Current Obesity Reports最新文献

{"title":"Correction to: The Role of Echocardiography in the Assessment of Epicardial Adipose Tissue: A Systematic Review and Meta-analysis.","authors":"Barbara Pala, Mariagrazia Piscione, Francesco Cribari, Serena De Mitri, Paola Gualtieri, Antonino De Lorenzo, Luigi Barrea, Marco Alfonso Perrone, Gianluca Iacobellis, Laura Di Renzo","doi":"10.1007/s13679-026-00769-6","DOIUrl":"https://doi.org/10.1007/s13679-026-00769-6","url":null,"abstract":"","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653811/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165383","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":"Adolescents' perspectives on socio-cultural influences on overweight and obesity in African countries: a systematic scoping review of qualitative studies.","authors":"Emmanuel Osei Bonsu, Steven Allender, Erik Martin, Richmond Aryeetey, Colin Bell","doi":"10.1007/s13679-026-00767-8","DOIUrl":"10.1007/s13679-026-00767-8","url":null,"abstract":"<p><strong>Introduction: </strong>Adolescent obesity is a global public health concern, with increasing prevalence rates in many African countries. Studies have highlighted diverse social and cultural influences on weight, but there is uncertainty about how adolescents in Africa perceive and experience these influences. This review aims to describe adolescents' perspectives on how cultural beliefs and norms, peers, family, and media influence weight-related behaviours, body weight, and experiences of weight stigma in African countries.</p><p><strong>Methods: </strong>We systematically searched Scopus, PubMed, Embase, Web of Science, CINAHL, PsycINFO and SocINDEX for qualitative studies on socio-cultural determinants of adolescents' overweight and obesity in African countries. Study quality was assessed using the Critical Appraisal Skills Programme (CASP) for qualitative research. Using a narrative synthesis approach guided by socio-cultural theory, we summarised and interpreted findings across studies to describe adolescents' perspectives on how cultural beliefs, peers, family, and media influence weight and experiences of weight stigma.</p><p><strong>Results: </strong>Of 1,410 articles identified, 17 met the inclusion criteria from eight African countries. Eight studies were conducted in South Africa, while the remaining studies were conducted in Benin, Botswana, Cameroon, Ethiopia, Gambia, Kenya, and Uganda, with no eligible studies identified from Northern or Central Africa. Synthesis of these studies revealed that adolescents perceived peers and parents/families as important influences on their food choices, in the direction of unhealthy options, and on their physical activity levels. Adolescents also described media as shaping these behaviours and perceptions of body image. Several studies reported that overweight or obesity was associated with wealth and health, while thinness was associated with disease or illness. Weight stigma was reported among adolescents irrespective of their weight status.</p><p><strong>Conclusion: </strong>Adolescents from eight African countries perceived peers, family members, and media as important socio-cultural influences on their weight-related behaviours, perceptions of body weight, and experiences of weight stigma. Interventions to prevent and manage adolescent obesity may be more effective and better received if these perceived socio-cultural influences are integrated into the design.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13627244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105094","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: Microbiota-Gut-Brain Axis Mechanisms in Cognitive Impairment Associated with Central Obesity.","authors":"Tianyun Huang, Zhou Hao, Jiaxin Shen, Tingxiao Lai, Yitong Wu, Xinyi Zhu, Huangan Wu, Chunhui Bao","doi":"10.1007/s13679-026-00766-9","DOIUrl":"https://doi.org/10.1007/s13679-026-00766-9","url":null,"abstract":"","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073810","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":"Beyond Pleasure: Unraveling the Multifaceted Role of Dopamine in Obesity and Metabolic Regulation.","authors":"Shurui Yang, Zhongyu Huang, Wei Lu, Wenyan Wang, Song Wu, Yayuan Wang, Liuyang Huang, Li Chen, Rui Chen, Fengxia Liang","doi":"10.1007/s13679-026-00763-y","DOIUrl":"10.1007/s13679-026-00763-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>Obesity is a heterogeneous chronic disease involving dysregulated energy intake and expenditure. Dopamine (DA) has traditionally been recognized as a key regulator of reward-driven feeding. However, accumulating evidence indicates that its functions extend beyond hedonic eating. This review examines the central and peripheral actions of DA in obesity. It focuses on neuronal and receptor diversity, DA-related circuits, metabolic interactions, and responses to anti-obesity interventions.</p><p><strong>Recent findings: </strong>DA neurons and receptor subtypes exhibit substantial molecular, anatomical, and functional diversity. Obesity-related alterations in DA release, receptor function, and downstream signaling vary across brain regions and metabolic contexts. DA regulates food reward, feeding, physical activity, and thermogenesis through VTA-centered reward circuits, hypothalamus-centered feeding circuits, and central-peripheral metabolic pathways. These circuits interact with neuropeptides, neurotransmitter and neuromodulatory systems, and metabolic hormones. In peripheral tissues, local DA signaling regulates gastrointestinal motility, pancreatic hormone secretion, adipose tissue function, and skeletal muscle glucose utilization. Dietary adjustment, exercise, microbiome interventions, bariatric surgery, glucagon-like peptide-1 receptor (GLP-1R) agonists, and other DA-modulating agents may alter these pathways. However, direct evidence that DA modulation mediates their clinical effects remains limited. Current evidence does not support a uniform pattern of dopaminergic (DAergic) dysfunction or a generalized reward-deficiency model in obesity. DA alterations vary across neural circuits, receptor subtypes, tissues, metabolic states, and feeding phases. Most human findings are associative, whereas mechanistic evidence is derived largely from animal models. It remains unclear whether DA alterations precede obesity or result from dietary exposure and metabolic dysfunction. The coordination between central and peripheral DA systems is also poorly defined. Longitudinal and mechanistically informed human studies are needed to identify clinically relevant DAergic biomarkers and therapeutic targets.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13601120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029736","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":"When Ultra-Processed Foods are Eaten: The Missing Dimension in Exposure Measurement for Obesity Research.","authors":"Jimmy Chun Yu Louie","doi":"10.1007/s13679-026-00765-w","DOIUrl":"10.1007/s13679-026-00765-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>Almost every study linking ultra-processed foods (UPFs) to obesity measures exposure as the proportion of energy or weight derived from Nova group 4 foods, averaged across days. This scalar is commonly treated as though it were the exposure itself, yet it embodies an untested assumption: that the timing and context of intake carry no information beyond total amount. This review examines what is lost when occasion-level intake is collapsed to a daily average and how that loss may affect epidemiological inference.</p><p><strong>Recent findings: </strong>Controlled circadian-misalignment protocols and time-restricted eating trials show that the metabolic response to a fixed quantity of food varies with its timing. Postprandial studies further show that meal sequence, co-ingestion and eating-occasion structure modify glycaemic and appetite responses at equal daily totals. These findings expose a mismatch between the timescale at which relevant processes operate and the daily scale at which UPF exposure is conventionally measured. Measurement-error and causal-inference frameworks show how such temporal collapse could attenuate or otherwise distort effect estimates, reduce transportability and obscure the intervention to which an association refers. The daily group 4 fraction is a modelling choice, not a complete representation of the diet. It discards temporal and contextual structure that may explain heterogeneity across UPF-obesity cohorts and determine the causal contrast represented by their estimates. This review proposes a time-resolved, context-aware construct and specifies the studies needed to test whether it adds information beyond the conventional scalar. The controlled timing literature manipulated total energy, macronutrients or glucose loads rather than Nova group 4 foods, so its extension to UPFs remains a testable inference rather than an established finding. The immediate priority is therefore not to replace the scalar, but to analyse cohorts whose dietary records retain item-level time stamps and determine whether the discarded structure predicts outcomes beyond total amount.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001052","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: Does the Carbohydrate-Insulin Model Explain Obesity? Evidence from Mechanistic and Clinical Studies: A Critical Review.","authors":"Damoon Ashtary-Larky","doi":"10.1007/s13679-026-00762-z","DOIUrl":"https://doi.org/10.1007/s13679-026-00762-z","url":null,"abstract":"","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988500","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":"Obesity-Associated Osteoarthritis: Mechanical-Metabolic Pathogenesis, Obesity Memory and Dual-Target Therapy.","authors":"Yudan Wang, Xinhao Fan, Jingyuan Gao, Lei Xing, Faming Tian","doi":"10.1007/s13679-026-00761-0","DOIUrl":"10.1007/s13679-026-00761-0","url":null,"abstract":"<p><strong>Purpose of review: </strong>Given the global obesity epidemic, osteoarthritis (OA) incidence is expected to rise, posing a substantial public health burden. This review covers epidemiological associations of obesity and OA, controversial mechanisms, and current prevention and treatment limitations. Based on these insights, we propose a dual‑target treatment strategy for obesity‑induced OA.</p><p><strong>Recent findings: </strong>Leptin signaling and mechanical overload from excess adiposity independently drive OA pathogenesis, whereas obesity‑related adipose dysfunction exerts its pathogenic effects only in the presence of mechanical loading. Obesity‑induced residual memory may persist and sustain joint damage even after weight loss and metabolic improvement. Evidence‑based weight loss strategies should be implemented to prevent OA, with the preventive window for obesity shifting to infancy. Given the limited and controversial structural benefits of current clinical interventions, a dual‑target strategy combining weight loss with memory‑targeted interventions is warranted. This review provides new insights into the debate on mechanical versus metabolic mechanisms in obesity‑induced OA, clarifying their relative contributions. Earlier obesity prevention interventions offer a broader window for OA prevention. Given these limitations, a dual‑target strategy addressing both excessive fat accumulation and its persistent adverse effects may represent a promising clinical direction, with particular potential for repurposing FDA‑approved agents such as semaglutide and metformin in this context.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148981915","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":"Hypothyroidism and Metabolic Dysfunction-Associated Steatotic Liver Disease: Mechanisms, Clinical Links, and Therapeutic Implications.","authors":"Amjad Mahmood Qadir, Rebaz Anwar Omer","doi":"10.1007/s13679-026-00764-x","DOIUrl":"10.1007/s13679-026-00764-x","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review evaluates the epidemiological, molecular, pathophysiological, and clinical relationships between hypothyroidism and metabolic dysfunction-associated steatotic liver disease (MASLD), with emphasis on hepatic lipid metabolism, mitochondrial function, insulin resistance, thyroid hormone signaling, and therapeutic implications.</p><p><strong>Recent findings: </strong>Recent observational studies and meta-analyses indicate a correlation between hypothyroidism, especially overt hypothyroidism, and a heightened risk of hepatic steatosis and fibrosis. Research indicates that thyroid-stimulating hormone might exert direct effects on the liver through signalling via thyroid-stimulating hormone receptors. Moreover, current research suggests that levothyroxine could enhance hepatic enzymes and steatosis in certain patients, whereas thyroid hormone receptor-β agonists have surfaced as potential liver-specific treatments for MASLD. The existing research indicates that thyroid dysfunction is a significant risk factor in MASLD. Regular evaluation of thyroid function might be suitable for certain patients with MASLD, and meticulous minimisation of metabolic risk is crucial. Nonetheless, the causal relationship is not fully determined, and additional longitudinal and mechanistic research is required to elucidate which patients would derive the greatest advantage from thyroid-targeted treatments.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966995","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":"Obesity-related Metabolic Dysfunction and Triple-negative Breast Cancer: Epidemiologic Signals, Mechanistic Pathways, and Opportunities for Prevention.","authors":"Naser Elkum, Abdelilah Aboussekhra","doi":"10.1007/s13679-026-00760-1","DOIUrl":"10.1007/s13679-026-00760-1","url":null,"abstract":"<p><strong>Purpose of review: </strong>Obesity is an established risk factor for postmenopausal hormone receptor-positive breast cancer, largely through estrogen-mediated pathways. Emerging evidence suggests that obesity-related metabolic dysfunction may also contribute to the risk and aggressive biology of receptor-negative breast cancer, particularly TNBC, among premenopausal women and populations undergoing rapid metabolic transition. This review evaluates epidemiologic, mechanistic, and translational evidence linking metabolic dysfunction to TNBC.</p><p><strong>Recent findings: </strong>Observational studies and pooled analyses report modest but reproducible associations between adiposity and TNBC, stronger in some metabolically high-risk populations but heterogeneous across studies. BMI-based Mendelian randomization generally yields inverse associations with overall breast cancer, whereas bariatric-surgery studies suggest lower overall incidence without establishing TNBC-specific effects. These discordant causal-inference findings do not demonstrate that obesity directly causes TNBC. Mechanistic studies indicate that adipose inflammation, adipokine imbalance, insulin/IGF-1 signaling, and immune remodeling can promote inflammatory signaling, metabolic adaptation, and epithelial plasticity. These processes support biologic plausibility but do not demonstrate de novo conversion to a receptor-negative subtype in vivo. Current evidence supports a model in which obesity-related metabolic dysfunction may create a breast microenvironment favoring tumor-promoting inflammation and aggressive features associated with TNBC. Priorities include refined metabolic phenotyping, biomarker-driven risk stratification, validation in human-relevant models, and biomarker-enriched feasibility studies testing whether modifying metabolic dysfunction alters intermediate metabolic or tissue endpoints. An evidence-graded framework is needed to distinguish association, biologic plausibility, and causal inference.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13569575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944205","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":"Obesity-Related Tendon Pathology: Cardiometabolic Mechanisms, Clinical Implications, and Management.","authors":"Hang Zhao, Jun Lu","doi":"10.1007/s13679-026-00759-8","DOIUrl":"10.1007/s13679-026-00759-8","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review evaluates obesity as the organizing exposure linking mechanical loading and adipose-tissue dysfunction with tendon pathology. It synthesizes site- and outcome-specific human evidence, candidate mechanisms, tendon xanthomas associated with familial hypercholesterolemia (FH), and implications for targeted assessment and management.</p><p><strong>Recent findings: </strong>Human studies associate obesity and related cardiometabolic abnormalities with tendinopathy, tendon rupture, and postoperative outcomes, but findings vary by exposure, site, and outcome and remain predominantly observational. Limited human tissue and predominantly preclinical studies support candidate roles for glycation, oxidized lipids, chronic inflammation, mitochondrial and redox dysfunction, and impaired repair, although their causal sequence and human relevance remain uncertain. Recent single-cell and spatial studies reveal tendon cellular heterogeneity but have not established obesity- or metabolism-specific endotypes. Recurrent, bilateral, atraumatic, or treatment-resistant manifestations have been proposed as features of a hypothesis-generating \"metabolic tendon phenotype\" rather than a validated diagnostic entity. FH-related tendon xanthomas represent a distinct manifestation of severe cumulative low-density lipoprotein cholesterol exposure. Standard tendon-directed rehabilitation remains central, whereas tendon-specific benefits of cardiometabolic optimization, glucagon-like peptide-1 receptor agonists, bariatric surgery, or lipid-lowering therapy remain unconfirmed. The proposed mechanometabolic continuum integrates obesity-associated systemic influences with local loading as a conceptual framework rather than a validated disease model or screening tool. Current evidence does not support universal cardiometabolic or cardiovascular screening based on nonspecific tendinopathy alone; targeted assessment may be considered in selected patients with relevant clinical cues or conventional risk factors. Longitudinal human studies and intervention trials are needed to clarify causality and clinical utility.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944189","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}