Obesity最新文献

{"title":"Tirzepatide for the Maintenance of Body Weight Reduction: Rationale, Design, and Baseline Characteristics of SURMOUNT-MAINTAIN","authors":"Deborah B. Horn,&nbsp;Louis J. Aronne,&nbsp;Sean Wharton,&nbsp;Harold E. Bays,&nbsp;Elisa Gomez-Valderas,&nbsp;Avigdor D. Arad,&nbsp;Palash Sharma,&nbsp;Julia P. Dunn,&nbsp;Cagri Senyucel,&nbsp;Clare J. Lee","doi":"10.1002/oby.70014","DOIUrl":"10.1002/oby.70014","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>SURMOUNT-MAINTAIN aims to evaluate the efficacy and safety of reducing the tirzepatide dose and/or continuing the maximum tolerated dose (MTD) versus placebo in maintaining body weight (BW) reduction achieved with tirzepatide MTD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This Phase 3b, multicenter, randomized, parallel-arm, double-blinded, placebo-controlled, 52-week clinical trial is in progress comparing treatment with once weekly tirzepatide (5 mg and/or MTD of 15 mg or 10 mg) versus placebo in achieving BW reduction maintenance from the initial 60-week open-label weight-loss period on tirzepatide MTD, in adults with obesity (BMI ≥ 30 kg/m² or ≥ 27 kg/m² with ≥ 1 obesity-related comorbidity, excluding type 2 diabetes). The primary endpoint is percent maintenance of BW reduction achieved during the weight-loss period at Week 112 among those who reached a BW plateau (i.e., &lt; 5% BW change) between Weeks 48 and 60.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Participants are mostly female (65%) with a mean ± SD age of 47 ± 13 years, BW 114 ± 27 kg, BMI 40 ± 8 kg/m², and waist circumference 119 ± 18 cm.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The SURMOUNT-MAINTAIN trial will evaluate whether reducing or continuing the tirzepatide dose as a long-term treatment option may help maintain the reduced BW initially achieved with tirzepatide MTD versus switching to placebo. Combined, this study may provide additional evidence to help tailor patient-centered strategies for maintenance of BW reduction in adults living with obesity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>ClinicalTrials.gov identifier: NCT06047548</p>\u0000 \u0000 <div>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"1873-1885"},"PeriodicalIF":4.7,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.70014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016912","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}

{"title":"Projecting Global Trends and Inequalities in Adult Overweight and Obesity, 2023–2040: Findings From the NCD-RisC Database","authors":"Jinli Liu,&nbsp;Zeping Fang,&nbsp;Qianhui Lu,&nbsp;Yanan Wang,&nbsp;Lei Zhang","doi":"10.1002/oby.24358","DOIUrl":"10.1002/oby.24358","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study quantifies the global burden of overweight and obesity, projects future trends, and examines associated health inequalities.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Overweight and obesity burden data were obtained from the NCD-RisC database. Trends from 1990 to 2022 were analyzed, and a Bayesian model was used to project changes for 2023–2040. Cross-national health inequalities were measured using the slope index of inequality (SII) and the relative concentration index (RCI).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Globally, overweight prevalence rose from 17.50% in 1990 to 28.00% in 2022 (average annual percentage change [AAPC] = 1.48%) and is projected to reach 43.97% by 2040 (AAPC = 1.13%). Obesity prevalence grew from 6.44% to 16.06% (AAPC = 2.46%) and is projected to surge to 38.96% by 2040 (AAPC = 4.96%). The SII for overweight burden dropped from 33.74% in 1990 to 16.24% in 2022, and it is projected to reverse to −2.42% by 2040. For obesity (BMI, ≥ 30.0 kg/m²) and mild obesity (BMI, 30.0–34.9 kg/m²), the SII declined from 20.12% to 18.58% and from 14.22% to 10.02%, respectively, with further drops to 9.35% and −1.70% by 2040. From 1990 to 2040, the share of the global prevalence burden of overweight and obesity in countries with the lowest GDP per capita rose from 15% to 22% and from 6% to 26%, respectively. The relative gradient inequality, measured by RCI, also showed similar findings.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The global burden of overweight and obesity has significantly increased from 1990 to 2040. Health inequalities decreased from 1990 to 2022, with the burden mainly in higher-income countries. However, by 2040, the burden of overweight and mild obesity is projected to shift to lower-income countries, highlighting the need for targeted health policies and interventions.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"1955-1967"},"PeriodicalIF":4.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.24358","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144983463","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}

{"title":"The Role of p53 in Adipocyte Differentiation and Lipid Metabolism in Obese Mice via Transcriptional Regulation of Lgals3","authors":"Huarui Li,&nbsp;Zhengze Yv,&nbsp;Shihua Tan,&nbsp;Peihua Li,&nbsp;Ning Jiang,&nbsp;Fenglin Peng","doi":"10.1002/oby.24363","DOIUrl":"10.1002/oby.24363","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study investigates the regulatory role of p53 on Lgals3 expression and its impact on preadipocyte differentiation, fatty acid synthesis, and oxidation in obesity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Bioinformatics analysis of six obesity-related microarray datasets and single-cell RNA sequencing (scRNA-seq) data identified Lgals3 as a key obesity-associated gene. A high-fat diet (HF) mouse model was established to evaluate obesity-related phenotypes, including body weight, hepatic Lgals3 expression, adipose tissue pathology, blood lipid profiles, and glucose tolerance. In vitro experiments using 3T3-L1 cells were conducted to assess adipocyte differentiation, fatty acid synthase (FAS) activity, and glucose uptake. The interaction between p53 and the Lgals3 promoter was analyzed via dual-luciferase reporter and chromatin immunoprecipitation assays. Key metabolic genes and proteins were quantified by RT-qPCR and Western blot.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>HF mice exhibited significant weight gain, elevated Lgals3 expression, and altered lipid profiles. In vitro, p53 was shown to transcriptionally repress Lgals3, thereby reducing adipocyte differentiation, FAS activity, and glucose uptake. In vivo, p53 overexpression led to downregulation of Lgals3 and improvement in obesity-related metabolic outcomes, whereas Lgals3 overexpression counteracted these effects.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>p53 inhibits Lgals3 expression, suppressing adipocyte differentiation and improving obesity-related metabolic dysfunction, highlighting its potential as a therapeutic target in obesity management.</p>\u0000 \u0000 <div>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"1895-1908"},"PeriodicalIF":4.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.24363","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144984081","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}

{"title":"FGF21 and GDF15 Act Synergistically to Regulate Systemic Metabolic Homeostasis in Mice Lacking OPA1 in Thermogenic Adipocytes","authors":"Joshua Peterson,&nbsp;Jayashree Jena,&nbsp;Ayushi Sood,&nbsp;Shelly Roitershtein,&nbsp;David Smith,&nbsp;Renata O. Pereira","doi":"10.1002/oby.70004","DOIUrl":"10.1002/oby.70004","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Our previous studies showed that mice lacking the mitochondrial fusion protein optic atrophy 1 (OPA1 BKO) in brown adipose tissue (BAT) have high metabolic rates and are resistant to diet-induced obesity (DIO) via effects partially mediated by independent actions of fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15) secretion from BAT. We examined whether FGF21 and GDF15 act synergistically, contributing to the systemic metabolic adaptations reported in OPA1 BKO mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We generated mice simultaneously lacking the <i>Opa1</i>, <i>Fgf21</i>, and <i>Gdf15</i> genes in thermogenic adipocytes (TKO) and assessed energy homeostasis and glucose metabolism after regular chow or high-fat diet feeding.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Young TKO mice fed regular chow had impaired glucose tolerance, while insulin sensitivity was unchanged. Notably, combined <i>Fgf21</i> and <i>Gdf15</i> deletion in OPA1 BKO significantly blunted the resistance to DIO and insulin resistance observed in OPA1 BKO mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>FGF21 and GDF15 act synergistically to maintain glucose homeostasis and promote resistance to DIO in mice lacking OPA1 in BAT, highlighting the potential of combined therapies using FGF21 and GDF15 for the treatment of metabolic disorders.</p>\u0000 \u0000 <div>\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"1909-1920"},"PeriodicalIF":4.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.70004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144984430","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}

{"title":"Real-World Efficacy and Safety of Setmelanotide in Adults With Monogenic or Syndromic Obesity: A Prospective Cohort Study","authors":"Francois Mifsud,&nbsp;Sarah Chalopin,&nbsp;Emilie Guillon,&nbsp;Pauline Faucher,&nbsp;Jean Muller,&nbsp;Johanne Le Bihan,&nbsp;Karine Clément,&nbsp;Christine Poitou","doi":"10.1002/oby.70002","DOIUrl":"10.1002/oby.70002","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The melanocortin-4 receptor agonist setmelanotide has demonstrated effectiveness in phase 3 clinical trials for patients with monogenic obesity caused by biallelic variants in the leptin receptor (LEPR) and pro-opiomelanocortin (POMC), as well as for individuals with Bardet–Biedl syndrome (BBS). However, real-world evidence remains limited. This study evaluates the long-term effectiveness and safety of setmelanotide in patients who received treatment under a pre-marketing early-access authorization.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This ongoing prospective monocentric cohort includes 17 patients with obesity due to BBS (<i>n</i> = 11) or biallelic variants in <i>LEPR</i> (<i>n</i> = 4) or <i>POMC</i> (<i>n</i> = 2) who either started setmelanotide in routine care between 2022 and 2024 or continued therapy after participating in the RM-493-022 clinical trial. The average follow-up time was 14.4 months.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Patients experienced a clinically significant weight reduction of 20% from their highest pre-treatment weight within the first year. Those previously treated in a clinical trial maintained their weight loss over time. Additionally, eating behavior improved, with significant reductions in hunger (−62%), food craving (−41%), and external eating evaluated by DEBQ. The overall safety profile was consistent with phase 3 trials data, without any new safety signals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These findings confirm the drug's long-term clinical benefit and safety profile in a routine-care setting.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"1865-1872"},"PeriodicalIF":4.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144983688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of Metal Mixtures During Early Pregnancy With Midlife Obesity and Body Composition: A Prospective Study","authors":"Mingyu Zhang,&nbsp;Izzuddin M. Aris,&nbsp;Andres Cardenas,&nbsp;Sheryl L. Rifas-Shiman,&nbsp;Pi-I Debby Lin,&nbsp;Long H. Ngo,&nbsp;Emily Oken,&nbsp;Stephen P. Juraschek,&nbsp;Marie-France Hivert","doi":"10.1002/oby.24368","DOIUrl":"10.1002/oby.24368","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To examine the prospective associations of metal mixtures during pregnancy with midlife adiposity and explore metal-folate interactions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In 500 participants from Project Viva, we measured six non-essential metals (arsenic, barium, cadmium, cesium, mercury, and lead) and five essential metals (copper, magnesium, manganese, selenium, and zinc) in red blood cells and folate in plasma collected during early pregnancy (mean gestational age: 10.0 weeks; mean age: 32.9 years). We assessed midlife (mean age: 51.2 years) adiposity using BMI and dual-energy X-ray absorptiometry (DXA) measures. We used multivariable-adjusted linear and multinomial logistic regression models to analyze individual exposures and Bayesian kernel machine regression to examine exposure mixtures.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Higher arsenic, cesium, and mercury levels were associated with lower midlife DXA percentage fat, total fat mass index, and/or trunk fat mass index, even after adjustments for diet in pregnancy. We observed an antagonistic interaction between folate and arsenic: arsenic was associated with higher obesity risk at lower folate levels but lower obesity risk at higher folate levels. The essential metal mixture tended to be associated with lower midlife BMI and obesity risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Higher pregnancy levels of arsenic, cesium, mercury, and the mixture of essential metals were associated with lower midlife adiposity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"1984-1994"},"PeriodicalIF":4.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144984421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alcoholic Use Disorder Outcomes After Roux-en-Y Gastric Bypass in Patients Taking GLP-1 RAs: A Multicenter Analysis","authors":"Olanrewaju Adeniran,&nbsp;Luis M. Nieto,&nbsp;Chima Amadi,&nbsp;Katherine Shepherd,&nbsp;Joshua Kirkpatrick,&nbsp;Kanith Farah,&nbsp;Farirai Marwizi,&nbsp;Budoor Alqinai,&nbsp;Sharon I. Narvaez,&nbsp;Samuel Mensah,&nbsp;Ayowumi Adekolu,&nbsp;Ethan M. Cohen,&nbsp;Raja S. Khan,&nbsp;Swapna Gayam,&nbsp;Lawrence E. Tabone,&nbsp;Laura Davisson","doi":"10.1002/oby.70001","DOIUrl":"10.1002/oby.70001","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Roux-en-Y gastric bypass (RYGB) has been linked with increased alcohol-related outcomes, whereas glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have been associated with reduced risks. We performed the first multicenter retrospective cohort study to identify alcohol use outcomes of GLP-1 RAs post RYGB.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using TriNetX, adults (≥ 18 years old) with obesity (BMI ≥ 30 kg/m²) who underwent RYGB between January 1, 2019, and May 31, 2023, were identified. Two cohorts were analyzed: patients initiated on GLP-1 RA versus non-GLP-1 RA users. Patients with other liver diseases and other bariatric surgeries were excluded. Covariates were balanced via propensity score matching (PSM). Participants were followed for at least 1 year post RYGB and GLP-1 RA initiation. Outcomes include the risk of alcohol use disorders (AUD), alcohol liver diseases (ALD), and all-cause mortality. Hazard ratio (HR) was calculated through Cox regression analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>After PSM, 3438 were matched in each cohort. GLP-1 RA initiation was associated with a reduced incidence rate of AUD versus control (1.1% vs. 1.8%) (HR 0.77, [95% CI: 0.549–0.840, <i>p</i> = 0.041]) and all-cause mortality (1.2% versus 3.9%) (HR 0.497, [95% CI: 0.346–0.715, <i>p</i> = 0.039]).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Post RYGB, GLP-1 RAs provide the potential to reduce AUD and all-cause mortality.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"1886-1894"},"PeriodicalIF":4.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144984427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multimodal Neuroimaging of Brain Structure, Metabolism, and Function in Obesity: Current Landscape and Future Perspectives","authors":"Tao Ju,&nbsp;Zhen Li,&nbsp;Xiaozu Zhang,&nbsp;Yang Liu,&nbsp;Xiaotian Gao,&nbsp;Haimo Zhang,&nbsp;Xizhen Wang,&nbsp;Xiaodong Sun,&nbsp;Xiaoli Wang","doi":"10.1002/oby.24353","DOIUrl":"10.1002/oby.24353","url":null,"abstract":"<div>\u0000 \u0000 <p>Obesity is a systemic disease that not only increases the incidence of diabetes and cardiovascular disease but also contributes to central nervous system disorders such as cognitive impairment, depression, and anxiety. Neuroimaging studies have confirmed that obesity leads to various forms of brain damage, as well as abnormalities in the function and metabolism of different brain regions. Multimodal neuroimaging, a collection of detection tools capable of visualizing neural diseases, has shown potential in diagnosing various brain disorders, and it provides insights from multiple perspectives to explore the pathological mechanisms of brain damage associated with obesity. Structural imaging techniques within multimodal imaging have identified changes in the volume and microstructure of the brain's gray and white matter. Functional imaging has detected abnormal activation and disrupted circuits in specific brain regions, while metabolic imaging has revealed neurochemical changes in the brain. In this review, we provide an overview of multimodal neuroimaging in obesity-related brain diseases, systematically analyzing these diseases from three aspects: structure, metabolism, and function. Additionally, we introduce novel multimodal imaging techniques that hold potential but have not yet been applied to obesity-related studies, aiming to provide a theoretical foundation for future clinical diagnosis and treatment.</p>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"1833-1844"},"PeriodicalIF":4.7,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144984456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evolution of multidisciplinary obesity treatments: past, present, and future role of nutrition","authors":"Steven B. Heymsfield,&nbsp;Philip J. Atherton,&nbsp;Sandra Christensen,&nbsp;Colleen Tewksbury,&nbsp;Amanda Velazquez,&nbsp;Jens Walter,&nbsp;Ellen E. Blaak","doi":"10.1002/oby.24340","DOIUrl":"10.1002/oby.24340","url":null,"abstract":"<p>Obesity is a complex chronic disease requiring lifelong comprehensive treatment. In addition to lifestyle counseling that improves nutrition and physical activity, a promising new generation of obesity medications has been added to bariatric procedures as therapeutic options to achieve weight reduction and improve health outcomes. With the promise of effective and safe treatments comes the need to emphasize maximal reduction of body fat and minimal loss of vital body components, including skeletal muscle and bone. Nutrition is a critical aspect of obesity care and is leveraged to support preservation of lean tissues, such as skeletal muscle, through adequate, daily, high-quality protein intake and intake of key micronutrients. More targeted nutrition approaches that promote muscle protein synthesis include amino acid supplementation with leucine and its metabolite β-hydroxy β-methylbutyrate. Another potential target for support is the gut microbiome, as its adequate function is increasingly seen as playing a role in human health and metabolism. Obesity is a heterogenous disease, and there is considerable interest in specific metabolic phenotypes that might be used to tailor nutrition strategies. As research advances on these and other fronts, there is the potential to identify precision nutrition strategies for individualized, more effective approaches to lifelong obesity management.</p>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"1819-1832"},"PeriodicalIF":4.7,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.24340","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144884705","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}

{"title":"Correction to “MicroRNA Profiling in Adipose Before and After Weight Loss Highlights the Role of miR-223-3p and the NLRP3 Inflammasome”","authors":"","doi":"10.1002/oby.70007","DOIUrl":"10.1002/oby.70007","url":null,"abstract":"<p>\u0000 \u0000 <span>Macartney-Coxson, D.</span>, <span>Danielson, K.</span>, <span>Clapham, J.</span>, et al., “ <span>MicroRNA Profiling in Adipose Before and After Weight Loss Highlights the Role of miR-223-3p and the NLRP3 Inflammasome</span>,” <i>Obesity</i> <span>28</span> (<span>2020</span>): <span>570</span>–<span>580</span>, https://doi.org/10.1002/oby.22722.\u0000 </p><p>In Table 2 of this article, the headings for columns 3 and 6 and footnote “a” are incorrect.</p><p>Below is the correct Table 2.</p><p>In addition, in the <i>Methods</i> section, under the heading \"Differential expression analysis of miRNA arrays,\" the text should read: “Fold change was calculated using 2^{absolute log2FC}. Decreased fold change (i.e. less expression after vs. before gastric bypass) is represented as −2^{absolute log2FC}.”</p><p>Under the \"RT-qPCR\" heading, in two instances, the text should read: “Fold change in expression between time points was calculated for each paired sample using 2^−ΔΔCt. For values &lt; 1 (indicating a decrease in gene expression after vs. before gastric bypass and weight loss) the negative reciprocal of 1/2^−ΔΔCt was calculated. Mean relative fold change for a given tissue and gene was calculated using each of these individual fold change values from the paired samples.”</p><p>We apologize for these errors.</p>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"33 10","pages":"2014-2015"},"PeriodicalIF":4.7,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.70007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144884694","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}