney metabolism in growth-restricted newborn rats and induces renal apoptosis. The results of our study have the potential to provide new insights into biomarkers and metabolic pathways that are involved in the kidney changes generated by IUGR.

背景:本研究通过检测宫内生长受限(IUGR)大鼠肾脏代谢变化,探讨子宫胎盘功能不全(UPI)对肾脏发育的影响。方法:在妊娠第17天选取妊娠大鼠,随机分为IUGR组和对照组。IUGR组接受了包括关闭双侧子宫血管的方案,而对照组则接受了假手术。在妊娠第22天自然分娩。在出生后第7天,从对照组和IUGR组随机招募幼犬。手术切除肾脏进行Western blot和代谢组学分析。结果:IUGR是由UPI产生的,在出生后第7天,IUGR幼崽的体重明显低于对照组幼崽。结论:UPI可改变生长受限新生大鼠肾脏代谢,诱导肾细胞凋亡。我们的研究结果有可能为IUGR产生的肾脏变化所涉及的生物标志物和代谢途径提供新的见解。
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引用次数: 0
A comparative study on indicators of vitamin A status and risk factors for sensitivity and specificity of the methods to detect vitamin A deficiency. 维生素A状态指标及危险因素对维生素A缺乏症检测方法敏感性和特异性的比较研究
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2023-11-16 DOI: 10.1186/s12986-023-00768-7
Olivier O Sombié, Augustin N Zeba, Jérome W Somé, Adama Kazienga, Michael Grahn, Sherry A Tanumihardjo, Stefaan De Henauw, Souheila Abbeddou

Background: Serum retinol (SR) and retinol-binding protein (RBP) are commonly used indicators, but they are affected by infections and inflammation. This study aimed to assess the sensitivity and specificity of VA indicators to detect vitamin A deficiency (VAD) in 36-59-month-old children living in a rural area in Burkina Faso.

Methods: In a community-based study, two cross-sectional surveys were carried out from November 2016 to September 2017 in the health district of Dandé in Burkina Faso. The surveys included 115 children 36-59 months old. Indicators of VA and inflammation assessed in all children included SR, RBP and total liver VA reserves (TLR) estimated by retinol isotope dilution, and inflammation markers (C-reactive protein (CRP) and alpha 1-acid glycoprotein (AGP)). We calculated the sensitivity, specificity, positive and negative predictive values. In addition, the effects of inflammation, helminth infection, and season on sensitivity and specificity were assessed.

Results: The prevalence of VAD assessed by SR (< 0.7 µmol/L), RBP (< 0.7 µmol/L), and TLR (< 0.1 µmol/g liver) were, respectively, 30.9%, 33.3%, and 0%. Compared to TLR, the specificity, positive predictive value, and negative predictive value of SR were 71.1%, 0%, and 100%, and of RBP, were 68.9%, 0%, and 100%, respectively. The sensitivity was indeterminable for SR and RBP. The specificity of SR and RBP was lower during the dry season. Elevated CRP (> 5.0 mg/L) and AGP (> 1.0 g/L) were detected in 1.9% and 28.6% of children, respectively. The adjustment of VA indicators for inflammation improved SR's specificity to 75.9% and decreased RBP's specificity to 67.8%.

Conclusion: No cases of VAD were identified by TLR. However, (inflammation-adjusted) SR and RBP had varying accuracy in the estimation of VAD.

Trial registration: The study was registered, retrospectively, on 22 March 2018 as a clinical trial with the Pan African Clinical Trials Registry under the number Cochrane South Africa; PACTR201803002999356.

背景:血清视黄醇(SR)和视黄醇结合蛋白(RBP)是常用的指标,但受感染和炎症的影响。本研究旨在评估VA指标在布基纳法索农村地区36-59个月儿童中检测维生素A缺乏症(VAD)的敏感性和特异性。方法:以社区为基础,于2016年11月至2017年9月在布基纳法索dand卫生区进行了两次横断面调查。调查对象包括115名年龄在36-59个月之间的儿童。所有患儿的VA和炎症指标包括:视黄醇同位素稀释法估计的SR、RBP和总肝脏VA储备(TLR),以及炎症标志物(c反应蛋白(CRP)和α 1-酸性糖蛋白(AGP))。计算敏感性、特异性、阳性预测值和阴性预测值。此外,还评估了炎症、寄生虫感染和季节对敏感性和特异性的影响。结果:以SR (5.0 mg/L)和AGP (> 1.0 g/L)评估的VAD患病率分别为1.9%和28.6%。调整VA炎症指标后,SR特异性提高至75.9%,RBP特异性降低至67.8%。结论:TLR未发现VAD病例。然而,(炎症调整)SR和RBP在VAD估计中的准确性不同。试验注册:该研究于2018年3月22日作为临床试验在泛非临床试验注册中心回顾性注册,编号为Cochrane South Africa;PACTR201803002999356。
{"title":"A comparative study on indicators of vitamin A status and risk factors for sensitivity and specificity of the methods to detect vitamin A deficiency.","authors":"Olivier O Sombié, Augustin N Zeba, Jérome W Somé, Adama Kazienga, Michael Grahn, Sherry A Tanumihardjo, Stefaan De Henauw, Souheila Abbeddou","doi":"10.1186/s12986-023-00768-7","DOIUrl":"10.1186/s12986-023-00768-7","url":null,"abstract":"<p><strong>Background: </strong>Serum retinol (SR) and retinol-binding protein (RBP) are commonly used indicators, but they are affected by infections and inflammation. This study aimed to assess the sensitivity and specificity of VA indicators to detect vitamin A deficiency (VAD) in 36-59-month-old children living in a rural area in Burkina Faso.</p><p><strong>Methods: </strong>In a community-based study, two cross-sectional surveys were carried out from November 2016 to September 2017 in the health district of Dandé in Burkina Faso. The surveys included 115 children 36-59 months old. Indicators of VA and inflammation assessed in all children included SR, RBP and total liver VA reserves (TLR) estimated by retinol isotope dilution, and inflammation markers (C-reactive protein (CRP) and alpha 1-acid glycoprotein (AGP)). We calculated the sensitivity, specificity, positive and negative predictive values. In addition, the effects of inflammation, helminth infection, and season on sensitivity and specificity were assessed.</p><p><strong>Results: </strong>The prevalence of VAD assessed by SR (< 0.7 µmol/L), RBP (< 0.7 µmol/L), and TLR (< 0.1 µmol/g liver) were, respectively, 30.9%, 33.3%, and 0%. Compared to TLR, the specificity, positive predictive value, and negative predictive value of SR were 71.1%, 0%, and 100%, and of RBP, were 68.9%, 0%, and 100%, respectively. The sensitivity was indeterminable for SR and RBP. The specificity of SR and RBP was lower during the dry season. Elevated CRP (> 5.0 mg/L) and AGP (> 1.0 g/L) were detected in 1.9% and 28.6% of children, respectively. The adjustment of VA indicators for inflammation improved SR's specificity to 75.9% and decreased RBP's specificity to 67.8%.</p><p><strong>Conclusion: </strong>No cases of VAD were identified by TLR. However, (inflammation-adjusted) SR and RBP had varying accuracy in the estimation of VAD.</p><p><strong>Trial registration: </strong>The study was registered, retrospectively, on 22 March 2018 as a clinical trial with the Pan African Clinical Trials Registry under the number Cochrane South Africa; PACTR201803002999356.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"20 1","pages":"49"},"PeriodicalIF":4.5,"publicationDate":"2023-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10652566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136398481","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
Early adulthood weight change, midlife "Life's essential 8" health status and risk of cardiometabolic diseases: a chinese nationwide cohort study. 成年早期体重变化、中年“生命必需8”健康状况和心脏代谢疾病风险:一项中国全国性队列研究。
IF 4.5 2区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2023-11-01 DOI: 10.1186/s12986-023-00765-w
Qiuyu Cao, Mian Li, Guijun Qin, Li Yan, Jiang He, Min Xu, Yu Xu, Tiange Wang, Yuhong Chen, Shuangyuan Wang, Hong Lin, Zhiyun Zhao, Zhengnan Gao, Tianshu Zeng, Ruying Hu, Xuefeng Yu, Gang Chen, Qing Su, Yiming Mu, Lulu Chen, Xulei Tang, Qin Wan, Guixia Wang, Feixia Shen, Zuojie Luo, Yingfen Qin, Li Chen, Yanan Huo, Qiang Li, Zhen Ye, Yinfei Zhang, Chao Liu, Youmin Wang, Shengli Wu, Tao Yang, Huacong Deng, Jiajun Zhao, Lixin Shi, Guang Ning, Weiqing Wang, Jieli Lu, Yufang Bi

Background: The association between weight change during early adulthood and cardiometabolic diseases remains uncertain in Chinese population. Whether the association varies with comprehensive cardiovascular health (CVH) in midlife assessed by "Life's Essential 8" has not been characterized. We aim to examine the associations of early adulthood weight change and midlife "Life's Essential 8" CVH status with cardiometabolic outcomes in a Chinese cohort.

Methods: The study participants were from the China Cardiometabolic Disease and Cancer Cohort (4 C) Study. This analysis included 72,610 middle-aged and older participants followed for a median of 3.6 years. At baseline, the participants recalled body weight at age 20 and 40 years, and we calculated change in weight and BMI between 20 and 40 years of age. Health behaviors information in "Life's Essential 8" was collected by questionnaire, and health factors were measured in the study center. During follow-up, we ascertained incident cardiovascular events based on medical records, and diagnosed incident diabetes according to the American Diabetes Association 2010 criteria.

Results: 72,610 study participants were included with a mean age of 56.0 ± 8.8 years and 29% of them were males. Weight gain of more than 10 kg between 20 and 40 years of age was associated with 22% increased risk of incident cardiovascular events (HR: 1.22; 95%CI: 1.04-1.43) and 38% increased risk of diabetes (HR: 1.38; 95%CI: 1.25-1.53) compared to stable weight. Besides, the association of weight gain more than 10 kg in early adulthood with cardiometabolic risk was even stronger in those with low CVH score in midlife (HR: 2.44; 95%CI: 2.01-2.97 for incident cardiovascular events; HR: 2.20; 95%CI: 1.90-2.55 for incident diabetes) or with few ideal cardiovascular health metrics in midlife.

Conclusions: Our study indicated that weight gain in early adulthood was associated with significantly increased risk of cardiometabolic diseases. And the association could be stronger in those with poor CVH profiles in midlife. These findings confirmed the significance of weight management during early adulthood and suggested that individuals who experienced substantial weight gain in early life should be encouraged to maintain good CVH status in Chinese population.

背景:在中国人群中,成年早期体重变化与心脏代谢疾病之间的关系尚不确定。这种关联是否与“生命的基本8”评估的中年综合心血管健康(CVH)有关,目前尚未确定。我们的目的是在一个中国队列中研究成年早期体重变化和中年“生命必需8”CVH状态与心脏代谢结果的关系。方法:研究参与者来自中国心脏代谢疾病和癌症队列(4C)研究。该分析包括72610名中老年参与者,平均随访3.6年。在基线时,参与者回忆了20岁和40岁时的体重,我们计算了20岁到40岁之间体重和BMI的变化。采用问卷调查的方法收集《生活必需品8》中的健康行为信息,并在研究中心对健康因素进行测量。在随访期间,我们根据医疗记录确定了心血管事件,并根据美国糖尿病协会2010年的标准诊断为糖尿病。结果:72610名研究参与者,平均年龄56.0岁 ± 8.8岁,其中男性占29%。与稳定体重相比,20至40岁期间体重增加超过10公斤与心血管事件风险增加22%(HR:1.22;95%CI:1.04-1.43)和糖尿病风险增加38%(HR:1.38;95%CI:1.25-1.53)相关。此外,在中年CVH评分较低的人群中,成年早期体重增加超过10公斤与心脏代谢风险的相关性更强(HR:2.44;95%CI:2.01-2.97,针对心血管事件;HR:2.20;95%CI:1.90-2.55,针对糖尿病事件),或中年时几乎没有理想的心血管健康指标。结论:我们的研究表明,成年早期的体重增加与心脏代谢疾病的风险显著增加有关。在中年CVH状况不佳的人群中,这种联系可能会更强。这些发现证实了成年早期体重管理的重要性,并建议应鼓励早期体重大幅增加的人在中国人群中保持良好的CVH状态。
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引用次数: 0
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Nutrition & Metabolism
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