Current Obesity Reports肥胖研究当前综述
Current Obesity Reports(英文缩写 CURR OBES REP),ISSN 2162-4968,eISSN 2162-4968,中文译名:肥胖研究当前综述 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 8.023 | Q1 |
| 2022 | 8.800 | Q1 |
| 2023 | 9.500 | Q1 |
| 2024 | 11.000 | Q1 |
| 2025 | 17.000 | Q1 |
Current Obesity Reports 最新收录文献
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1. Adolescents' perspectives on socio-cultural influences on overweight and obesity in African countries: a systematic scoping review of qualitative studies.
1. 青少年对非洲国家超重和肥胖的社会文化影响的看法：对定性研究的系统性范围综述PMID:日期:2026-09-30Adolescent 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. 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. 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. 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.
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2. Beyond Pleasure: Unraveling the Multifaceted Role of Dopamine in Obesity and Metabolic Regulation.
2. 超越快感：揭示多巴胺在肥胖和代谢调节中的多重作用PMID:日期:2026-09-23[中文摘要] 肥胖是一种涉及能量摄入和消耗失调的异质性慢性疾病。多巴胺（DA）传统上被认为是奖赏驱动性进食的关键调节因子。然而，越来越多的证据表明其功能远超享乐性进食。本综述探讨了DA在肥胖中的中枢和外周作用，重点关注神经元与受体的多样性、DA相关神经环路、代谢相互作用以及对减肥干预的反应。DA神经元和受体亚型在分子、解剖和功能层面表现出显著的多样性。肥胖相关的DA释放、受体功能及下游信号改变因脑区和代谢背景而异。DA通过以VTA为中心的奖赏环路、以下丘脑为中心的进食环路以及中枢-外周代谢通路，调节食物奖赏、进食、体力活动和产热。这些环路与神经肽、神经递质和神经调质系统以及代谢激素相互作用。在外周组织中，局部DA信号调节胃肠动力、胰腺激素分泌、脂肪组织功能和骨骼肌葡萄糖利用。饮食调整、运动、微生物组干预、减重手术、胰高血糖素样肽-1受体（GLP-1R）激动剂及其他DA调节剂可能改变这些通路。然而，直接证明DA调节介导其临床效应的证据仍然有限。当前证据不支持肥胖中存在一致的多巴胺能（DAergic）功能障碍模式或泛化的奖赏缺陷模型。DA改变因神经环路、受体亚型、组织、代谢状态和进食阶段而异。大多数人类研究结果属于关联性发现，而机制性证据主要来自动物模型。DA改变是先于肥胖发生还是由饮食暴露和代谢功能障碍所致，目前尚不清楚。中枢与外周DA系统之间的协调关系也尚不明确。需要纵向和机制导向的人体研究来识别具有临床相关性的DAergic生物标志物和治疗靶点。
[英文摘要] 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. 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.
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3. When Ultra-Processed Foods are Eaten: The Missing Dimension in Exposure Measurement for Obesity Research.
3. 当食用超加工食品时：肥胖研究中暴露测量的缺失维度PMID:日期:2026-09-18Almost 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. 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.
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4. Correction: Does the Carbohydrate-Insulin Model Explain Obesity? Evidence from Mechanistic and Clinical Studies: A Critical Review.
4. 更正：碳水化合物-胰岛素模型能解释肥胖吗？来自机制与临床研究的证据：一篇批判性综述PMID:日期:2026-09-18该文献暂无摘要。
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5. Obesity-Associated Osteoarthritis: Mechanical-Metabolic Pathogenesis, Obesity Memory and Dual-Target Therapy.
5. 肥胖相关骨关节炎：机械-代谢发病机制、肥胖记忆与双靶点治疗PMID:日期:2026-09-16Given 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. 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.
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6. Hypothyroidism and Metabolic Dysfunction-Associated Steatotic Liver Disease: Mechanisms, Clinical Links, and Therapeutic Implications.
6. 甲状腺功能减退与代谢功能障碍相关脂肪性肝病：机制、临床关联及治疗意义PMID:日期:2026-09-14This 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. 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.
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7. Obesity-Related Tendon Pathology: Cardiometabolic Mechanisms, Clinical Implications, and Management.
7. 肥胖相关肌腱病变：心脏代谢机制、临床意义与管理PMID:日期:2026-09-11This 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. 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.
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8. State of the Science on Ultra-processed Foods and the Ultra-processed Food Addiction Construct.
8. 关于超加工食品与超加工食品成瘾构念的科学现状PMID:日期:2026-09-11We 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. 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.
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9. Obesity-related Metabolic Dysfunction and Triple-negative Breast Cancer: Epidemiologic Signals, Mechanistic Pathways, and Opportunities for Prevention.
9. 肥胖相关代谢功能障碍与三阴性乳腺癌：流行病学信号、机制通路及预防机会PMID:日期:2026-09-11Obesity 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. 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.
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10. Adipose Tissue Remodeling Beyond Weight Loss: New Insights Into Incretin-Based Therapies and Bariatric Surgery.
10. 脂肪组织重塑超越减重：胰高血糖素样肽-1疗法与减重手术的新见解PMID:日期:2026-09-10This 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. 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.