Metabolism open最新文献_第10页

SPT: A new contributor to trans fatty acid-induced atherosclerosis SPT：反式脂肪酸诱导的动脉粥样硬化的新贡献者

Metabolism open

Pub Date : 2025-03-01 DOI: 10.1016/j.metop.2024.100340

Chengbin Li, Junli Liu, Bin Liang

引用次数: 0

The role of lipoprotein sulfatides in MASLD fibrosis transition: A new frontier in hepatic immunomodulation 脂蛋白硫脂在MASLD纤维化转变中的作用：肝脏免疫调节的新前沿

Metabolism open

Pub Date : 2025-03-01 DOI: 10.1016/j.metop.2024.100335

Yifan Zhou, Junli Liu

引用次数: 0

Lipidomics reveals potential biomarkers and pathophysiological insights in the progression of diabetic kidney disease 脂质组学揭示了糖尿病肾病进展中的潜在生物标志物和病理生理学见解

Metabolism open

Pub Date : 2025-03-01 DOI: 10.1016/j.metop.2025.100354

Xiaozhen Guo , Zixuan Zhang , Cuina Li , Xueling Li , Yutang Cao , Yangyang Wang , Jiaqi Li , Yibin Wang , Kanglong Wang , Yameng Liu , Cen Xie , Yifei Zhong

Background

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease, affecting over 30 % of diabetes mellitus (DM) patients. Early detection of DKD in DM patients can enable timely preventive therapies, and potentially delay disease progression. Since the kidney relies on fatty acid oxidation for energy, dysregulated lipid metabolism has been implicated in proximal tubular cell damage and DKD pathogenesis. This study aimed to identify lipid alterations during DKD development and potential biomarkers differentiating DKD from DM.

Methods

lipidomics analysis was performed on serum collected from 55 patients with DM, 21 with early DKD stage and 32 with advanced DKD, and 22 healthy subjects. Associations between lipids and DKD risk were evaluated by logistic regression.

Results

Lipid profiling revealed elevated levels of certain lysophosphatidylethanolamines (LPEs), phosphatidylethanolamines (PEs), ceramides (Cers), and diacylglycerols (DAGs) in the DM-DKD transition, while most LPEs, lysophosphatidylcholines (LPCs), along with several monoacylglycerol (MAG) and triacylglycerols (TAGs), increased further from DKD-E to DKD-A. Logistic regression indicated positive associations between LPCs, LPEs, PEs, and DAGs with DKD risk, with most LPEs correlating significantly with urinary albumin-to-creatinine ratio (UACR) and inversely with estimated glomerular filtration rate (eGFR). A machine-learning-derived biomarker panel, Lipid9, consisting of LPC(18:2), LPC(20:5), LPE (16:0), LPE (18:0), LPE (18:1), LPE (24:0), PE (34:1), PE (34:2), and PE (36:2), accurately distinguished DKD (AUC: 0.78, 95 % CI 0.68–0.86) from DM. Incorporating two clinical indexes, serum creatinine and blood urea nitrogen, the Lipid9-SCB model further improved DKD detection (AUC: 0.83, 95 % CI 0.75–0.90) from DM, and was notably more sensitive for identifying DKD-E (AUC: 0.79, 95 % CI 0.67–0.91).

Conclusion

This study deciphers the lipid signature in DKD progression, and suggests the Lipid9-SCB panel as a promising tool for early DKD detection in DM patients.

背景：糖尿病肾病（DKD）是终末期肾脏疾病的主要原因，影响了超过30%的糖尿病（DM）患者。早期发现糖尿病患者的DKD可以及时预防治疗，并有可能延缓疾病进展。由于肾脏依赖脂肪酸氧化提供能量，脂质代谢失调与近端小管细胞损伤和DKD发病机制有关。本研究旨在确定DKD发展过程中的脂质改变以及区分DKD和DM的潜在生物标志物。方法对55名DM患者、21名早期DKD患者和32名晚期DKD患者以及22名健康受试者的血清进行滑质组学分析。通过逻辑回归评估脂质与DKD风险之间的关系。结果在DM-DKD转化过程中，某些溶血磷脂酰乙醇胺（LPEs）、磷脂酰乙醇胺（PEs）、神经酰胺（Cers）和二酰基甘油（dag）水平升高，而大多数LPEs、溶血磷脂酰胆碱（LPCs）以及一些单酰基甘油（MAG）和三酰基甘油（TAGs）在DKD-E到DKD-A之间进一步升高。Logistic回归显示LPCs、LPEs、PEs和dag与DKD风险呈正相关，大多数LPEs与尿白蛋白与肌酐比（UACR）显著相关，与肾小球滤过率（eGFR）估算呈负相关。由LPC（18:2）、LPC（20:5）、LPE（16:0）、LPE（18:0）、LPE（18:1）、LPE（24:0）、PE（34:1）、PE（34:2）和PE（36:2）组成的机器学习衍生的生物标志物面板Lipid9准确区分了DKD和DM （AUC: 0.78, 95% CI 0.68-0.86）。结合血清肌酐和血尿素氮两项临床指标，Lipid9- scb模型进一步提高了DKD和DM的检测（AUC: 0.83, 95% CI 0.75-0.90），对DKD- e的识别（AUC: 0.79, 95% CI 0.67-0.91）更为敏感。结论：本研究揭示了DKD进展中的脂质特征，并提示Lipid9-SCB面板是DM患者早期DKD检测的有希望的工具。

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引用次数: 0

An updated review of popular dietary patterns during pregnancy and lactation: Trends, benefits, and challenges 妊娠和哺乳期流行饮食模式的最新综述：趋势、益处和挑战

Metabolism open

Pub Date : 2025-02-08 DOI: 10.1016/j.metop.2025.100353

Maria Chouli , Anastasia Bothou , Giannoula Kyrkou , Sofia Kaliarnta , Aikaterini Dimitrakopoulou , Athina Diamanti

This review examines nutritional needs during pregnancy and lactation, focusing on the critical nutrients required for both maternal and fetal health. Essential nutrients such as folic acid, vitamin D, iron, calcium, and omega-3 fatty acids play a significant role in supporting fetal development and minimizing the risk of complications like gestational diabetes, hypertension, and preterm birth. Various dietary patterns, including the Mediterranean, vegetarian/vegan, and gluten-free diets, were evaluated for their adequacy and potential benefits. The Mediterranean diet was highlighted for its protective effects against pregnancy-related health issues. In contrast, the review identified vegetarian and vegan diets as requiring careful planning to ensure sufficient intake of key nutrients. Additionally, the review explored the implications of gestational diabetes and dietary strategies for managing blood sugar levels. The effects of intermittent fasting during pregnancy were also discussed, with mixed evidence regarding its safety and impact on pregnancy outcomes. Overall, the review stresses the importance of tailored nutritional guidance to ensure optimal health for both the mother and the developing fetus during pregnancy and lactation.

这篇综述探讨了孕期和哺乳期的营养需求，重点是孕产妇和胎儿健康所需的关键营养素。叶酸、维生素D、铁、钙和omega-3脂肪酸等必需营养素在支持胎儿发育和减少妊娠糖尿病、高血压和早产等并发症的风险方面发挥着重要作用。各种饮食模式，包括地中海，素食/纯素食和无麸质饮食，评估了它们的充分性和潜在益处。与会者强调了地中海饮食对预防与怀孕有关的健康问题的保护作用。相比之下，该综述认为素食和纯素饮食需要仔细规划，以确保关键营养素的充足摄入。此外，该综述还探讨了妊娠糖尿病和饮食策略对控制血糖水平的影响。研究还讨论了妊娠期间间歇性禁食的影响，关于其安全性和对妊娠结局的影响，证据不一。总的来说，该综述强调了量身定制的营养指导的重要性，以确保在怀孕和哺乳期间母亲和发育中的胎儿的最佳健康。

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引用次数: 0

Causal relationship of familial hypercholesterolemia with risk of intestinal vascular disorders: A mendelian randomization study 家族性高胆固醇血症与肠道血管疾病风险的因果关系：一项孟德尔随机研究

Metabolism open

Pub Date : 2025-01-31 DOI: 10.1016/j.metop.2025.100352

Gang Wei , Cheng Zhang , Feng-Jie Shen , Hua-Qi Guo , Lin Liu

Background

The causal relationship between the familial hypercholesterolemia (FH) and intestinal vascular diseases was unnoticed. This study aims to investigate the cause-and-effect relationship of FH with risk of intestinal vascular diseases in human.

Methods

A Mendelian randomization (MR) analysis was performed by extracting summary-level datasets for FH or FH concurrently with ischemic heart disease (IHD) and intestinal vascular diseases from the FinnGen study including 329,115, 316,290 and 350,505 individuals. The inverse-variance weighted (IVW) method and the weighted median method were applied to analyze the causal relationships between FH or FH concurrently with IHD and the risk of intestinal vascular diseases. Cochran's Q statistic method and MR-Egger regression were used to assess heterogeneity and pleiotropy.

Results

The IVW method demonstrated that FH was significantly associated with higher odds of intestinal vascular diseases [OR (95%CI): 1.22 (1.03, 1.45)] (P = 0.02) without significant heterogeneity (P = 0.54) and horizontal pleiotropy (P = 0.43). Rs7575840 in 6.5kda upstream of ApoB gene, rs11591147 in PCSK9 gene and rs9644862 in the CDKN2B-AS1 (or named ANRIL; p15AS; PCAT12; CDKN2BAS; CDKN2B-AS; NCRNA00089) gene were illustrated to mostly influence the risk of intestinal vascular diseases. However, no significant causal relationship between FH concurrently with IHD and intestinal vascular diseases was observed.

Conclusion

In conclusion, FH was causally positive-associated with the increased risk of intestinal vascular diseases, revealing a potential unfortunate outcome for FH. Therefore, patients with FH should pay closely attention to the risk of intestinal vascular diseases. Our study may provide evidence for new diagnostic and therapeutic strategies in clinical practices.

背景家族性高胆固醇血症（FH）与肠道血管疾病之间的因果关系一直未引起重视。本研究旨在探讨FH与人类肠道血管疾病风险的因果关系。方法通过提取FinnGen研究中FH或FH合并缺血性心脏病（IHD）和肠道血管疾病的汇总数据集，分别包括329,115、316,290和350,505人，进行孟德尔随机化（MR）分析。应用反方差加权（IVW）法和加权中位数法分析FH或FH合并IHD与肠道血管疾病风险的因果关系。采用Cochran's Q统计方法和MR-Egger回归评估异质性和多效性。结果IVW方法显示，FH与较高的肠道血管疾病发生率显著相关[OR (95%CI): 1.22 (1.03, 1.45)] (P = 0.02)，无显著异质性（P = 0.54）和水平多效性（P = 0.43）。Rs7575840位于ApoB基因上游6.5kda， rs11591147位于PCSK9基因，rs9644862位于CDKN2B-AS1(或称为ANRIL；p15AS;PCAT12;CDKN2BAS;CDKN2B-AS;NCRNA00089)基因是影响肠道血管疾病风险的主要基因。然而，FH合并IHD与肠道血管疾病之间没有明显的因果关系。总之，FH与肠道血管疾病风险增加呈因果正相关，揭示了FH潜在的不幸结局。因此，FH患者应密切关注肠道血管疾病的风险。我们的研究可能为临床实践提供新的诊断和治疗策略。

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引用次数: 0

The role of vitamin D deficiency in placental dysfunction: A systematic review 维生素D缺乏在胎盘功能障碍中的作用：一项系统综述

Metabolism open

Pub Date : 2025-01-31 DOI: 10.1016/j.metop.2025.100350

Eleni Gerovasili, Antigoni Sarantaki, Anastasia Bothou, Anna Deltsidou, Aikaterini Dimitrakopoulou, Athina Diamanti

Introduction

Vitamin D plays a critical role in pregnancy, supporting placental function via angiogenesis, immune regulation, and nutrient transport. Deficiency in vitamin D during gestation is associated with complications such as preeclampsia, intrauterine growth restriction (IUGR), and preterm birth. However, the mechanisms linking vitamin D deficiency to placental dysfunction remain inadequately understood, highlighting the need for systematic evaluation.

Methods

A systematic review was conducted in adherence to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, with searches in PubMed, Scopus, and Web of Science for studies published within the last 20 years. Inclusion criteria targeted human studies examining the association between vitamin D and placental function, including randomized controlled trials, cohort studies, and case-control studies. A total of 10 studies were included following rigorous screening and quality assessment.

Results

Findings from human studies indicate that maternal vitamin D deficiency significantly impairs placental function by reducing vascular integrity, downregulating nutrient transporters, and promoting inflammation. Mechanistic evidence highlights decreased expression of vascular endothelial growth factor (VEGF) and increased inflammatory cytokines in vitamin D-deficient pregnancies. Supplementation with active vitamin D [1α,25(OH)2D3] mitigated these adverse effects, restoring placental growth, improving nutrient transport, and reducing inflammation. Notably, population-specific differences and sex-specific responses to vitamin D sufficiency were observed.

Conclusions

Vitamin D is essential for optimal placental function and pregnancy outcomes. This review underscores the need for standardized supplementation protocols and further research into long-term and population-specific effects of vitamin D. Addressing these gaps can inform targeted interventions to reduce pregnancy complications and improve maternal-fetal health.

维生素D在妊娠中起着至关重要的作用，通过血管生成、免疫调节和营养运输支持胎盘功能。妊娠期维生素D缺乏与子痫前期、宫内生长受限（IUGR）和早产等并发症有关。然而，将维生素D缺乏与胎盘功能障碍联系起来的机制仍然没有得到充分的了解，因此需要进行系统的评估。方法根据系统评价和荟萃分析（PRISMA）指南的首选报告项目进行系统评价，并在PubMed， Scopus和Web of Science中检索近20年发表的研究。纳入标准针对的是研究维生素D与胎盘功能之间关系的人类研究，包括随机对照试验、队列研究和病例对照研究。经过严格的筛选和质量评估，共纳入10项研究。结果人体研究结果表明，母体维生素D缺乏通过降低血管完整性、下调营养转运蛋白和促进炎症显著损害胎盘功能。机制证据强调在维生素d缺乏的妊娠中血管内皮生长因子（VEGF）的表达减少和炎症细胞因子的增加。补充活性维生素D [1α，25(OH)2D3]可以减轻这些不良反应，恢复胎盘生长，改善营养运输，减少炎症。值得注意的是，观察到人群特异性差异和对维生素D充足性的性别特异性反应。结论维生素D对优化胎盘功能和妊娠结局至关重要。这篇综述强调需要标准化的补充方案，并进一步研究维生素d的长期和人群特异性影响。解决这些差距可以为有针对性的干预提供信息，以减少妊娠并发症，改善母胎健康。

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引用次数: 0

The development of a food-group, tree classification method and its use in exploring dietary associations with metabolic dysfunction-associated Steatotic liver disease (MASLD) and other health-related outcomes in a UK population 食物组、树分类方法的发展及其在英国人群中探索饮食与代谢功能障碍相关脂肪变性肝病（MASLD）和其他健康相关结局的关联的应用

Metabolism open

Pub Date : 2025-01-30 DOI: 10.1016/j.metop.2025.100351

Amina A. Alawadi , Amrita Vijay , Jane I. Grove , Moira A. Taylor , Guruprasad P. Aithal

Background

Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) affects up to one in five people in the UK, with persistent overeating and a sedentary lifestyle being significant risk factors. Exploring dietary patterns at a food level is a novel approach to understand associations between diet and disease.

Methods

This cross-sectional case-control study included 168 MASLD patients and 34 healthy controls from Nottingham (UK). Dietary data were collected using the EPIC-food frequency questionnaire. A food-group, tree classification method was developed which categorized 923 ingredients into three levels (main food group, sub-types, and cooking methods) and intakes were associated with clinical outcomes using logistic regression and degree of liver fibrosis using linear regression.

Results

Significant associations were found for red meat intake with MASLD (OR [CI]: 1.013 [1.001–1.025]) and fibrosis (Beta [SE]: +0.048 [0.013]); intakes of nuts (OR [CI]: 0.951 [0.905–0.999]); and fish (OR [CI]: 0.985 [0.971–0.999]) with MASLD; “Cereals and cereals products”, “salt and gravy” and baked foods with fibrosis (Beta [SE]: +0.018 to +0.057 [0.005–0.23]); white and organ meat (Beta [SE]: −0.04 to −0.61 [0.015–0.249]); diet soda (OR [CI]: +0.01 [1–1.003]) and red meat intakes (OR [CI]:+0.002 [1.002–1.016]) with T2DM; wholegrain wheat, red meat, and semi-skimmed dairy intakes with hypercholesterolemia (ORs [CI]: −0.003 to −0.023 [1–1.043]); “herbs and spices” and wholegrain rice with hypercholesterolaemia (ORs [CI]: −0.08 to −0.98 [0.159–0.989); fresh herbs and boiled foods intakes with hypertension (ORs [CI]: −0.001 to −2.21 [0.013–1]).

Conclusion

The study introduces a new food-group, tree classification method to characterise UK diet data and identify risk factors for MASLD, potentially informing the development of culturally applicable dietary guidelines designed to improve public health.

在英国，多达五分之一的人患有代谢功能障碍相关的脂肪变性肝病（MASLD），持续暴饮暴食和久坐不动的生活方式是重要的危险因素。在食物水平上探索饮食模式是理解饮食与疾病之间关系的一种新方法。方法本横断面病例对照研究纳入来自英国诺丁汉的168例MASLD患者和34例健康对照者。饮食数据采用epic -食物频率问卷收集。开发了一种食物组树分类方法，将923种成分分为三个层次（主要食物组、亚类型和烹饪方法），并使用逻辑回归将摄入量与临床结果相关联，使用线性回归将肝纤维化程度与临床结果相关联。结果红肉摄入与MASLD （OR [CI]: 1.013[1.001-1.025]）和纤维化（Beta [SE]: +0.048[0.013]）有显著相关性；坚果摄入量（OR [CI]: 0.951 [0.905-0.999]）；鱼（OR [CI]: 0.985 [0.971-0.999]）；“谷类及谷类制品”、“盐及肉汁”及有纤维化的烘焙食品（Beta [SE]: +0.018至+0.057 [0.005-0.23]）；白色和器官肉（Beta [SE]:−0.04至−0.61 [0.015-0.249]）；无糖汽水（OR [CI]:+ 0.01[1-1.003]）和红肉摄入（OR [CI]:+0.002[1.002-1.016]）与T2DM；摄入全麦、红肉和半脱脂乳制品会导致高胆固醇血症（or [CI]:−0.003至−0.023 [1-1.043]）；“香草和香料”和全谷物大米与高胆固醇血症（or [CI]:−0.08至−0.98 [0.159-0.989]）；新鲜草药和煮熟食物摄入与高血压（or [CI]:−0.001至−2.21[0.013-1]）。该研究引入了一种新的食物组、树分类方法来描述英国饮食数据，并确定MASLD的风险因素，可能为制定文化上适用的饮食指南提供信息，旨在改善公众健康。

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引用次数: 0

Gender based difference in glycemic control and diabetes related chronic complications among type 2 diabetic patients in Debre Berhan city public hospitals 德伯尔汉市公立医院2型糖尿病患者血糖控制及糖尿病相关慢性并发症的性别差异

Metabolism open

Pub Date : 2025-01-23 DOI: 10.1016/j.metop.2025.100349

Enguday Demeke Gebeyaw , Girma Deshimo Lema

Introduction

Type 2 diabetes mellitus (T2DM) is a growing public health concern, particularly in low- and middle-income countries like Ethiopia. There is limited data on gender differences in glycemic control and diabetes related chronic complications in Ethiopia. This study aimed to assess gender-based difference in glycemic control and diabetes related chronic complications among T2DM patients in Debre Berhan public hospitals, Ethiopia.

Methods

A comparative cross-sectional study was carried out at public hospitals in Debre Berhan. Data were gathered from 258 T2DM patients (129 men and 129 women). Using Hemoglobin A1c (HgA1c), level of glycemic control was assessed. To compare gender differences in diabetes related chronic complications and glycemic control, the chi-square test and Independent sample t-test were employed. However logistic regression was employed to identify gender-specific factors of poor glycemic control.

Results

Women had poorer glycemic control, with a mean difference of 0.51 (95 % CI: 0.04–0.97) as compared with men. Alcohol consumption (AOR = 3.2; 95 % CI: 1.25–7.98), drug non-adherence (AOR = 4.1; 95 % CI: 1.01–17.54) and diabetic complications (AOR = 0.3; 95 % CI: 0.10–0.88) were significant factors for poor glycemic control in men. For women, rural residence (AOR = 0.2; 95 % CI: 0.03–0.58), duration of diabetes >5 years (AOR = 4.3; 95 % CI: 1.15–16.17), and drug non-adherence (AOR = 4.7; 95 % CI: 1.14–19.42) were significant factors for poor glycemic control. There were no significant gender differences in diabetes related chronic complications.

Conclusion

This study revealed significant gender differences in glycemic control among T2DM patients. Female patients experienced worse glycemic control. There were no gender differences in the prevalence of diabetes related chronic complications. This study highlights the importance of considering both general and specific factors when assessing and improving glycemic control in T2DM. Future studies should involve large sample sizes and gender focused studies to gain a deeper understanding of the relevant factors.

2型糖尿病（T2DM）是一个日益严重的公共卫生问题，特别是在埃塞俄比亚等低收入和中等收入国家。在埃塞俄比亚，关于血糖控制和糖尿病相关慢性并发症的性别差异的数据有限。本研究旨在评估埃塞俄比亚Debre Berhan公立医院T2DM患者血糖控制和糖尿病相关慢性并发症的性别差异。方法采用比较横断面研究方法，对德伯尔省公立医院进行调查。数据来自258名T2DM患者（129名男性和129名女性）。采用糖化血红蛋白（HgA1c）评估血糖控制水平。比较糖尿病相关慢性并发症和血糖控制的性别差异，采用卡方检验和独立样本t检验。然而，采用逻辑回归来确定血糖控制不良的性别特异性因素。结果与男性相比，女性血糖控制较差，平均差值为0.51 （95% CI: 0.04-0.97）。饮酒(AOR = 3.2；95% CI: 1.25-7.98)，药物不依从(AOR = 4.1；95% CI: 1.01-17.54)和糖尿病并发症(AOR = 0.3；95% CI: 0.10-0.88)是男性血糖控制不良的重要因素。对于妇女，农村居住(AOR = 0.2；95% CI: 0.03-0.58)，糖尿病病程>；5年(AOR = 4.3；95% CI: 1.15-16.17)和药物不依从(AOR = 4.7；95% CI: 1.14-19.42)是血糖控制不良的重要因素。糖尿病相关慢性并发症的性别差异不显著。结论T2DM患者血糖控制存在显著的性别差异。女性患者血糖控制较差。糖尿病相关慢性并发症的患病率没有性别差异。本研究强调了在评估和改善T2DM患者血糖控制时综合考虑一般因素和特殊因素的重要性。今后的研究应包括大样本量和以性别为重点的研究，以便更深入地了解有关因素。

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引用次数: 0

Exploring the anti-inflammatory potential of vitamin D in cardiometabolic diseases 探索维生素D在心血管代谢疾病中的抗炎作用。

Metabolism open

Pub Date : 2025-01-09 DOI: 10.1016/j.metop.2025.100348

Kabelo Mokgalaboni

The prevalence of cardiometabolic diseases is rising, and this is fuelled by inflammation, which tends to be worse in individuals with vitamin D (VD) deficiency. While non-steroidal anti-inflammatory interventions are available, they present with coagulation events. Hence, alternative therapy in the form of VD supplements is gaining research interest. This study reviewed the effect of VD supplementation on inflammation, focusing on nuclear factor kappa-beta (NF-κβ), tumour necrosis factor-alpha (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) across different cardiometabolic disease. Thirty-seven studies, 16 rodent models and 21 clinical studies were evaluated. The study considered evidence from rodent models to understand the effect of VD on these markers of inflammation and its translatability to clinical studies. While the potential benefits of VD were notable in rodents, these effects were less consistent in clinical studies. Notably, rodent models showed a more pronounced impact of VD in reducing NF-κβ and TNF-α; however, clinical trials reported conflicting findings. Furthermore, the VD was important in reducing MCP-1 across different rodent models; this was partially demonstrated in clinical trials. Based on these findings, VD modulates inflammation in cardiometabolic disease by inhibiting the activation of NF-κβ and suppressing the production of TNF-α and MCP-1. Although VD has some possible benefits in rodent models, the translatability of these findings in clinical trials is limited. Hence, the presented evidence in this study calls for further randomised controlled trials to assess the effect of VD on inflammation in patients living with different conditions as a therapy to curb the inflammation and the risk thereof. Future trials should also focus on exploring the VD dose-response, optimal dose, and duration of VD intervention among these patients that may offer optimal benefits on inflammation.

心脏代谢疾病的发病率正在上升，这是由炎症引起的，而炎症在维生素D （VD）缺乏的个体中往往更严重。虽然非甾体抗炎干预措施是可用的，但它们存在凝血事件。因此，以VD补充剂形式的替代疗法正在获得研究兴趣。本研究综述了VD补充对炎症的影响，重点关注不同心脏代谢疾病的核因子κβ (NF-κβ)、肿瘤坏死因子α (TNF-α)和单核细胞趋化蛋白-1 （MCP-1）。对37项研究、16种啮齿动物模型和21项临床研究进行了评价。该研究考虑了来自啮齿动物模型的证据，以了解VD对这些炎症标志物的影响及其对临床研究的可翻译性。虽然VD的潜在益处在啮齿类动物中是显著的，但这些影响在临床研究中不太一致。值得注意的是，在啮齿动物模型中，VD对NF-κβ和TNF-α的降低作用更为明显；然而，临床试验报告了相互矛盾的结果。此外，VD在不同啮齿动物模型中对降低MCP-1有重要作用；这在临床试验中得到了部分证明。基于这些发现，VD通过抑制NF-κβ的激活和抑制TNF-α和MCP-1的产生来调节心脏代谢疾病的炎症。虽然VD在啮齿动物模型中有一些可能的益处，但这些发现在临床试验中的可翻译性是有限的。因此，本研究提出的证据需要进一步的随机对照试验来评估VD对不同条件患者炎症的影响，作为一种抑制炎症及其风险的治疗方法。未来的试验还应该集中在探索这些患者的VD剂量反应、最佳剂量和VD干预的持续时间，这些患者可能对炎症有最佳的益处。

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引用次数: 0

Unveiling the link between chronic inflammation and cancer 揭示慢性炎症和癌症之间的联系。

Metabolism open

Pub Date : 2025-01-09 DOI: 10.1016/j.metop.2025.100347

Siddhant Tripathi , Yashika Sharma , Dileep Kumar

The highly nuanced transition from an inflammatory process to tumorigenesis is of great scientific interest. While it is well known that environmental stimuli can cause inflammation, less is known about the oncogenic modifications that chronic inflammation in the tissue microenvironment can bring about, as well as how these modifications can set off pro-tumorigenic processes. It is clear that no matter where the environmental factors come from, maintaining an inflammatory microenvironment encourages carcinogenesis. In addition to encouraging angiogenesis and metastatic processes, sustaining the survival and proliferation of malignant transformed cells, and possibly altering the efficacy of therapeutic agents, inflammation can negatively regulate the antitumoral adaptive and innate immune responses. Because chronic inflammation has multiple pathways involved in tumorigenesis and metastasis, it has gained recognition as a marker of cancer and a desirable target for cancer therapy. Recent advances in our knowledge of the molecular mechanisms that drive cancer's progression demonstrate that inflammation promotes tumorigenesis and metastasis while suppressing anti-tumor immunity. In many solid tumor types, including breast, lung, and liver cancer, inflammation stimulates the activation of oncogenes and impairs the body's defenses against the tumor. Additionally, it alters the microenvironment of the tumor. As a tactical approach to cancer treatment, these findings have underscored the importance of targeting inflammatory pathways. This review highlights the role of inflammation in cancer development and metastasis, focusing on its impact on tumor progression, immune suppression, and therapy resistance. It examines current anti-inflammatory strategies, including NSAIDs, cytokine modulators, and STAT3 inhibitors, while addressing their potential and limitations. The review emphasizes the need for further research to unravel the complex mechanisms linking inflammation to cancer progression and identify molecular targets for specific cancer subtypes.

从炎症过程到肿瘤发生的高度微妙的转变引起了极大的科学兴趣。众所周知，环境刺激可引起炎症，但对组织微环境中的慢性炎症可带来的致癌修饰以及这些修饰如何引发促肿瘤过程知之甚少。很明显，无论环境因素来自哪里，维持炎症微环境都会促进癌变。除了促进血管生成和转移过程，维持恶性转化细胞的生存和增殖，并可能改变治疗药物的疗效外，炎症还可以负向调节抗肿瘤适应性和先天免疫反应。由于慢性炎症在肿瘤发生和转移过程中有多种途径参与，它已被公认为癌症的标志物和癌症治疗的理想靶点。最近我们对驱动癌症进展的分子机制的了解表明，炎症促进肿瘤的发生和转移，同时抑制抗肿瘤免疫。在许多实体肿瘤类型中，包括乳腺癌、肺癌和肝癌，炎症刺激致癌基因的激活，损害身体对肿瘤的防御。此外，它改变了肿瘤的微环境。作为癌症治疗的一种战术方法，这些发现强调了靶向炎症途径的重要性。本文综述了炎症在癌症发展和转移中的作用，重点关注其对肿瘤进展、免疫抑制和治疗抵抗的影响。研究了当前的抗炎策略，包括非甾体抗炎药、细胞因子调节剂和STAT3抑制剂，同时指出了它们的潜力和局限性。该综述强调需要进一步研究，以揭示炎症与癌症进展之间的复杂机制，并确定特定癌症亚型的分子靶点。

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