International Journal of Obesity最新文献_第9页

Whole blood TNF-α expression and apoptotic endothelial microparticles reveal early vascular injury in pediatric obesity 全血TNF-α表达和内皮细胞凋亡微粒揭示儿童肥胖早期血管损伤。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-18 DOI: 10.1038/s41366-025-01954-8

Fernanda Thomazini, Mauro Eugênio Medina Nunes, Paula Regina de Souza, Alexandre Budu, Ronaldo de Carvalho Araujo, Maria do Carmo Franco

Childhood obesity is increasingly recognized as a trigger for early cardiovascular risk, partly mediated by subclinical inflammation and endothelial dysfunction. This study aimed to evaluate the expression of pro-inflammatory cytokines (TNF-α, IL-17A, and IL-2) in whole blood and investigate their associations with anthropometric measures, blood pressure, microvascular endothelial function, and circulating apoptotic endothelial microparticles (EMPs) in children with healthy weight versus those with overweight/obesity. A cross-sectional study was conducted with 113 children aged 6–11 years, categorized as children with healthy weight (n = 82) or children with overweight/obesity (n = 31) based on BMI-for-age criteria. Endothelial function was assessed using peripheral arterial tonometry by measurement of reactive hyperemia index (RHI) and circulating apoptotic EMPs were measured by flow cytometry. Whole blood mRNA levels of inflammatory cytokines were quantified using qRT-PCR. Children with overweight/obesity exhibited significantly lower RHI values, indicating early endothelial dysfunction. RHI negatively correlated with BMI (r = −0.485; P < 0.001), waist circumference (r = −0.466; P < 0.001), SBP (r = −0.317, P = 0.001), DBP (r = −0.246; P = 0.009), and LDL-C levels (r = −0.191; P = 0.043). Circulating levels of apoptotic EMPs were elevated in these children and positively associated with adiposity and blood pressure, while inversely correlated with RHI (r = −0.496; P < 0.001). TNF-α expression was significantly upregulated in the overweight/obesity group and correlated positively with BMI (r = 0.468; P = 0.001), waist circumference (r = 0.492; P < 0.001), SBP (r = 0.294; P = 0.040), apoptotic EMPs (r = 0.326; P = 0.022), and negatively with RHI (r = −0.543; P < 0.001). No significant differences were observed for IL-17A or IL-2 expression. The linear regression analysis indicated that high circulating levels of both apoptotic EMPs and TNF-α mRNA were recognized as predictors factors of lower RHI value in the study population. TNF-α gene expression in whole blood and elevated levels of apoptotic endothelial microparticles are closely associated with early endothelial microvascular dysfunction in pediatric obesity. The observed associations underscore the role of inflammation-driven endothelial dysfunction in the pathophysiology of obesity-related cardiovascular risk.

背景：儿童肥胖越来越被认为是早期心血管风险的触发因素，部分由亚临床炎症和内皮功能障碍介导。本研究旨在评估全血中促炎细胞因子（TNF-α、IL-17A和IL-2）的表达，并研究它们与健康体重儿童与超重/肥胖儿童的人体测量、血压、微血管内皮功能和循环内皮细胞凋亡微粒（EMPs）的关系。方法：对113名6-11岁儿童进行横断面研究，根据年龄bmi标准将其分为健康体重儿童（n = 82）和超重/肥胖儿童（n = 31）。外周动脉血压计通过测量反应性充血指数（RHI）评估内皮功能，流式细胞术测量循环凋亡emp。采用qRT-PCR定量检测全血炎症细胞因子mRNA水平。结果：超重/肥胖儿童表现出明显较低的RHI值，表明早期内皮功能障碍。结论：全血TNF-α基因表达和内皮细胞凋亡微粒水平升高与儿童肥胖早期内皮微血管功能障碍密切相关。观察到的关联强调了炎症驱动的内皮功能障碍在肥胖相关心血管风险的病理生理中的作用。

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引用次数: 0

The prevalence of prediabetes is high and has rapidly increased, independent of the degree of obesity, in Finnish children with overweight or obesity 在芬兰超重或肥胖儿童中，前驱糖尿病的患病率很高，并且与肥胖程度无关，而且迅速增加。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-18 DOI: 10.1038/s41366-025-01950-y

Hanna Riekki, Linnea Aitokari, Antti Saari, Laura Kivelä, Heini Huhtala, Anna Viitasalo, Sonja Soininen, Eero A. Haapala, Timo Lakka, Kalle Kurppa

The global increase in obesity predisposes individuals to prediabetes and type 2 diabetes, but data on their prevalence, temporal trends, and associated factors in children remain limited. We examined these issues in well-defined patient and population cohorts. Data were collected from 602 patients aged 6–16 years, who were examined in healthcare for overweight/obesity once in 2002–2020. Controls comprised 483 population-representative children aged 7–16, who participated in 1–3 prospective visits. Prediabetes signified fasting glucose 5.6–6.9 mmol/L or 2h-post-challenge glucose 7.8–11.0 mmol/L, and diabetes as values ≥7.0 mmol/L or ≥11.1 mmol/L, respectively. Factors associated with prediabetes in patients were studied using logistic regression. The prevalence of prediabetes was compared between patients having their first healthcare visit in different years between 2002 and 2019. Altogether, 89.2% of patients and 3.3–4.7% of controls had obesity. The prevalence of prediabetes was 34.2% and of type 2 diabetes 1.3% among patients, and 6.9% and 0% in controls respectively, with prediabetes increasing significantly with age and stage of puberty. Both conditions were associated with presence of metabolic dysfunction-associated steatotic liver disease (OR 1.69, 95% CI 1.01–2.80) and acanthosis nigricans (1.83, 1.05–3.21), after adjusting for age. Prevalence of prediabetes increased steeply over time from 11.4% in patients examined in 2002–2004 to 50.0% in patients examined in 2017–2019 (OR 1.16, CI 1.10–1.21 p < 0.001) without concurrent changes in the degree of obesity, body mass index, other metabolic conditions, age, sex, or gestational/neonatal factors, except for an increase in maternal prepregnancy/pregnancy overweight (20.0–68.8%, OR 1.14, CI 1.08–1.21, p < 0.001). Prediabetes was decidedly prevalent in pediatric patients with obesity and was associated particularly with steatotic liver disease. Its prevalence increased steeply over time, independent of the degree of obesity.

目的：全球肥胖的增加使个体易患前驱糖尿病和2型糖尿病，但关于其在儿童中的患病率、时间趋势和相关因素的数据仍然有限。我们在明确的患者和人群队列中检查了这些问题。方法：收集2002-2020年在医疗保健机构接受过一次超重/肥胖检查的602例6-16岁患者的资料。对照组包括483名具有人口代表性的7-16岁儿童，他们参加了1-3次预期访问。糖尿病前期空腹血糖5.6-6.9 mmol/L或攻毒后2h血糖7.8-11.0 mmol/L，糖尿病分别为≥7.0 mmol/L或≥11.1 mmol/L。采用logistic回归分析与糖尿病前期患者相关的因素。比较了2002年至2019年不同年份首次就诊的患者的前驱糖尿病患病率。结果：89.2%的患者和3.3-4.7%的对照组存在肥胖。糖尿病前期患病率为34.2%，2型糖尿病患病率为1.3%，对照组为6.9%和0%，糖尿病前期患病率随年龄和青春期阶段的增加而显著增加。在调整年龄后，这两种情况都与代谢功能障碍相关的脂肪变性肝病（OR 1.69, 95% CI 1.01-2.80）和黑棘皮病（OR 1.83, 1.05-3.21）的存在相关。随着时间的推移，糖尿病前期的患病率从2002-2004年的11.4%急剧上升到2017-2019年的50.0% （OR 1.16, CI 1.10-1.21 p）。结论：糖尿病前期在儿童肥胖患者中明显普遍存在，尤其是与脂肪变性肝病相关。随着时间的推移，它的患病率急剧上升，与肥胖程度无关。

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引用次数: 0

The Physiology Of the WEight Reduced State (POWERS) study: assessing energy balance. 减重状态（POWERS）的生理学研究：评估能量平衡。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-17 DOI: 10.1038/s41366-025-01935-x

Michael Rosenbaum, Kelly C Allison, Maren R Laughlin, Kathryn Whyte, John M Jakicic, Laurel E S Mayer, Maxine Ashby-Thompson, Matthew R Hayes, John Speakman, Rudolph L Leibel, Sai Krupa Das, Dympna Gallagher, Susan B Roberts

Background/objectives: We provide the rationale for and description of energy balance measures (i.e., energy intake and energy expenditure) in The Physiology Of the WEight Reduced State (POWERS) study which aims to understand the contribution of the many factors that influence weight regain following behavioral weight loss.

Methods: The primary dependent variable is weight regain over 1 year following a 7% or greater supervised weight loss. The balance between energy intake and expenditure is the primary determinant of weight regain. Healthy adults (target n = 205), aged 25- < 60 years, with body mass index (BMI) 30- < 40 kg/m² are being recruited. Energy intake and expenditure phenotypes are measured prior to weight loss (baseline, BL), immediately following weight loss (T0), and then four (T4) and 12 months (T12) after weight loss. Weight stability is required before BL and T0 measurement periods. Weight change at T12 from T0 is the primary outcome variable. Energy intake is measured with serial doubly labeled water (DLW) measurements combined with dual x-ray absorptiometry (DXA) to assess changes in fat and lean mass; DLW is also used to measure twenty-four-hour energy expenditure (TEE). Components of TEE including resting energy expenditure (REE) and non-resting and activity energy expenditure (NREE and AEE), as well as skeletal muscle chemomechanical efficiency and grip strength are assessed. Self-reported dietary intake is assessed with interviewer-administered multiple-pass 24-hour food recalls.

Discussion: This manuscript describes the rationale for the methods chosen to assess energy balance and the analytical methods employed to normalize and express data in the setting of changes in body weight and composition immediately following behavioral weight loss and thereafter at 4- and 12-months post-weight loss.

背景/目的：我们在体重减轻状态的生理学（POWERS）研究中提供了能量平衡测量（即能量摄入和能量消耗）的基本原理和描述，旨在了解影响行为减肥后体重恢复的许多因素的贡献。方法：主要的因变量是在7%或更高的监督下体重减轻1年后体重恢复。能量摄入和消耗之间的平衡是体重恢复的主要决定因素。正在招募25- 2岁的健康成年人（目标n = 205）。在减肥前（基线，BL）、减肥后（T0）、减肥后4个月（T4）和12个月（T12）分别测量能量摄入和消耗表型。在BL和T0测量周期前要求重量稳定。从T0到T12的体重变化是主要的结局变量。通过连续双标记水（DLW）测量结合双x线吸收仪（DXA）来测量能量摄入，以评估脂肪和瘦质量的变化；DLW也用于测量24小时能量消耗（TEE）。TEE的组成包括静息能量消耗（REE）和非静息和活动能量消耗（NREE和AEE），以及骨骼肌化学力学效率和握力进行评估。自我报告的饮食摄入量通过访谈者管理的24小时多次食品召回进行评估。讨论：本文描述了所选择的评估能量平衡的方法的基本原理，以及在行为减肥后立即以及减肥后4个月和12个月体重和成分变化的背景下，用于规范化和表达数据的分析方法。

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引用次数: 0

Maternal monosodium glutamate exposure disrupts leptin and insulin signaling in the hypothalamus, activating NF-κB and mTOR inflammatory pathways, contributing to metabolic dysfunction in male offspring 母体暴露于味精会破坏下丘脑的瘦素和胰岛素信号，激活NF-κB和mTOR炎症通路，导致雄性后代代谢功能障碍。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-17 DOI: 10.1038/s41366-025-01941-z

Alshehri Hanan Hassan, Eman Mohamad El Nashar, Norah Saeed Al-Zahrani, Hind Zafrah, Hanan M. A. El Henafy

Maternal nutrition during critical developmental windows is increasingly recognised as a key determinant of offspring health, a concept central to the developmental origins of health and disease paradigm. Monosodium glutamate (MSG), a common food additive and neuroendocrine stimulant, warrants investigation in this context. The impact of maternal MSG exposure (120 mg/kg) during gestation and/or lactation on metabolic programming in first-generation male rat offspring. Metabolic, hormonal, and molecular parameters in pups following maternal MSG administration, body weight, food intake, adiposity, glucose homeostasis (insulin sensitivity and resistance), lipid profiles, oxidative stress markers, and inflammatory mediators were measured. Furthermore, we analyzed microRNA expression profiles in relevant tissues. Maternal MSG exposure resulted in significant metabolic perturbations in offspring. Key findings included a reduced survival index, impaired glucose homeostasis (manifesting as decreased insulin sensitivity and increased insulin resistance), increased body weight, and elevated adiposity. We observed elevated oxidative stress, dyslipidemia, altered lipid peroxidation, and hormonal imbalances. Quantitative PCR analysis revealed altered expression of metabolic and inflammatory genes in both adipocytes and the hypothalamus. MicroRNA expression analysis identified significant alterations in miR-27a, miR-34a, miR-335, and miR-30a, suggesting potential regulatory roles in adipogenesis and metabolic control. Maternal MSG exposure during gestation and lactation induces profound and adverse metabolic effects in male offspring. The observed alterations in metabolic indices suggest an increased risk of metabolic disease later in life. This study underscores the critical importance of maternal nutrition during sensitive developmental periods and has implications for public health recommendations and nutritional guidelines (Graphical abstract).

背景：在关键的发育窗口期间，产妇营养越来越被认为是后代健康的关键决定因素，这是健康和疾病范式的发展起源的核心概念。味精（MSG），一种常见的食品添加剂和神经内分泌兴奋剂，值得在这方面进行调查。方法：研究妊娠期和/或哺乳期母体味精暴露（120 mg/kg）对第一代雄性大鼠后代代谢程序的影响。研究人员测量了母鼠服用味精后的代谢、激素和分子参数、体重、食物摄入、肥胖、葡萄糖稳态（胰岛素敏感性和抵抗）、脂质谱、氧化应激标志物和炎症介质。此外，我们分析了相关组织中的microRNA表达谱。结果：母体接触味精会导致后代显著的代谢紊乱。主要发现包括生存指数降低、葡萄糖稳态受损（表现为胰岛素敏感性降低和胰岛素抵抗增加）、体重增加和肥胖增加。我们观察到氧化应激升高、血脂异常、脂质过氧化改变和激素失衡。定量PCR分析显示脂肪细胞和下丘脑中代谢和炎症基因的表达改变。MicroRNA表达分析发现miR-27a、miR-34a、miR-335和miR-30a显著改变，提示在脂肪形成和代谢控制中具有潜在的调节作用。结论：母体在妊娠期和哺乳期接触味精会对雄性后代产生深远的不良代谢影响。观察到的代谢指标的变化表明，在以后的生活中，代谢性疾病的风险增加。这项研究强调了敏感发育时期产妇营养的至关重要性，并对公共卫生建议和营养指南产生了影响（图形摘要）。

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引用次数: 0

Plasma metabolites may inhibit childhood obesity by regulating ferroptosis through SMPD1 and SIRT3 血浆代谢物可能通过SMPD1和SIRT3调控铁下垂来抑制儿童肥胖。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-17 DOI: 10.1038/s41366-025-01951-x

Ji-Gan Wang, Xiu-Hua Pan, Yan Li

To investigate the causal relationship between plasma metabolites and ferroptosis-related genes in childhood obesity and to explore the potential mediating role of ferroptosis-related genes in the association between plasma metabolites and childhood obesity risk. A bidirectional two-step Mendelian randomization (MR) approach was applied, leveraging publicly available genome-wide association study (GWAS) datasets to analyze the causal relationship among 1400 plasma metabolites, 159 ferroptosis-related genes, and childhood obesity. In the first step, protein quantitative trait loci (pQTL) data corresponding to ferroptosis-related genes were identified as mediators to evaluate the causal effects of plasma metabolites and ferroptosis-related genes on childhood obesity. In the second step, MR analysis was conducted on ferroptosis-related genes and plasma metabolites identified in the first step to confirm their causal association. The inverse-variance weighted (IVW) method was primarily used for meta-analysis, while MR-PRESSO was employed to detect pleiotropy and outliers. Four ferroptosis-related genes (SMPD1 and SIRT3 suppressing obesity, GSTZ1 and ADAMTS13 promoting obesity) and nine plasma metabolites were found to be significantly associated with childhood obesity (six negatively correlated and three positively correlated). Further mediation analysis indicated that the ferroptosis mechanism regulated by SMPD1 and SIRT3 partially mediated the association between specific plasma metabolites and childhood obesity, with the highest mediation proportion reaching 9.62%. Sensitivity analysis confirmed the robustness of the results (no heterogeneity or horizontal pleiotropy), and reverse Mendelian randomization ruled out causal interference. This study is the first to reveal, through Mendelian randomization analysis, the potential mediating role of ferroptosis-related genes in the association between plasma metabolites and childhood obesity. It suggests that the ferroptosis mechanism may influence childhood obesity risk by regulating specific metabolites. These findings contribute to understanding the role of ferroptosis in the pathological mechanisms of childhood obesity and provide novel molecular targets and intervention strategies for obesity prevention and treatment in children.

目的：探讨血浆代谢物与吸铁相关基因在儿童肥胖中的因果关系，探讨吸铁相关基因在血浆代谢物与儿童肥胖风险之间的潜在中介作用。方法：采用双向两步孟德尔随机化（MR）方法，利用公开的全基因组关联研究（GWAS）数据集，分析1400种血浆代谢物、159种铁沉相关基因与儿童肥胖之间的因果关系。第一步，鉴定出与嗜铁相关基因对应的蛋白数量性状位点（pQTL）数据作为介质，评估血浆代谢物和嗜铁相关基因对儿童肥胖的因果关系。第二步，对第一步鉴定的嗜铁相关基因和血浆代谢物进行MR分析，确认两者之间的因果关系。meta分析主要采用逆方差加权法（IVW），多效性和异常值检测采用MR-PRESSO。结果：发现4个凋亡相关基因（SMPD1和SIRT3抑制肥胖，GSTZ1和ADAMTS13促进肥胖）和9个血浆代谢物与儿童肥胖显著相关（6个负相关，3个正相关）。进一步的中介分析表明，SMPD1和SIRT3调控的铁下沉机制部分介导了特定血浆代谢物与儿童肥胖的关联，最高的中介比例可达9.62%。敏感性分析证实了结果的稳健性（无异质性或水平多效性），反向孟德尔随机化排除了因果干扰。结论：本研究首次通过孟德尔随机化分析揭示了嗜铁相关基因在血浆代谢物与儿童肥胖之间的潜在中介作用。提示铁下垂机制可能通过调节特定代谢物影响儿童肥胖风险。这些发现有助于理解铁下垂在儿童肥胖病理机制中的作用，并为儿童肥胖的预防和治疗提供新的分子靶点和干预策略。

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引用次数: 0

Long-term trends in central obesity in England: an age-period-cohort approach. 英格兰中枢性肥胖的长期趋势：一种年龄期队列方法。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-17 DOI: 10.1038/s41366-025-01949-5

Laura A Gray, Magdalena Opazo Breton

Background: Central obesity measures, such as waist circumference (WC), waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR) have previously outperformed body mass index (BMI) in predicting health risks. BMI has been shown to underdiagnose obesity in older adults.

Methods: We used data from the Health Survey for England (2005-2021) for 120,024 individuals aged 11-89 years, born in 1919-2008. High-risk classifications for WC, WHR, WHtR, and BMI were defined using established thresholds (World Health Organisation and the UK National Institute for Health and Care Excellence). Age, period (changes over time), and cohort effects were assessed using logistic regression with grouped variables to address the identification problem inherent in age-period-cohort (APC) models.

Results: The prevalence of high-risk increased over time for all obesity measures. Central obesity measures showed a consistent linear increase with age until around 70 years of age. BMI exhibited an inverted U-shaped age trend. Obesity increased over time across all measures, while there was little evidence for a cohort effect. WHtR trends closely mirrored BMI at the population level but identified different high-risk individuals. The odds of high-risk WHtR increased with age, with odds ratios (OR) 4.91 (95% CI: 1.95-12.39) for females and 6.15 (95% CI: 2.24-16.89) for males by 85-89 years compared to 18-19 years. Period effects for WHtR showed ORs of 1.41 (95% CI: 1.16-1.72) for females and 1.25 (95% CI: 1.01-1.55) for males in 2019-2021 compared to 2005-2006.

Conclusions: Central obesity measures, particularly WHtR, could provide a more consistent reflection of age-related increases in obesity risk. The linear increase in high-risk with age for central obesity measures aligns better with known age-related increases in obesity-related comorbidities. Age plays a significant role in driving obesity trends meaning an aging population could leading to further increases in the prevalence of obesity.

背景：中心性肥胖测量，如腰围（WC）、腰臀比（WHR）和腰高比（WHtR），在预测健康风险方面优于体重指数（BMI）。BMI已被证明对老年人肥胖的诊断不足。方法：我们使用了英格兰健康调查（2005-2021）的数据，涉及120,024名年龄在11-89岁、出生于1919-2008年的个体。使用既定阈值（世界卫生组织和英国国家健康与护理卓越研究所）定义腰围、腰臀比、腰臀比和身体质量指数的高危分类。年龄、时期（随时间的变化）和队列效应使用分组变量的逻辑回归进行评估，以解决年龄-时期-队列（APC）模型固有的识别问题。结果：在所有肥胖测量中，高危人群的患病率随着时间的推移而增加。中心性肥胖测量显示，直到70岁左右，随着年龄的增长，肥胖率呈线性增长。BMI呈倒u型年龄趋势。在所有测量中，肥胖都随着时间的推移而增加，但几乎没有证据表明存在队列效应。WHtR趋势密切反映了人群水平的BMI，但确定了不同的高危个体。与18-19岁相比，85-89岁女性的比值比（OR）为4.91 (95% CI: 1.95-12.39)，男性的比值比（OR）为6.15 (95% CI: 2.24-16.89)，高危WHtR的几率随年龄增加而增加。与2005-2006年相比，2019-2021年女性WHtR的周期效应or为1.41 (95% CI: 1.16-1.72)，男性为1.25 （95% CI: 1.01-1.55）。结论：中心性肥胖测量，特别是腰宽比，可以更一致地反映年龄相关的肥胖风险增加。在中心肥胖测量中，高风险随年龄的线性增加与已知的肥胖相关合并症的年龄相关增加更一致。年龄在推动肥胖趋势方面起着重要作用，这意味着人口老龄化可能会导致肥胖患病率进一步上升。

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引用次数: 0

Weight loss normalizes plasma and adipose tissue vitamin D metabolism, and gene expression involved in the vitamin D metabolism in male mice with obesity 体重减轻使肥胖雄性小鼠血浆和脂肪组织维生素D代谢以及参与维生素D代谢的基因表达正常化。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-15 DOI: 10.1038/s41366-025-01953-9

Lauriane Bonnet, Amine Hachemi, Esma Karkeni, Charlène Couturier, Julien Astier, Catherine Defoort, Ljubica Svilar, Franck Tourniaire, Jean-Charles Martin, Jean-François Landrier

Obesity has consistently been linked to lower circulating total and free 25-hydroxyvitamin D (25(OH)D), and weight loss has been shown to enhance 25(OH)D levels in individuals with obesity. We examined whether weight loss would alter total and free 25(OH)D in a mouse model of diet-induced obesity, with controlled cholecalciferol intake. Mice were fed either a low-fat (LF, n = 10) or a high-fat diet (HF, n = 20). After 7 weeks, half of the HF group transitioned to a low-fat diet (HF/LF) for 5 weeks, while the other mice maintained the same diet. The HF diet for 12 weeks increased body weight, adiposity, total 25(OH)D, and PTH plasma concentrations while reducing free 25(OH)D and cholecalciferol plasma levels. The LF-fed switch in mice resulted in a decrease in body weight. By the end of the experiment, HF/LF mice were comparable to LF animals in terms of total body weight, adiposity, and plasma PTH concentration. Interestingly, weight loss normalized most parameters related to vitamin D metabolism, including adipose tissue cholecalciferol and 25(OH)D content, as well as plasma total and free 25(OH)D; however, plasma cholecalciferol levels appeared reduced in the plasma of HF/LF mice compared to LF mice. The expression of genes related to vitamin D metabolism indicated that renal and adipose tissue uptake of protein-bound vitamin D was altered in HF/LF, which may partially explain the decrease in plasma cholecalciferol after weight loss. The data demonstrate the overall reversibility of the changes induced by diet-induced obesity in vitamin D metabolism; however, they also highlight that some parameters may be impacted chronically.

背景：肥胖一直与循环总25-羟基维生素D （25(OH)D）和游离25-羟基维生素D （25(OH)D）降低有关，体重减轻已被证明可提高肥胖个体的25(OH)D水平。在控制胆骨化醇摄入量的饮食性肥胖小鼠模型中，我们研究了体重减轻是否会改变总25(OH)D和游离25(OH)D。方法：小鼠分别饲喂低脂（LF, n = 10）和高脂（HF, n = 20）饮食。7周后，HF组一半的小鼠过渡到低脂饮食（HF/LF） 5周，而其他小鼠保持相同的饮食。结果：12周的HF饮食增加了体重、肥胖、总25(OH)D和PTH血浆浓度，同时降低了游离25(OH)D和胆骨化醇血浆水平。在小鼠中，低脂喂养的开关导致体重下降。实验结束时，HF/LF小鼠在总体重、脂肪和血浆甲状旁腺激素浓度方面与LF动物相当。有趣的是，体重减轻使大多数与维生素D代谢相关的参数正常化，包括脂肪组织胆骨化醇和25(OH)D含量，以及血浆总25(OH)D和游离25(OH)D；然而，与LF小鼠相比，HF/LF小鼠血浆中胆骨化醇水平明显降低。维生素D代谢相关基因的表达表明，HF/LF患者肾脏和脂肪组织对蛋白结合维生素D的摄取发生了改变，这可能部分解释了体重减轻后血浆胆骨化醇的下降。结论：饮食性肥胖引起的维生素D代谢变化具有总体可逆性；然而，他们也强调了一些参数可能会长期受到影响。

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引用次数: 0

Bridging the nutrition guidance gap for GLP-1 receptor agonist therapy assisted weight loss: lessons from bariatric surgery 弥合GLP-1受体激动剂治疗辅助减肥的营养指导差距：来自减肥手术的经验教训。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-15 DOI: 10.1038/s41366-025-01952-w

Marie Spreckley, Cara F. Ruggiero, Adrian Brown

引用次数: 0

Prediabetes as an indication for GLP-1 therapy. Clarifying evidence thresholds and clinical guardrails 糖尿病前期作为GLP-1治疗的适应症。明确证据阈值和临床护栏。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-15 DOI: 10.1038/s41366-025-01959-3

Jian-Ying Wang

引用次数: 0

Maternal pre-pregnancy body mass index and the risk of neurodevelopmental disorders in offspring 孕妇孕前体重指数与后代神经发育障碍的风险。

IF 3.8 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

International Journal of Obesity

Pub Date : 2025-11-15 DOI: 10.1038/s41366-025-01955-7

Hye Won Park, Tae-Eun Kim, Sanghyun Park, Yoo Jinie Kim, Jinyoung Shin

The global increase in maternal obesity has raised concerns regarding its potential impact on offspring neurodevelopment. This study investigated the association between maternal pre-pregnancy body mass index (BMI) and the risk of neurodevelopmental disorders in offspring using a large-scale national cohort in South Korea. We conducted a retrospective cohort study using data from the Korean National Health Information Database merged with the National Health Screening Program data. Maternal BMI, measured within three years prior to delivery, was categorized based on the Asia-Pacific guidelines. Neurodevelopmental disorders, including epilepsy, cerebral palsy, intellectual disability, autism spectrum disorder, and attention-deficit/hyperactivity disorder, were identified using diagnostic codes from the International Classification of Diseases, Tenth Revision (ICD-10) up to five years of age. Multivariable Poisson and Cox regression models were used to estimate the relative risks and hazard ratios, adjusting for neonatal and maternal covariates. This study analyzed a cohort of 2,285,943 live births in South Korea (January 1, 2014–December 31, 2021) to assess the association between maternal pre-pregnancy BMI and neurodevelopmental disorders in offspring. After excluding neonates lacking complete medical records or follow-up data, 779,091 neonates were included in the study. Maternal obesity (BMI ≥ 30.0) was independently associated with an elevated risk of epilepsy (adjusted hazard ratio 1.13; 95% CI, 1.08–1.18) and intellectual disability (aHR 1.37; 95% CI, 1.12–1.68), following adjustment for neonatal and maternal covariates. Maternal underweight status (BMI < 18.5) was not significantly associated with neurodevelopmental outcomes. Elevated maternal BMI prior to conception was independently associated with an increased risk of epilepsy and intellectual disability in offspring. The results underscore the importance of preconception weight management and support public health strategies to reduce neurodevelopmental disorders in children of mothers with overweight or obesity.

背景：全球孕产妇肥胖的增加引起了人们对其对后代神经发育的潜在影响的关注。本研究在韩国进行了一项大规模的国家队列研究，调查了母亲孕前体重指数（BMI）与后代神经发育障碍风险之间的关系。方法：我们进行了一项回顾性队列研究，数据来自韩国国家健康信息数据库和国家健康筛查计划数据。产妇在分娩前三年内测量的BMI指数是根据亚太指南进行分类的。神经发育障碍，包括癫痫、脑瘫、智力残疾、自闭症谱系障碍和注意力缺陷/多动障碍，使用国际疾病分类第十版（ICD-10）中的诊断代码进行鉴定，年龄为5岁。多变量泊松和Cox回归模型用于估计相对风险和风险比，调整新生儿和产妇协变量。结果：本研究分析了韩国2,285,943例活产婴儿（2014年1月1日- 2021年12月31日）的队列，以评估母亲孕前BMI与后代神经发育障碍之间的关系。排除缺乏完整医疗记录或随访资料的新生儿后，共有779,091名新生儿纳入研究。孕妇肥胖（BMI≥30.0）与癫痫（校正危险比1.13,95% CI 1.08-1.18）和智力残疾（aHR 1.37, 95% CI 1.12-1.68）风险升高独立相关，校正后为新生儿和孕妇协变量。结论：研究结果强调了孕前体重管理的重要性，并支持公共卫生策略，以减少超重或肥胖母亲所生儿童的神经发育障碍。

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引用次数: 0