Journal of Obesity最新文献

{"title":"Association Between Metabolic Syndrome and Incident Cervical Cancer: A Retrospective Cohort Study.","authors":"Linjun Jiang, Akira Okada, Risa Ishida, Hideo Yasunaga","doi":"10.1155/jobe/3691654","DOIUrl":"10.1155/jobe/3691654","url":null,"abstract":"<p><strong>Objective: </strong>To determine whether metabolic syndrome is associated with an elevated risk of cervical cancer.</p><p><strong>Methods: </strong>We retrospectively analyzed data on 1,410,650 women without a history of cancer, using the JMDC Claims Database, a nationwide epidemiological database in Japan, between 2005 and 2022. The look-back period was set at 2 years. Cox regression analyses were conducted to assess cervical cancer risk associated with metabolic syndrome and its components (waist circumference, blood pressure, triglycerides, high-density lipoprotein cholesterol, and fasting plasma glucose). Further, we conducted age-stratified analyses.</p><p><strong>Results: </strong>Metabolic syndrome was diagnosed in 43,029 participants (median age: 53 years), and 1579 cervical cancer cases were recorded over a median follow-up of 942 days. Multivariable Cox regression analyses showed that metabolic syndrome was associated with a higher cervical cancer incidence (hazard ratio [HR], 1.38; 95% confidence interval [CI], 1.04-1.82). Among the metabolic factors, cancer risk was associated with higher plasma glucose (per 10 mg/dL increase) (HR, 1.04; 95% CI, 1.01-1.08) and lower high-density lipoprotein cholesterol levels (per 10 mg/dL decrease) (HR, 1.06; 95% CI, 1.02-1.10), whereas waist circumference, blood pressure, or triglyceride levels showed no significant relationship. Metabolic syndrome was associated with an increased risk of cervical cancer, with a stronger association observed in younger women in age-stratified analyses (<i>p</i> for interaction = 0.004).</p><p><strong>Conclusion: </strong>Metabolic syndrome was associated with an increased risk of cervical cancer, with a stronger association observed among younger women. Elevated plasma glucose and low high-density lipoprotein cholesterol levels were identified as significant contributing factors.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"3691654"},"PeriodicalIF":3.9,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12500346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Determinants Associated With Obesity in Children of Low Socioeconomic Status Families: A Narrative Review.","authors":"Zeena Harakeh, Wilma Otten, Pepijn van Empelen","doi":"10.1155/jobe/4992624","DOIUrl":"10.1155/jobe/4992624","url":null,"abstract":"<p><p>Children of families with low socioeconomic status (SES) are at higher risk for obesity and obesity-related lifestyle behaviors, i.e., unhealthy eating and low physical activity. This review aims to identify changeable determinants of obesity and obesity-related lifestyle behaviors in children aged 0-12, with a focus on those specific to low SES. A literature search was conducted in PsycINFO/Ovid and PubMed, using terms related to SES, obesity, and individual or environmental determinants. We included 42 systematic review/meta-analysis articles, written in English, that focused on children (0-12 years) and assessed obesity or obesity-related lifestyle behavior outcomes. We extracted modifiable individual and environmental determinants, and the role of SES in their association with obesity and obesity-related lifestyle behaviors in children. Nine reviews examined the relationship between determinants and obesity and obesity-related lifestyle behaviors in children, and the role of SES. These reviews focused mainly on environmental determinants (<i>n</i> = 8), particularly family and peer factors (<i>n</i> = 6). The findings suggest that SES may influence obesity and lifestyle behaviors indirectly through parental factors, such as parental BMI, maternal smoking during pregnancy, and parental TV viewing behaviors. SES may also moderate the impact of parental factors, such as parental BMI, maternal depression, or permissive/indulgent parenting. Our review showed that research on determinants of obesity and obesity-related lifestyle behaviors of children with low SES is limited, with scarce and inconsistent evidence and lacking theoretical explanations. The (parent-related) mechanisms which influence child obesity in families with low SES are still unclear. To develop effective (family) interventions to prevent or decrease obesity in children of families with low SES, future research needs to examine individual and environmental determinants and underlying mechanisms through which SES has its influence on childhood obesity.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"4992624"},"PeriodicalIF":3.9,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12496157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MRI-Based Genetic Studies Reveal Specific Genetic Variants and Disease Risks Associated With Fat Distribution Across Anatomical Sites.","authors":"Altayeb Ahmed, Madeleine Cule, Afreen Naz, Marjola Thanaj, Elena P Sorokin, Chiemela S Odoemelam, Brandon Whitcher, Naveed Sattar, Jimmy D Bell, E Louise Thomas, Hanieh Yaghootkar","doi":"10.1155/jobe/7792701","DOIUrl":"10.1155/jobe/7792701","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the genetic determinants of fat distribution across anatomical sites and their implications for health outcomes. <b>Methods:</b> We analyzed neck-to-knee MRI data from the UK Biobank (<i>n</i> = 37,589) to measure fat at various locations and used Mendelian randomization to assess effects on 26 obesity-related diseases and 94 biomarkers from FinnGen and other consortia. <b>Result:</b> We identified genetic loci associated with 10 fat depots: abdominal subcutaneous adipose tissue (<i>n</i> = 2 loci), thigh subcutaneous adipose tissue (25), thigh intermuscular adipose tissue (15), visceral adipose tissue (7), liver proton density fat fraction (PDFF) (8), pancreas PDFF (11), paraspinal adipose tissue (9), pelvic bone marrow fat (28), thigh bone marrow fat (27), and vertebrae bone marrow fat (5). Genetically higher abdominal subcutaneous adipose tissue was associated with an adverse metabolic profile and higher risks of Type 2 diabetes, and cardiovascular outcomes. Conversely, higher thigh subcutaneous adipose tissue was associated with a favorable profile and lower risks of Type 2 diabetes and cardiovascular outcomes. Higher visceral adipose tissue was associated with gallstones; higher liver PDFF was associated with elevated tyrosine levels, higher Type 2 diabetes risk, and fatty liver disease; pancreas PDFF was associated with thrombotic events; and thigh bone marrow fat was associated with osteoporosis. <b>Conclusion:</b> These results further suggest a unique contribution of fat deposition in different anatomical locations to disease risk, emphasizing the potential, beyond weight loss per se, for future research into depot-specific therapeutic strategies.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"7792701"},"PeriodicalIF":3.9,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12414625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Weight Loss Efficacy of Tirzepatide Compared to Placebo or GLP-1 Receptor Agonists in Adults With Obesity or Overweight: A Meta-Analysis of Randomized Controlled Trials With ≥ 20 Weeks Treatment Duration.","authors":"Alhussain Khawaji, Abdulaziz A Jaly, Hanan A Bakri, Renju Ravi, Ahmed Hattan, Abdullah Khawaji, Wael Najmi","doi":"10.1155/jobe/3442754","DOIUrl":"10.1155/jobe/3442754","url":null,"abstract":"<p><p><b>Introduction:</b> Tirzepatide, a dual glucose-dependent insulinotropic peptide (GIP) and glucagon-like Peptide 1 (GLP-1) analogue, is a novel medication with comparable pharmacological characteristics and has demonstrated promising weight reduction outcomes in its antidiabetic trials following the approval of liraglutide and semaglutide for long-term weight control. Nonetheless, this efficacy has not been fully explored, so this meta-analysis was aimed to measure the weight loss efficacy and safety of tirzepatide in adults with overweight or obesity. <b>Methods:</b> We searched the PubMed, Cochrane, and Embase databases for RCTs of once-weekly tirzepatide vs. placebo or GLP-1 receptor agonists. We included studies involving adult participants who were overweight or obese despite T2DM or OHA use, with a trial duration of at least 20 weeks. The primary outcomes accounted for the mean difference in weight from baseline in the three doses of tirzepatide compared to placebo and GLP-1 receptor agonists, separately. The secondary outcomes included safety profiles and achievement of categorical weight loss of 5%, 10% and 15%. We performed the statistical analysis on RevMan 5.4, GRADE assessment using GRADEpro GDT and the quality of the included studies assessed using the Cochrane risk-of-bias (Version 2) tool. <b>Results:</b> We identified six RCTs in which the data of 6266 subjects were analysed. Once-weekly doses (5, 10 and 15 mg) of tirzepatide were more effective than placebo and GLP-1 RAs. Also, the proportion of patients achieving categorical weight loss goals was higher in the tirzepatide groups than in others. GRADE assessment also indicated high-certainty evidence for ≥ 15% weight loss with tirzepatide and moderate-to-low certainty for lower thresholds. Gastrointestinal side effects appeared similar between the three doses of tirzepatide and GLP-1 RAs, but they were significantly higher than placebo might impact tolerability for certain patients. <b>Conclusion:</b> A dose-dependent tirzepatide was superior to placebo and GLP-1 RAs in weight reduction. However, the lean mass reduction and tolerability require further investigation. <b>Trial Registration:</b> ClinicalTrials.gov identifier: NCT04255433.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"3442754"},"PeriodicalIF":3.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12313391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Landscape of Obesity in Children: Research Advances and Prospects.","authors":"Rita Khusainova, Ildar Minniakhmetov, Olga Vasyukova, Bulat Yalaev, Ramil Salakhov, Darya Kopytina, Raisat Guseinova, Ekaterina Dobreva, Galina Melnichenko, Ivan Dedov, Natalia Mokrysheva","doi":"10.1155/jobe/9186826","DOIUrl":"10.1155/jobe/9186826","url":null,"abstract":"<p><p>Obesity is a chronic metabolic disease characterized by excessive accumulation or uneven distribution of fat in the body, which poses a serious threat to health. Obesity significantly increases the risk of developing сonditions such as type 2 diabetes, coronary heart disease, hypertension, obstructive sleep apnea, and some types of cancer. The prevalence of obesity, especially in childhood, has increased significantly worldwide over the past few decades. The World Health Organization predicts that 250 million children and adolescents aged 5-19 years will be obese by 2030, which indicates a global problem with far-reaching consequences. Advances in genomic technologies have led to the identification of multiple genetic loci associated with the disease ranging from severe cases with early onset to common multifactorial polygenic forms. Epigenetic changes driven by dietary and lifestyle factors are now recognized as crucial contributors to obesity. These modifications can alter gene expression and thereby link environmental influences to the observable clinical features of the disease. Significant progress has been made in deciphering the genetic architecture of obesity, particularly in pediatric populations. However, further advancement requires integrative multiomics analyses that encompass genomic, epigenomic, transcriptomic, proteomic, metabolomic, and microbiome data. To better understand the complex molecular underpinnings and clinical variability of obesity, researchers are increasingly applying methods from machine learning and artificial intelligence. These technologies help analyze large-scale genomic and phenotypic datasets, allowing for the identification of biological pathways involved in weight regulation. In the future, this may support the design of individualized diagnostic tools and targeted treatment plans that reflect a patient's genetic profile, lifestyle, and environmental exposures. To implement the principles of personalized and precision medicine in the treatment of obesity, it is crucial to identify risk profiles by assessing multiple contributing factors. This approach not only enables the prediction of an individual's risk of obesity and its associated diseases but also facilitates the optimization of treatment based on the patient's genetic profile. This study provides a comprehensive overview of the current understanding of childhood obesity, including its prevalence, genetic determinants, and pathophysiological mechanisms. It highlights the contribution of genetic factors to hereditary and syndromic forms, the role of gene-environment interactions (including nutrition and environmental pollutants), and the influence of epigenetic modifications on metabolic disturbances associated with polygenic obesity.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"9186826"},"PeriodicalIF":3.8,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12274101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Genetic, Environmental, and Nutritional Factors With Metabolic Phenotypes of Obesity: A Scoping Review.","authors":"Haniyeh Danesh Doost, Milad Nasiri Jounaghani, Roya Riahi, Motahar Heidari-Beni, Mohsen Hosseini, Fariborz Sharifianjazi, Roya Kelishadi","doi":"10.1155/jobe/8472196","DOIUrl":"10.1155/jobe/8472196","url":null,"abstract":"<p><p><b>Background:</b> There are inconsistent findings regarding the different metabolic phenotypes of obesity and associated risk factors. This scoping review aims to provide a comprehensive summary of the literature that has evaluated the relationship between genetic, environmental, and nutritional factors and metabolic heterogeneity in obese and normal-weight individuals. <b>Methods:</b> This scoping review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR) guidelines. A literature search was conducted in Web of Science, the MEDLINE database (PubMed), Scopus, and Google Scholar up to the beginning of April 2024. All observational studies (cross-sectional, case-control, and cohort) were included. <b>Results:</b> Ninety-two studies were included. Of these studies, 20, 38, and 20 were evaluated for the association between genetic, nutritional, and environmental factors with metabolic phenotypes, respectively. Genetic background could be a significant factor in obesity's metabolic phenotypes. Unhealthy dietary patterns, physical inactivity, improper sleep habits, smoking, and alcohol consumption could be related to an increased risk of metabolic phenotypes. <b>Conclusion:</b> Environmental and nutritional factors can increase metabolic abnormalities. Metabolic phenotype categories are useful for predicting disease risk and for developing personalized diets and environmental interventions. These findings may help develop strategies to improve metabolic health.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"8472196"},"PeriodicalIF":3.8,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259317/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calcium/Calmodulin-Dependent Protein Kinase II Inhibitors Mitigate High-Fat Diet-Induced Obesity in Mice.","authors":"Naoyuki Kawao, Ryosuke Satoh, Yuya Mizukami, Katsumi Okumoto, Genzoh Tanabe, Osamu Muraoka, Reiko Sugiura, Hiroshi Kaji","doi":"10.1155/jobe/5530467","DOIUrl":"10.1155/jobe/5530467","url":null,"abstract":"<p><p>Calcium signaling contributes to obesity and its related disorders, such as diabetes. We herein investigated the effects of calcium/calmodulin-dependent protein kinase II (CaMKII) inhibitors on diet-induced obesity in mice. In mice fed a high-fat diet (HFD), the administration of the CaMKII inhibitor KN-93 and the glycolipid acremomannolipin A with the suppression of CaMKII phosphorylation reduced fat mass in the whole body, epididymal and subcutaneous white adipose tissue weights, and lipid accumulation in epididymal and subcutaneous white adipose tissues, but not muscle mass or bone mineral density at the tibia. Moreover, the administration of KN-93 and acremomannolipin A improved glucose intolerance in HFD-fed mice. In an in vitro study on preadipocytic 3T3-L1 cells and mouse adipose tissue-derived stromal cells, KN-93 and acremomannolipin A suppressed adipogenic differentiation, proliferation, and lipid accumulation. In conclusion, this is the first study to demonstrate that CaMKII inhibitors mitigated the development of diet-induced obesity in mice partly through the suppression of adipogenic differentiation, cell proliferation, and lipid accumulation in adipocytes. Inhibiting CaMKII could be a potential strategy for obesity treatment.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"5530467"},"PeriodicalIF":3.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic Exploration of Nonalcoholic Fatty Liver Disease: Insights From Gene Expression and Variation in Morbidly Obese Individuals.","authors":"Tamadher Abbas Rafaa, Safa Abbas Khudhair, Zahraa Yassen Mohammed, Ahmed AbdulJabbar Suleiman","doi":"10.1155/jobe/9245699","DOIUrl":"10.1155/jobe/9245699","url":null,"abstract":"<p><p>Nonalcoholic fatty liver disease (NAFLD) is a common liver condition resulting from metabolic syndrome characterized by fat accumulation in the liver. It is often associated with obesity and diabetes, contributing to hepatic steatosis in liver cells. The prevalence of NAFLD is increasing globally, with 32% of the adult population affected. Genetic modifiers, such as single nucleotide polymorphisms, can increase susceptibility to the disease. Gene expression analysis and genetic variation can help identify disease-causing pathways and reveal biomarkers involved in NAFLD. This study employed integrative bioinformatics analysis, including bulk RNA-seq and single-cell RNA-seq, to explore differentially expressed genes and their genetic variants in NAFLD vs. control and NAFLD vs. cirrhosis, highlighting genes influencing NAFLD progression. Moreover, this study identified <i>AKR1D1, LIPC, UGT2B17, DGAT2,</i> and <i>SERPINE1</i> implicated in metabolic, immune, and lipid functions while being overexpressed in both hepatocyte cells among obese patients identified and validated through Liver Cell Atlas, highlighting their pivotal role in the pathogenesis of the disease in obese patients through perturbed hepatocytes. Furthermore, novel pathogenic variants of <i>AKR1D1, LIPC,</i> and <i>SERPINE1</i>, associated with congenital bile acid synthesis defects, abnormal circulating lipid concentrations, and plasminogen activator inhibitor type 1 deficiency conditions, were identified. Conclusively, this integrative multiomics study highlights the novel pathogenic variants of <i>AKR1D1</i>, <i>LIPC</i>, and <i>SERPINE1</i> in metabolic, immune, and lipid pathways that are highly expressed among hepatocytes in obese patients while possibly carrying pathogenic mutations that may be associated with NAFLD, emphasizing their potential as novel targets for therapeutic strategies and biomarker development in early diagnosis and treatment before the onset of cirrhosis or hepatocellular carcinoma.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"9245699"},"PeriodicalIF":3.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12069845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144023831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Complex Network of Obesity-Risk Genes Revealed by Systematic Bioinformatics and Single-Cell Transcriptomic Analyses.","authors":"Yuenan Liu, Haolin Yuan, Junhui Hu, Xu Xu, Shankai Yin, Yiming Hu, Feng Liu","doi":"10.1155/jobe/7821115","DOIUrl":"10.1155/jobe/7821115","url":null,"abstract":"<p><p>The development of obesity is closely linked to genetic factors. Despite the identification of numerous genes associated with an increased risk of obesity in humans, a comprehensive understanding of their biological roles has not been achieved. In our extensive bioinformatics study, we identified 802 core genes implicated in obesity. Our protein-protein interaction (PPI) network analysis revealed that these genes form a tightly connected functional network primarily involved in neurological and metabolic regulatory processes. Moreover, our in-depth analysis of single-cell transcriptomic datasets from the human hypothalamus, pancreatic islets, adipose tissue, and liver has shed light on the distinct expression profiles of these obesity-linked genes across various tissue and cell types. This analysis also highlighted the biological processes they influence and the upstream transcriptional regulatory networks involved. Our study not only uncovers the complicated regulatory role of genetic factors in the pathogenesis and progression of obesity but also establishes a close link between the expression patterns and functional roles of these obesity-associated genes. This study provides crucial insights for advancing our understanding of the genetic mechanisms underlying obesity.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"7821115"},"PeriodicalIF":3.8,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976034/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Laparoscopic One Anastomosis Gastric Bypass as a Revisional Procedure After Failed Vertical Banded Gastroplasty: Our Center Experience.","authors":"Hosam Elghadban, Ashraf Shoma, Emad Abdallah, Ahmed Negm, Elsayed Abdullah, Hossam Hamed, Sameh Ghareeb, Ahmed Lotfy, Ahmed Taki-Eldin","doi":"10.1155/jobe/4161005","DOIUrl":"10.1155/jobe/4161005","url":null,"abstract":"<p><p><b>Background:</b> Vertical banded gastroplasty (VBG) was historically a popular restrictive bariatric procedure, but long-term failure rates due to weight regain, stenosis, and gastroesophageal reflux have necessitated revisional interventions. One anastomosis gastric bypass (OAGB), also known as mini-gastric bypass, has emerged as a viable revisional option due to its technical simplicity, lower complication rates, and promising metabolic outcomes. This study evaluates the safety, efficacy, and outcomes of OAGB as a revisional procedure following failed VBG, based on our center's experience and a review of the current literature. <b>Methods:</b> Seventy-one patients who underwent revisional OAGB after failed open VBG between February 2014 and February 2020 were included in this retrospective study. Three years outcomes regarding weight loss (the percentage of excess body weight loss (EBWL %) and change in body mass index (BMI)), co-morbidities resolution, morbidity, and mortality were assessed. <b>Results:</b> The EBWL % after revisional OAGB was 68.2 ± 9.4%, 65.9 ± 2.5%, and 59.6 ± 7.4% after 1, 2, and 3 years, respectively. The mean BMI before revisional surgery was 41.8 ± 3.7 kg/m²,which decreased to 31.9 ± 4.2 kg/m² 3 years after the revisional surgery. After 1 year, there was a remarkable resolution of obesity-related co-morbidities, the remission of type 2 diabetes mellitus was 85.7%, and of hypertension was 80%. Remission of other comorbidities was also observed. Bile reflux was encountered in 6 cases (8.5%), two of them required surgical intervention. <b>Conclusions:</b> OAGB is a feasible and effective revisional procedure after failed open VBG. However, the risk of bile reflux should be considered to justify these findings; further prospective randomized controlled trials are required.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":"2025 ","pages":"4161005"},"PeriodicalIF":3.8,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11972859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}