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The various pathological roles of oxidized LDL in diseases 氧化LDL在疾病中的各种病理作用
Q2 Medicine Pub Date : 2025-09-01 DOI: 10.1016/j.obmed.2025.100646
Abdullatif Taha Babakr
Oxidized low-density lipoprotein (Ox-LDL) represents a chemically altered version of low-density lipoprotein where oxidative damage modifies both its protein and lipid constituents. This oxidation can occur through direct interaction with radical molecules or via lipid peroxidation byproducts. The presence of Ox-LDL is closely associated with the development of atherosclerosis and various pathological conditions, although the precise mechanisms by which it contributes to these processes continue to be comprehensively elucidated.
The recognition of Ox-LDL marked a paradigm shift, emphasizing oxidative modification as a key driver of atherogenesis and metabolic pathologies. This discovery also encouraged the development of various biomarkers and therapeutic strategies aimed at reducing LDL oxidation as a potential way to prevent or treat cardiovascular diseases. Thus, the discovery of Ox-LDL continues to shape modern cardiovascular research and treatment approaches.
This article aims to elucidate the process of LDL oxidation and its association with various diseases. A thorough investigation was carried out across multiple databases, such as PubMed, Scopus, Google Scholar, and Ovid, to gather relevant literature and studies that explore the relationship between Ox-LDL and the pathogenesis of diseases, thereby creating a clear understanding of the topic. This review will examine the characteristics of the Ox-LDL particle, emphasizing its contributions to various pathological conditions and diseases. Finally, this review will shed light on the challenges facing the use of this biomarker in clinical practice and future recommendations.
氧化低密度脂蛋白(Ox-LDL)代表了低密度脂蛋白的化学改变版本,其中氧化损伤改变了其蛋白质和脂质成分。这种氧化可以通过与自由基分子的直接相互作用或通过脂质过氧化副产物发生。Ox-LDL的存在与动脉粥样硬化和各种病理状况的发展密切相关,尽管其促进这些过程的确切机制仍有待全面阐明。对Ox-LDL的认识标志着范式的转变,强调氧化修饰是动脉粥样硬化和代谢病理的关键驱动因素。这一发现也鼓励了各种生物标志物和治疗策略的发展,旨在减少LDL氧化,作为预防或治疗心血管疾病的潜在方法。因此,Ox-LDL的发现继续影响着现代心血管研究和治疗方法。本文旨在阐明LDL氧化过程及其与多种疾病的关系。通过对PubMed、Scopus、谷歌Scholar、Ovid等多个数据库进行深入调查,收集相关文献和研究,探讨Ox-LDL与疾病发病机制之间的关系,从而对该主题有一个清晰的认识。本文将研究Ox-LDL颗粒的特性,强调其在各种病理条件和疾病中的作用。最后,这篇综述将阐明在临床实践中使用这种生物标志物所面临的挑战和未来的建议。
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引用次数: 0
Obesity driven autoimmune dysregulation and its implications in rheumatoid arthritis, lupus, and multiple sclerosis 肥胖驱动自身免疫失调及其在类风湿关节炎、狼疮和多发性硬化症中的意义
Q2 Medicine Pub Date : 2025-09-01 DOI: 10.1016/j.obmed.2025.100636
Manisha M , Arun Elamurugan , Nishvanth F , Pavithra N , Nivetha S , Anuragh Singh , Harikrishnan N , Ankul Singh S
Obesity, long considered a metabolic disorder, is now recognized as a key driver of immune dysregulation and chronic low-grade inflammation, significantly contributing to the onset and progression of autoimmune diseases. This review critically explores the mechanistic links between obesity and major autoimmune disorders like rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis, highlighting the roles of adipokines, neuroendocrine-immune crosstalk, and chronic systemic inflammation. Special attention is given to the emerging role of gut microbiota dysbiosis in mediating neuroimmune responses through the gut–brain axis. Specific microbiota, such as Akkermansia muciniphila, Prevotella histicola, and Desulfovibrio, are discussed in terms of their contribution to immune modulation, intestinal barrier integrity, and neuroinflammation. Furthermore, we examine how obesity impairs treatment efficacy via pharmacokinetic alterations and propose microbiota-targeted and adipokine-modulating interventions as potential therapeutic strategies. Lifestyle modifications, including diet, physical activity, and bariatric surgery, are also evaluated for their immunomodulatory and clinical benefits. By integrating current evidence from immunometabolism, neuroimmunology, and microbiome research, this review underscores the urgent need for holistic, obesity-informed approaches in autoimmune disease management.
肥胖,长期以来被认为是一种代谢紊乱,现在被认为是免疫失调和慢性低度炎症的关键驱动因素,在自身免疫性疾病的发生和发展中起着重要作用。这篇综述批判性地探讨了肥胖与主要自身免疫性疾病(如类风湿关节炎、系统性红斑狼疮和多发性硬化症)之间的机制联系,强调了脂肪因子、神经内分泌免疫串扰和慢性全身性炎症的作用。特别关注肠道微生物群失调在通过肠-脑轴介导神经免疫反应中的新作用。具体的微生物群,如嗜粘液阿克曼氏菌,历史普雷沃氏菌和脱硫弧菌,讨论了他们的免疫调节,肠道屏障完整性和神经炎症的贡献。此外,我们研究了肥胖如何通过药代动力学改变损害治疗效果,并提出了针对微生物群和脂肪因子调节的干预措施作为潜在的治疗策略。生活方式的改变,包括饮食、体育活动和减肥手术,也被评估其免疫调节和临床效益。通过整合目前来自免疫代谢、神经免疫学和微生物组研究的证据,本综述强调了在自身免疫性疾病管理中迫切需要全面的、肥胖信息的方法。
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引用次数: 0
Clinico-epidemiology analysis of hypertension and dyslipidaemia among patients with congestive heart failure in Douala, Cameroon 喀麦隆杜阿拉充血性心力衰竭患者高血压和血脂异常的临床流行病学分析
Q2 Medicine Pub Date : 2025-09-01 DOI: 10.1016/j.obmed.2025.100638
Djeukeu Asongni William , Julien Armel Agamou Assiene , Loick Pradel Kojom Foko , Pierre Mintom , Moni Michelle , William Dakam , Christine Fernande Nyangono Biyegue

Background

Cardiovascular and atherosclerotic vascular diseases are important cause of mortality worldwide. This study was designed to determine the prevalence, patterns, and determinants of hypertension (HTA) and dyslipidaemia in Cameroonian patients living with congestive heart failure.

Methods

Between March 2017 and August 2018, a cross-sectional study was conducted at the Deido District Hospital involving 98 patients diagnosed with heart failure. Data on socio-demographic, clinical, anthropometric, and physiological features were documented. Lipid profile components (i.e., total cholesterol – TC, low density lipoprotein cholesterol – LDL-c, high density lipoprotein cholesterol – HDL-c, and triglycerides – TG) were determined from overnight fasting blood. HTA was diagnosed using clinical standard procedures.

Results

The overall prevalence of HTA and dyslipidaemia was 45.9 % and 82.7 %. Disorders in lipid profile were found, which were mainly represented by hypercholesteremia (66.3 %) and hyper-LDL cholesterolemia (68.4 %). HTA was more prevalent in patients with dyslipidaemia, hypercholesterolemia, and hypertriglyceridemia. A one-unity increase in blood level of TC was associated with an increase in HTA risk by 1.04 times (95 %CI 1.02–1.06, p < 0.0001). The risk of dyslipidaemia was reduced in females by 77 % (aOR = 0.23, p = 0.007) compared to males. Glycaemia was consistently found to be a risk factor for hypercholesteremia (aOR = 1.87, p < 0.05), hypo-HDL cholesterolemia (aOR = 6.38, p < 0.05), and hyper-LDL cholesterolemia (aOR = 10.22, p < 0.05).

Conclusions

These findings call for systematic monitoring of HTA status and lipid profiles in this population to alleviate cardio-metabolic complications.
背景:心血管和动脉粥样硬化性血管疾病是世界范围内重要的死亡原因。本研究旨在确定喀麦隆充血性心力衰竭患者高血压(HTA)和血脂异常的患病率、模式和决定因素。方法2017年3月至2018年8月,在Deido地区医院进行了一项横断面研究,涉及98名诊断为心力衰竭的患者。记录了社会人口学、临床、人体测量学和生理特征的数据。血脂成分(即总胆固醇- TC,低密度脂蛋白胆固醇- LDL-c,高密度脂蛋白胆固醇- HDL-c,甘油三酯- TG)从空腹血液中测定。HTA的诊断采用临床标准程序。结果HTA和血脂异常的总患病率分别为45.9%和82.7%。血脂异常,主要表现为高胆固醇血症(66.3%)和高ldl胆固醇血症(68.4%)。HTA在血脂异常、高胆固醇血症和高甘油三酯血症患者中更为普遍。血液中TC水平的增加与HTA风险增加1.04倍相关(95% CI 1.02-1.06, p < 0.0001)。与男性相比,女性患血脂异常的风险降低了77% (aOR = 0.23, p = 0.007)。血糖一直被发现是高胆固醇血症(aOR = 1.87, p < 0.05)、低hdl胆固醇血症(aOR = 6.38, p < 0.05)和高ldl胆固醇血症(aOR = 10.22, p < 0.05)的危险因素。结论这些发现要求系统监测HTA状态和脂质谱,以减轻心脏代谢并发症。
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引用次数: 0
Gut microbiota-derived metabolites as early biomarkers for childhood obesity: A policy commentary from urban African populations 肠道微生物衍生代谢物作为儿童肥胖的早期生物标志物:来自非洲城市人口的政策评论
Q2 Medicine Pub Date : 2025-09-01 DOI: 10.1016/j.obmed.2025.100641
Okechukwu Paul-Chima Ugwu , Fabian C. Ogenyi , Chinyere N. Ugwu , Melvin Nnaemeka Ugwu
Obesity among children is rapidly increasing in urban African settings due to the Westernisation of diets and decreased physical exercise, as well as socioeconomic inequality. Changes in the composition of gut microbiota, especially depletion of short-chain fatty acids (SCFAs), increase in branched-chain amino acids (BCAAs), and alterations in the bile acid metabolism, are becoming early, non-invasive predictors of metabolic risk. Though comparable microbiome-based early-detection models have been designed regarding Latin American and Asian paediatric populations, the commentary aims at the African urban setting, where a combination of undernutrition and obesity, the use of street foods and the rapid urban-rural migration generate unique microbial profiles. We synthesise data in Nairobi, Kampala, and Lagos, including region-specific taxa such as Succinivibrio, Treponema, and Methanobrevibacter. Our suggestions are specific, low-cost interventions, such as the incorporation of fiber-rich foods into national school feeding programs and the use of Ghana-developed lateral-flow SCFA assays that cost less than US$2 per test. This is a policy-orientated narrative with no collection of primary data. The search of literature in PubMed, Scopus, and African health research repositories (2015–2025) was carried out with the use of the terms associated with gut microbiota, childhood obesity, microbial metabolites, and Africa. Our focus is to transform microbiome science into scalable, culturally appropriate, and cost-effective public health interventions.
由于饮食西化、体育锻炼减少以及社会经济不平等,非洲城市儿童肥胖人数正在迅速增加。肠道菌群组成的变化,特别是短链脂肪酸(SCFAs)的消耗、支链氨基酸(BCAAs)的增加和胆汁酸代谢的改变,正在成为代谢风险的早期、非侵入性预测指标。虽然针对拉丁美洲和亚洲儿科人群设计了可比较的基于微生物组的早期检测模型,但该评论针对的是非洲城市环境,在那里,营养不良和肥胖、街头食品的使用以及城乡快速迁移共同产生了独特的微生物图谱。我们综合了内罗毕、坎帕拉和拉各斯的数据,包括特定区域的分类群,如琥珀酸弧菌、密螺旋体和甲烷杆菌。我们的建议是具体的、低成本的干预措施,例如将富含纤维的食物纳入国家学校供餐计划,以及使用加纳开发的每次检测成本低于2美元的横向流动SCFA检测方法。这是一种以政策为导向的叙述,没有收集原始数据。在PubMed、Scopus和非洲卫生研究资料库(2015-2025)中检索文献,使用与肠道微生物群、儿童肥胖、微生物代谢物和非洲相关的术语。我们的重点是将微生物组科学转化为可扩展的、文化上适当的、具有成本效益的公共卫生干预措施。
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引用次数: 0
Phase angle decline after Roux-en-Y gastric bypass reflects fluid redistribution during the weight loss: A 12-month follow-up study Roux-en-Y胃旁路术后相位角下降反映体重减轻期间液体再分配:一项12个月的随访研究
Q2 Medicine Pub Date : 2025-09-01 DOI: 10.1016/j.obmed.2025.100644
Beatriz Bobbio de Brito , João Arthur Souza Fiorido , Doglas Gobbi Marchesi , Luís Carlos Lopes Júnior , Luciane Bresciani Salaroli , Blanca Elena Guerrero Daboin , Andressa Bolsoni Lopes , Fabiano Kenji Haraguchi

Aims

Phase angle (PhA), an indicator of cellular integrity and fluid balance, is underexplored in individuals with severe obesity, particularly during postoperative weight loss. This study evaluated PhA trajectories and their body composition determinants over 12 months following Roux-en-Y gastric bypass (RYGB).

Methods

Sixty participants meeting inclusion criteria were assessed at four time points: before surgery, and at 2, 6, and 12 months after RYGB. Body composition and PhA were evaluated at each follow-up. The Friedman test (α = 0.05) was used to examine changes over time. Spearman's correlation and multiple linear regression explored associations between PhA and body composition variables.

Results

PhA declined significantly after surgery and showed a consistent inverse association with the extracellular to intracellular water (ECW:ICW) ratio at all postoperative assessments (p < 0.05). Significant reductions were also observed in weight, BMI, waist circumference, fat mass, fat-free mass, and total body water (p < 0.05).

Conclusion

The ECW:ICW ratio was the primary determinant of PhA decline, reflecting fluid redistribution and early metabolic adaptation during rapid weight loss. PhA may serve as a practical marker for monitoring physiological responses to bariatric surgery.
AimsPhase角(PhA)是细胞完整性和液体平衡的指标,在严重肥胖患者中,特别是在术后减肥期间,尚未得到充分研究。本研究评估了Roux-en-Y胃旁路术(RYGB)后12个月的PhA轨迹及其体成分决定因素。方法60名符合纳入标准的参与者在四个时间点进行评估:手术前,RYGB后2、6和12个月。在每次随访中评估体成分和PhA。采用Friedman检验(α = 0.05)检验随时间的变化。Spearman相关和多元线性回归探讨了PhA与身体成分变量之间的关系。结果术后spha显著下降,且在所有术后评估中均与细胞外/细胞内水(ECW:ICW)比呈一致的负相关(p < 0.05)。体重、BMI、腰围、脂肪量、无脂肪量和全身水分也有显著降低(p < 0.05)。结论ECW:ICW比值是PhA下降的主要决定因素,反映了快速减肥过程中体液再分配和早期代谢适应。PhA可作为监测减肥手术生理反应的实用标记物。
{"title":"Phase angle decline after Roux-en-Y gastric bypass reflects fluid redistribution during the weight loss: A 12-month follow-up study","authors":"Beatriz Bobbio de Brito ,&nbsp;João Arthur Souza Fiorido ,&nbsp;Doglas Gobbi Marchesi ,&nbsp;Luís Carlos Lopes Júnior ,&nbsp;Luciane Bresciani Salaroli ,&nbsp;Blanca Elena Guerrero Daboin ,&nbsp;Andressa Bolsoni Lopes ,&nbsp;Fabiano Kenji Haraguchi","doi":"10.1016/j.obmed.2025.100644","DOIUrl":"10.1016/j.obmed.2025.100644","url":null,"abstract":"<div><h3>Aims</h3><div>Phase angle (PhA), an indicator of cellular integrity and fluid balance, is underexplored in individuals with severe obesity, particularly during postoperative weight loss. This study evaluated PhA trajectories and their body composition determinants over 12 months following Roux-en-Y gastric bypass (RYGB).</div></div><div><h3>Methods</h3><div>Sixty participants meeting inclusion criteria were assessed at four time points: before surgery, and at 2, 6, and 12 months after RYGB. Body composition and PhA were evaluated at each follow-up. The Friedman test (α = 0.05) was used to examine changes over time. Spearman's correlation and multiple linear regression explored associations between PhA and body composition variables.</div></div><div><h3>Results</h3><div>PhA declined significantly after surgery and showed a consistent inverse association with the extracellular to intracellular water (ECW:ICW) ratio at all postoperative assessments (p &lt; 0.05). Significant reductions were also observed in weight, BMI, waist circumference, fat mass, fat-free mass, and total body water (p &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>The ECW:ICW ratio was the primary determinant of PhA decline, reflecting fluid redistribution and early metabolic adaptation during rapid weight loss. PhA may serve as a practical marker for monitoring physiological responses to bariatric surgery.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"57 ","pages":"Article 100644"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145007700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Soluble receptor for advanced glycation end products and diabetes in Black and White Americans: the REGARDS study 美国黑人和白人晚期糖基化终产物和糖尿病的可溶性受体:REGARDS研究
Q2 Medicine Pub Date : 2025-09-01 DOI: 10.1016/j.obmed.2025.100647
Brittney J. Palermo , Katherine S. Wilkinson , Timothy B. Plante , Suzanne E. Judd , Debora Kamin Mukaz , D. Leann Long , Nels C. Olson , Melissa J. Smith , Mary Cushman

Background

Diabetes is a leading cause of morbidity and mortality in the United States, affecting Black more than White adults. The soluble receptor for advanced glycation end products (sRAGE) prevents signaling that induces inflammation and is implicated in diabetes pathogenesis. This analysis investigated if low sRAGE is associated with diabetes risk, and if sRAGE mediates the racial disparity in diabetes.

Methods

The REasons for Geographic and Racial Differences in Stroke prospective cohort included 30,239 Black and White adults aged ≥45 with baseline and follow up exam. We studied a 4400 participant sub-cohort with 9.5-year follow-up to classify diabetes, with analyses being survey weighted to the larger cohort. Baseline sRAGE was measured in 3400 at risk for diabetes; modified Poisson regression estimated relative risk (RR) by sRAGE. Inverse odds weighting mediation analysis examined the contribution of sRAGE to the racial disparity in diabetes.

Results

Ten percent of White and 18 % of Black participants experienced incident diabetes. The RR of diabetes was elevated in lower quartiles of sRAGE compared to the fourth quartile. With diabetes risk factor adjustment, the RR was 1.32 (95 % CI 0.97–1.79) in the lowest compared to the highest quartile (p-trend across quartiles 0.06). sRAGE did not mediate any of the racial disparity in diabetes.

Conclusions

Among Black and White Americans, low sRAGE was associated with increased risk of developing diabetes; associations attenuated and became non-significant with covariate adjustment. sRAGE may serve as a marker for diabetes risk, but clinical utility is unlikely given small non-significant associations, and no identified mediation of the association by sRAGE.
背景:糖尿病是美国发病率和死亡率的主要原因,对黑人的影响大于白人。晚期糖基化终产物的可溶性受体(sRAGE)阻止诱导炎症的信号传导,并参与糖尿病的发病机制。该分析调查了低sRAGE是否与糖尿病风险相关,以及sRAGE是否介导了糖尿病的种族差异。方法对30239名年龄≥45岁的黑人和白人进行卒中前瞻性队列研究,并进行基线和随访检查。我们研究了4400名参与者的亚队列,随访9.5年,对糖尿病进行分类,并对更大的队列进行调查加权分析。在3400名有糖尿病风险的患者中测量了基线sRAGE;修正泊松回归用sRAGE估计相对危险度(RR)。反向优势加权中介分析检验了sRAGE对糖尿病种族差异的贡献。结果:10%的白人和18%的黑人参与者经历了偶发性糖尿病。与第四个四分位数相比,低四分位数的sRAGE中糖尿病的RR升高。调整糖尿病危险因素后,与最高四分位数相比,最低四分位数的RR为1.32 (95% CI 0.97-1.79)(四分位数的p趋势为0.06)。sRAGE并没有调节糖尿病的种族差异。结论:在美国黑人和白人中,低sRAGE与患糖尿病的风险增加有关;协变量调整后,相关性减弱并变得不显著。sRAGE可以作为糖尿病风险的标记物,但由于较小的非显著相关性,并且没有确定sRAGE的关联中介,因此临床应用不太可能。
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引用次数: 0
Dysbiosis as a driving force for the relationship between obesity and secondary osteoporosis 生态失调是肥胖和继发性骨质疏松症之间关系的驱动力
Q2 Medicine Pub Date : 2025-08-27 DOI: 10.1016/j.obmed.2025.100637
Ferah Armutcu , Eugene McCloskey
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引用次数: 0
The UPR-oxidative stress nexus in diabetes and obesity: Exploring innovative therapeutic approaches for metabolic control 糖尿病和肥胖中的ubr -氧化应激关系:探索代谢控制的创新治疗方法
Q2 Medicine Pub Date : 2025-07-10 DOI: 10.1016/j.obmed.2025.100634
Clinton Ayodeji Akanbi , Oluwafemi Adeleke Ojo
Maintaining cellular protein homeostasis requires the endoplasmic reticulum (ER); however, the unfolded protein response (UPR) can be triggered by the accumulation of misfolded proteins, which can cause ER stress. The goal of the UPR is to bring the body back into balance. Nevertheless, long-term ER stress can cause β-cell dysfunction and apoptosis, which greatly exacerbates metabolic diseases such as diabetes and obesity. ER stress worsens insulin resistance and reduces glucose metabolism in pancreatic β-cells. Moreover, the ER is further damaged by oxidative stress, which is defined by an excess of reactive oxygen species (ROS), which prolongs metabolic dysfunction. This review delves into the molecular mechanisms that underlie ER stress, its consequences for diabetes and obesity, and possible treatment approaches. We discuss interventions to mitigate ER stress, including chemical chaperones, UPR modulators, and dietary strategies. Current pharmacological approaches, such as chemical chaperones and UPR modulators, have demonstrated efficacy in reducing ER stress, but they often present challenges, including inconsistent treatment responses and off-target effects. Antioxidant-rich dietary strategies, while promising for long-term management, require further validation to ensure their safety and effectiveness. Additionally, advances in CRISPR–Cas9 gene-editing technology provide new opportunities for addressing genetic defects associated with these disorders. These findings emphasize the need for integrated therapies that address both oxidative and ER stress to effectively mitigate metabolic dysfunction.
维持细胞蛋白稳态需要内质网(ER);然而,未折叠蛋白反应(UPR)可由错误折叠蛋白的积累触发,从而导致内质网应激。普遍定期审议的目标是使身体恢复平衡。然而,内质网长期应激可引起β细胞功能障碍和凋亡,大大加重糖尿病、肥胖等代谢性疾病。内质网应激加重胰岛素抵抗,降低胰腺β细胞的葡萄糖代谢。此外,内质网还会受到氧化应激的进一步损害,氧化应激的定义是活性氧(ROS)过量,从而延长代谢功能障碍。本文将深入探讨内质网应激的分子机制、内质网应激对糖尿病和肥胖症的影响以及可能的治疗方法。我们讨论了缓解内质网应激的干预措施,包括化学伴侣、UPR调节剂和饮食策略。目前的药理学方法,如化学伴侣和UPR调节剂,已经证明了减少内质网应激的有效性,但它们经常面临挑战,包括不一致的治疗反应和脱靶效应。富含抗氧化剂的饮食策略虽然有望长期管理,但需要进一步验证以确保其安全性和有效性。此外,CRISPR-Cas9基因编辑技术的进步为解决与这些疾病相关的遗传缺陷提供了新的机会。这些发现强调需要综合治疗,同时解决氧化应激和内质网应激,以有效减轻代谢功能障碍。
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引用次数: 0
Type 2 diabetes remission with very low-energy ketogenic treatment: a retrospective real-world study 低能量生酮治疗缓解2型糖尿病:一项真实世界的回顾性研究
Q2 Medicine Pub Date : 2025-07-10 DOI: 10.1016/j.obmed.2025.100633
Daniela Sofra , Maitane Nuñez-Garcia , Ignacio Sajoux , Massimiliano Caprio , Francesca Amati

Aims

The role of Very Low-Energy Ketogenic Treatment (VLEKT) in managing type 2 diabetes mellitus (T2DM) remains underexplored. This retrospective, single-center study evaluated the effectiveness of a structured VLEKT protocol in achieving diabetes remission or improving glycemic control (reversal) in overweight and obese T2DM patients in a real-world setting.

Methods

Thirty-eight patients underwent a three-phase VLEKT intervention. The initial phase included three consecutive very low-energy ketogenic stages with calibrated meal replacements, aimed at reducing endogenous insulin secretion, stimulating lipolysis, and promoting fat loss. The second phase involved transitioning to a low-calorie diet and increased physical activity, followed by a maintenance phase to sustain metabolic benefits. Anthropometric data, HbA1c, and medication use were recorded at each visit.

Results

VLEKT significantly improved weight and glycemic control. After 6 months, 47.4 % of patients achieved diabetes remission, with 28.9 % maintaining remission at 2 years. Nearly half of the patients showed a trend toward remission within 3 months, based on early medication discontinuation and normalized glucose values, but this did not meet the formal criteria for remission. Shorter diabetes duration and fewer baseline glucose-lowering drugs predicted remission. The intervention also enabled sustained weight loss and reduced medication reliance over 18 months. Limitations include the retrospective design, small sample size, single-center scope, and potential selection bias due to self-funded participation.

Conclusion

VLEKT is a feasible, safe, and effective non-pharmacological approach to induce T2DM remission in routine clinical practice. These findings support integrating ketogenic nutritional protocols into multidisciplinary diabetes care, offering clinicians valuable alternatives to conventional drug therapies.
极低能量生酮治疗(VLEKT)在2型糖尿病(T2DM)治疗中的作用仍未得到充分研究。本回顾性单中心研究评估了结构化VLEKT方案在现实世界中实现超重和肥胖T2DM患者糖尿病缓解或改善血糖控制(逆转)的有效性。方法38例患者接受三阶段VLEKT干预。初始阶段包括三个连续的低能量生酮阶段和校准的代餐,旨在减少内源性胰岛素分泌,刺激脂肪分解,促进脂肪减少。第二阶段包括过渡到低热量饮食和增加体力活动,随后是维持代谢益处的维持阶段。每次就诊时记录人体测量数据、糖化血红蛋白和药物使用情况。结果vlekt能显著改善体重和血糖控制。6个月后,47.4%的患者达到糖尿病缓解,28.9%的患者在2年内保持缓解。根据早期停药和正常血糖值,近一半的患者在3个月内出现缓解趋势,但这并不符合缓解的正式标准。较短的糖尿病病程和较少的基线降糖药物预测缓解。在18个月的时间里,干预还使体重持续下降,减少了对药物的依赖。局限性包括回顾性设计、小样本量、单中心范围和自费参与的潜在选择偏倚。结论在常规临床实践中,vlekt是一种可行、安全、有效的非药物诱导T2DM缓解方法。这些发现支持将生酮营养方案整合到多学科糖尿病治疗中,为临床医生提供了替代传统药物治疗的宝贵选择。
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引用次数: 0
Molecular mechanisms underlying obesity-altered brain functions: the alteration of BDNF production 肥胖改变脑功能的分子机制:BDNF产生的改变
Q2 Medicine Pub Date : 2025-07-01 DOI: 10.1016/j.obmed.2025.100632
Reem M. Al Haj Ahmad , Dalia M. Abu Al-Haijaa
Obesity adversely impacts the quality of life; people with obesity are more vulnerable to chronic diseases such as T2DM, insulin resistance, and dementia. Brain-derived neurotrophic factor (BDNF) has a significant role in cognition and brain health; it influences synaptic plasticity and neurogenesis. BDNF has been proposed as mechanistic a modulator to explain the association between peripheral dysmetabolism and cognitive decline. This review highlights the metabolic alterations associated with obesity including, insulin resistance, inflammation, and BDNF levels. It illustrates, as well, the mechanistic crosstalk between adiposity and the decline of brain health and cognition explained by the BDNF alteration. A narrative review of the recent research focusing on BDNF molecular biology and functions, the effect of obesity on its regulation, and neuronal health and cognition during obesity and its allied metabolic changes. Although the results of the related published research were contradicted, obesity was related to BDNF expression and signaling dysregulation. This dysregulation leads to neuroinflammation a condition that impairs synaptic plasticity and neurogenesis, and increases apoptosis. These fluctuations were linked to cognitive decline and different types of neurodegeneration. Insulin resistance and hyperinsulinemia were the main hubs for connecting adiposity, BDNF, and dementia. Correction of BDNF expression and signaling may offer an evolving therapeutic practice for the treatment and prevention of obesity-related cognitive decline. Further longitudinal and clinical trial studies are needed to clarify the causal direction and expand our vision of treatment and prevention regimes for cognitive disorders.
肥胖对生活质量产生不利影响;肥胖的人更容易患上慢性疾病,如2型糖尿病、胰岛素抵抗和痴呆。脑源性神经营养因子(BDNF)在认知和脑健康中具有重要作用;它影响突触可塑性和神经发生。BDNF被认为是外周代谢障碍和认知能力下降之间的机制调节剂。这篇综述强调了与肥胖相关的代谢改变,包括胰岛素抵抗、炎症和BDNF水平。它还说明了肥胖与脑健康和认知能力下降之间的机制相互作用,这可以通过BDNF的改变来解释。本文综述了近年来BDNF分子生物学和功能、肥胖对其调控的影响、肥胖及其相关代谢变化过程中神经元健康和认知的研究进展。尽管已发表的相关研究结果存在矛盾,但肥胖与BDNF表达和信号失调有关。这种失调导致神经炎症,损害突触可塑性和神经发生,并增加细胞凋亡。这些波动与认知能力下降和不同类型的神经变性有关。胰岛素抵抗和高胰岛素血症是连接肥胖、BDNF和痴呆的主要枢纽。纠正BDNF表达和信号传导可能为治疗和预防肥胖相关的认知衰退提供一种不断发展的治疗实践。需要进一步的纵向和临床试验研究来澄清因果方向,并扩大我们对认知障碍治疗和预防制度的看法。
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Obesity Medicine
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