Current Obesity Reports最新文献

{"title":"State of the Science on Ultra-processed Foods and the Ultra-processed Food Addiction Construct.","authors":"Erica M LaFata, Adrienne S Juarascio, Meghan L Butryn, Charlotte J Hagerman, Evan M Forman","doi":"10.1007/s13679-026-00758-9","DOIUrl":"10.1007/s13679-026-00758-9","url":null,"abstract":"<p><strong>Purpose of review: </strong>We synthesize recent developments across two linked literatures, ultra-processed foods (UPFs) and the construct of UPF addiction, engaging contested questions of health harm, classification, assessment, and recognition.</p><p><strong>Recent findings: </strong>Advances include: 1) feeding trials and diet-quality-adjusted cohorts indicating harm from processing itself; 2) analyses linking critiques of UPF classification predominantly to industry-affiliated authors; 3) findings consistent with the addictive-substance hypothesis: GLP-1 agonists reduce UPF intake and addictive-substance use, and analyses identify UPF attributes driving addictive-like eating; 4) the first clinician-administered UPF addiction interview extends assessment beyond self-report; and 5) Delphi consensus and regulatory and legislative attention signaling recognition of UPF addiction. Evidence increasingly supports treating UPFs and UPF addiction as one problem, the substance and the disorder, reshaping research and policy priorities. The evidence base for recognition rivals that of some recognized disorders, though its sufficiency remains debated. Gaps include targeted interventions and clinician-administered assessment data.</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":"148944203","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":"Adipose Tissue Remodeling Beyond Weight Loss: New Insights Into Incretin-Based Therapies and Bariatric Surgery.","authors":"Gabriela Ferreira Abud, Ellen Cristini de Freitas, Kristin I Stanford","doi":"10.1007/s13679-026-00756-x","DOIUrl":"10.1007/s13679-026-00756-x","url":null,"abstract":"<p><strong>Purpose of the review: </strong>This review summarizes obesity-induced adaptations in subcutaneous and visceral white adipose tissue (WAT) depots and discusses how incretin-based pharmacotherapies and bariatric surgery may influence WAT remodeling beyond weight loss, drawing on evidence from animal models and human studies.</p><p><strong>Recent findings: </strong>In obesity, adipose tissue undergoes pathological remodeling characterized by structural and cellular changes, extracellular matrix (ECM) remodeling, altered endocrine signaling, and impaired mitochondrial function that contribute to metabolic comorbidities. Weight-loss interventions, including incretin-based therapies and bariatric surgery, are associated with improvements in adiposity and metabolic outcomes, and multiple studies suggest accompanying changes in inflammatory, mitochondrial/thermogenic, and endocrine pathways within WAT; however, mechanistic evidence in humans remains heterogeneous and is often limited by tissue accessibility and study design. This review highlights candidate cellular and molecular mechanisms through which incretin-based pharmacotherapies and bariatric surgery may modulate WAT plasticity, emphasizing convergent and distinct effects across depots and the need for more longitudinal, tissue-level human studies to define weight-dependent remodeling versus changes not fully explained by weight loss.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929251","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":"Digital Health in Obesity Care: Current Evidence, Challenges, and Future Directions.","authors":"Sherry Pagoto, Richard Bannor","doi":"10.1007/s13679-026-00757-w","DOIUrl":"10.1007/s13679-026-00757-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>The purpose of this review is to highlight areas in which digital technologies including mobile apps, wearables, telehealth, and AI have improved obesity care, where gaps remain, and future directions.</p><p><strong>Recent findings: </strong>Technology is being used in myriad ways to support lifestyle, pharmacological, and surgical obesity care. Mobile apps and wearables reduce the burden of behavior change strategies (e.g., self-monitoring) and telehealth eliminates numerous barriers to in-person obesity care. However, low engagement is a persistent problem with digitally-delivered interventions. An emerging area is the use of AI in obesity care to glean personalized insights from data collected by wearables and mobile apps and to deliver lifestyle coaching. Technology increases access to obesity care, facilitates personalized care, and reduces burden. Future research should examine ways to improve engagement, to design adaptive interventions that are responsive to patients' evolving care needs, and to facilitate implementation in healthcare settings.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929216","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":"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/s13679-026-00755-y","DOIUrl":"10.1007/s13679-026-00755-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>Central obesity (CO), characterized by excessive visceral adipose tissue (VAT) accumulation, is increasingly recognized as a risk factor for cognitive decline, dementia, and Alzheimer's disease (AD). This review summarizes current evidence linking CO, particularly VAT accumulation, to cognitive impairment and discusses the microbiota-gut-brain axis as a mechanistic framework for interpreting this association.</p><p><strong>Recent findings: </strong>Studies published in recent years suggest that VAT-related indices, such as waist circumference, waist-to-hip ratio, and imaging-derived VAT measures, are more closely associated with cognitive dysfunction than body mass index. Recent neuroimaging studies have linked VAT accumulation with brain atrophy, white matter abnormalities, altered functional connectivity, and increased AD-related pathological burden. Emerging multi-omics evidence further indicates that VAT expansion shows an association with gut microbial dysbiosis, altered microbial metabolites, impaired intestinal barrier function, systemic low-grade inflammation, insulin resistance, and neuroendocrine disturbances. These findings support a model in which VAT-related metabolic and inflammatory alterations may influence brain structure and function through microbiota-mediated, immune, endocrine, and barrier-related pathways. Current evidence is consistent with a VAT-centered model in which CO is associated with cognitive impairment through interconnected inflammatory, metabolic, endocrine, and microbiota-mediated mechanisms. The microbiota-gut-brain axis may provide a useful mechanistic framework linking peripheral metabolic dysfunction with AD vulnerability. Future longitudinal cohort studies and mechanistically informed intervention studies are needed to clarify temporal relationships and to determine whether VAT reduction or microbiota-targeted strategies can improve cognitive or neuroimaging outcomes.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905275","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 and Iron Metabolism: Mechanisms, Status Assessment, and Clinical Implications.","authors":"Sixtus Aguree, Xiangqi Meng","doi":"10.1007/s13679-026-00753-0","DOIUrl":"10.1007/s13679-026-00753-0","url":null,"abstract":"<p><strong>Purpose of review: </strong>Obesity reshapes systemic iron handling, yet the resulting iron phenotype is frequently misclassified at the bedside and in population studies. This review examines how excess adiposity disturbs iron metabolism and complicates iron-status assessment, with balanced attention to biology and measurement problems across adults and children.</p><p><strong>Recent findings: </strong>Adipose tissue is an endocrine, inflammatory, and iron-handling organ. In obesity, interleukin-6 drives hepatic hepcidin through JAK/STAT3 signaling, while leptin, adipose hypoxia, and adipose hepcidin expression may contribute additional signals. Hepcidin degrades ferroportin, reducing duodenal iron export and limiting macrophage iron release, producing hypoferremia and iron-restricted erythropoiesis despite normal or elevated ferritin. We and others have shown that women with obesity may have higher hepcidin, ferritin, and inflammatory markers but lower serum iron. Stable-isotope and intervention studies suggest weight loss reduces inflammation and hepcidin and improves iron absorption, whereas the World Health Organization and Biomarkers of Nutrition for Development frameworks recommend interpreting ferritin relative to inflammation. Iron status in obesity spans a continuum from absolute or functional iron deficiency to sufficiency and, in some individuals, hyperferritinemia with possible dysmetabolic iron overload. Reliable assessment requires a multi-marker strategy: ferritin interpreted alongside an inflammation marker such as C-reactive protein and supported by transferrin saturation, soluble transferrin receptor, reticulocyte hemoglobin, or other context-appropriate indices. Management should address reversible inflammation through weight loss and metabolic risk reduction, use oral or intravenous iron according to the likelihood of true deficiency and hepcidin-mediated oral refractoriness, and avoid reflexive phlebotomy for dysmetabolic hyperferritinemia without confirmed overload.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13546355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896741","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":"Emerging Topics In Obesity Treatment in the Setting of Organ Transplantation.","authors":"Ethan Maahs, Zoe Zimmerman, Vandana Khungar, Bubu A Banini","doi":"10.1007/s13679-026-00749-w","DOIUrl":"10.1007/s13679-026-00749-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review summarizes current evidence on the treatment of obesity in the solid organ transplant setting and identifies evidence gaps.</p><p><strong>Recent findings: </strong>Lifestyle modification, pharmacotherapy, and metabolic and bariatric surgery are all potential options for management of obesity in the setting of solid organ transplantation. Limited available data on use of incretin-based pharmacotherapy in solid organ transplantation support its safety and effectiveness in appropriately-selected patients, however prospective large-scale studies are needed. Obesity treatment is an important component of transplant care, as obesity is associated with increased mortality and adverse graft outcomes. Lifestyle modification, anti-obesity pharmacotherapy, and metabolic and bariatric surgery can be employed safely in both pre- and post-transplant settings. Newer incretin-based pharmacotherapy, including glucagon-like peptide 1 (GLP-1) receptor agonists and dual GLP-1 receptor agonist/gastric inhibitory polypeptide offer potential for substantial weight loss and improved cardiometabolic outcomes. Bariatric and endoscopic metabolic procedures can be beneficial in carefully selected patients pre- or post-transplant. Precision approaches including sarcopenic obesity and measurement of body composition can help tailor interventions. These developments highlight the importance of multidisciplinary management and underscore the need for additional research within transplant populations.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886172","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":"PIEZO Channels in Metabolism and Metabolic Diseases: Research Advances and Therapeutic Strategies.","authors":"Zhiying Feng, Jiawang Huang, Jiacheng He, Peixun Luo, Yunfeng Yu, Ling Li, Rong Yu","doi":"10.1007/s13679-026-00754-z","DOIUrl":"10.1007/s13679-026-00754-z","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review aims to summarize the current knowledge on the role of mechanical-gated ion channel PIEZO in body metabolism and metabolic diseases, as well as the latest evidence of PIEZO1 channels as a therapeutic strategy for metabolic diseases.</p><p><strong>Recent findings: </strong>PIEZO channels are mechanosensitive ion channels that play a crucial role in converting mechanical stimuli into biological signals. They participate in numerous physiological and pathological processes within the human body. Recently, the importance of PIEZO channels in body metabolism and metabolic diseases has garnered significant attention. This review summarizes the current status of research in carbohydrate and lipid metabolism, energy metabolism, and bone metabolism. It also examines the role and mechanisms of PIEZO channels in obesity, diabetes and its complications, osteoporosis, metabolic syndrome, and other diseases. Furthermore, we organize and discuss the potential for targeting PIEZO channels through multi-faceted therapeutic strategies to treat metabolic diseases. PIEZO channels play a crucial role in the body's metabolism, regulating the body's glucose metabolism, energy metabolism, lipid metabolism, and bone metabolism. Moreover, PIEZO channels are potential therapeutic targets for metabolic diseases, capable of preventing and treating obesity, diabetes and its complications, osteoporosis, metabolic syndrome, and other diseases.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886207","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":"Exerkine-Mediated Inter-Organ Crosstalk and Translational Perspectives in Metabolic Diseases.","authors":"Bojun Zhou, Shiyan Zhang, Zhanbo Zhang, Shuman Ran, Haining Guo, Siqi Wang, Hua Meng","doi":"10.1007/s13679-026-00752-1","DOIUrl":"10.1007/s13679-026-00752-1","url":null,"abstract":"<p><strong>Purpose of review: </strong>Exercise is a cornerstone intervention for obesity and related metabolic diseases. However, its systemic benefits cannot be fully explained by increased energy expenditure, enhanced skeletal muscle glucose uptake, reduced adiposity, or improved peripheral insulin sensitivity alone. We review recent advances in exercise-responsive exerkines, with a focus on how these factors coordinate inter-organ crosstalk among major metabolic organs, including skeletal muscle, adipose tissue, liver, pancreas, and intestine.</p><p><strong>Recent findings: </strong>Both acute exercise and chronic training change the secretory profiles of multiple organs, giving rise to a broad spectrum of exercise-responsive factors, including proteins, metabolites, lipids, nucleic acids, and extracellular vesicle-associated cargo. Collectively, these exerkines coordinate inter-organ communication and regulate systemic energy homeostasis, inflammation, and tissue function, thereby promoting metabolic adaptation and mitigating lipotoxicity and insulin resistance. Among the candidates identified to date, IL-6, FGF21, GDF15, and myostatin have undergone relatively advanced translational investigation. Their development highlights both the therapeutic promise and the limitations of exerkine-based strategies, as illustrated by FGF21 analogues for metabolic diseases and the limited efficacy or tolerability reported for some GDF15-targeted interventions. Exerkines provide a molecular framework for understanding how exercise produces coordinated metabolic adaptations across organs. However, most candidate exerkines still require stronger human validation, clearer tissue-source attribution, defined receptor pathways, dose-response characterization, and long-term safety assessment. Exerkine-based strategies should therefore be viewed not as replacements for exercise, but as potential complementary approaches for populations with limited exercise capacity, including frail older adults, patients with cardiopulmonary disease, individuals with severe obesity or neuromuscular disorders, and those recovering from surgery or prolonged bed rest.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886147","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":"Remodeling the Immune Landscape: How Obesity-Induced SASPs Create a Pro-Tumorigenic Niche.","authors":"Eslam E Abd El-Fattah, Gary Ngai, Rachael Mooney, Karen S Aboody","doi":"10.1007/s13679-026-00750-3","DOIUrl":"10.1007/s13679-026-00750-3","url":null,"abstract":"<p><strong>Purpose of review: </strong>Obesity is a potent risk factor for cancer, primarily driven by a state of chronic inflammation. A key mechanism linking adipose tissue dysfunction to tumorigenesis is the induction of cellular senescence and the related Senescence-Associated Secretory Phenotype (SASP), which is not clearly defined.</p><p><strong>Recent findings: </strong>In obesity, expanding adipose tissue becomes hypoxic and stressed, triggering premature senescence in adipocytes and stromal cells. These senescent cells persistently secrete a robust arsenal of SASP factors, including pro-inflammatory cytokines (e.g., IL-6, IL-1β) and chemokines (e.g., IL-8, MCP-1). This review delineates how obesity-related SASPs create a permissive environment for cancer initiation and progression. Systemically, these SASPs establish a low-grade inflammatory milieu that promotes genomic instability and epithelial cell transformation. Within the tumor microenvironment, SASP components directly stimulate cancer cell survival, proliferation, invasion, and angiogenesis, concurrently through immune modulation. Crucially, obesity-related metabolic hormones regulate this process; hyperleptinemia, hyperinsulinemia, and hyperresistinemia amplify SASPs, while hypoadiponectinemia removes a key inhibitory brake. Obesity-induced SASPs act as critical endocrine and paracrine signals that remodel tissue landscapes to be pro-tumorigenic. Targeting the SASPs or the metabolic drivers of senescence presents a promising therapeutic strategy to mitigate the potential oncogenic consequences of obesity.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788883","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":"Does the Carbohydrate-Insulin Model Explain Obesity? Evidence from Mechanistic and Clinical Studies: A Critical Review.","authors":"Damoon Ashtary-Larky","doi":"10.1007/s13679-026-00751-2","DOIUrl":"10.1007/s13679-026-00751-2","url":null,"abstract":"<p><strong>Purpose of review: </strong>The Carbohydrate-Insulin Model (CIM) of obesity proposes that dietary carbohydrates particularly high-glycemic carbohydrates, drive weight gain by stimulating insulin secretion, thereby promoting fat storage, increasing hunger, and reducing energy expenditure (EE). According to this framework, hyperinsulinemia is viewed as the primary causal factor in obesity, with positive energy balance emerging as a downstream consequence of altered fuel partitioning. In contrast, the Energy Balance Model (EBM) conceptualizes obesity as the result of sustained excess energy intake (EI) relative to expenditure, with insulin dysregulation arising secondary to increased adiposity.</p><p><strong>Recent findings: </strong>This review critically evaluates the CIM across eleven complementary lines of evidence, including isocaloric and ad libitum dietary interventions, EE studies, population-level dietary trends, glycemic index (GI) manipulations, Glucagon-like peptide-1 receptor agonist (GLP-1 RA) therapies, overfeeding experiments, the insulinotropic effects of protein, central effects of insulin on appetite, insulin spikes and 24-hour fat balance, temporal relationships between hyperinsulinemia and obesity, and de novo lipogenesis (DNL). Although some findings remain compatible with contemporary formulations of the CIM, several lines of evidence are difficult to reconcile with some of its central predictions (i.e. the insulinotropic yet anti-obesogenic effects of dietary protein, the central anorexigenic role of insulin). However, many studies aimed at directly testing its predictions are limited in their ability to definitively distinguish between competing models owing to design constraints, intervention-related confounding, or limitations in the available data. Any single line of evidence reviewed in this article may be insufficient, in isolation, to draw definitive conclusions regarding the validity of the CIM. However, when considered collectively, the available mechanistic, clinical, and epidemiological evidence suggests that the CIM may not provide a fully comprehensive explanation for the etiology of common obesity. While insulin dynamics and carbohydrate quality are undoubtedly relevant to metabolic health and body-weight regulation, the available evidence does not consistently support their role as the primary drivers of obesity proposed by contemporary formulations of the CIM.</p>","PeriodicalId":10846,"journal":{"name":"Current Obesity Reports","volume":"15 1","pages":""},"PeriodicalIF":17.0,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788907","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}