Reviews in Endocrine & Metabolic Disorders最新文献

{"title":"A biopsychosocial perspective on obesity and eating disorders: A narrative overview and exploratory study of ghrelin, LEAP2, trait impulsivity, and eating psychopathology.","authors":"Isabel Baenas, Lucía Camacho-Barcia, Roser Granero, Sara Tamarit, Sulay Tovar, Isabel Sánchez, Carlos Diéguez, Chloe Tezenas du Montcel, Philip Gorwood, Stefan Ehrlich, Roger Ah Adan, Suzanne L Dickson, Susana Jiménez-Murcia, Fernando Fernandez-Aranda","doi":"10.1007/s11154-026-10096-9","DOIUrl":"https://doi.org/10.1007/s11154-026-10096-9","url":null,"abstract":"<p><p>Dysregulated eating in obesity and eating disorders (ED) is associated with complex relationships between peripheral hormonal signals and neurobehavioral characteristics. Ghrelin and its endogenous antagonist liver-expressed antimicrobial peptide-2 (LEAP2) have been implicated in the regulation of energy homeostasis and food intake, while trait impulsivity has been proposed as a transdiagnostic characteristic associated with dysregulated eating. This study aimed to integrate narrative evidence with exploratory empirical data to examine associations between ghrelin, LEAP2, and trait impulsivity in women with obesity, with and without ED, and to explore their associations with food addiction (FA) and eating psychopathology. A total of 164 adult women (67 with obesity, 35 with obesity + ED, 62 healthy controls) completed anthropometric assessments, fasting ghrelin and LEAP2 determinations, and psychometric measures of trait impulsivity, FA, and eating psychopathology. Group comparisons and exploratory structural equation modeling (SEM) were used to explore associations between endocrine and behavioral variables. Women with obesity (with or without ED) showed significantly lower ghrelin levels than controls, while LEAP2 concentrations did not differ between groups. Trait impulsivity and FA scores were higher in the obesity + ED group. Within this subgroup, SEM analyses identified positive associations of trait impulsivity and FA with eating psychopathology, while LEAP2 was positively associated with trait impulsivity and FA scores. Previous research has pointed to potential associations of ghrelin and LEAP2 with obesity and ED, as well as with behavioral characteristics related to dysregulated eating, although the available evidence remains limited and heterogeneous. In our study, ghrelin was lower in women with obesity, whereas LEAP2 did not differ between groups. The observed associations involving LEAP2 emerged only in the exploratory SEM analysis and should therefore be interpreted cautiously. These findings are hypothesis-generating and do not provide evidence of mechanistic or causal relationships. Further research in larger and longitudinal samples is needed to replicate these findings and clarify the relationships among endocrine and behavioral factors.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228658","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":"Functional connectivity and treatment response in obesity and eating disorders: Current evidence and empirical data.","authors":"Romina Miranda-Olivos, Carles Soriano-Mas, Víctor De la Peña-Arteaga, Isabel Baenas, Ignacio Lucas, Lucía Camacho-Barcia, Isabel Sánchez, Roser Granero, Anahi Gaspar-Perez, Jessica Sánchez-González, José A Fernández-Formoso, Fernando Guerrero-Pérez, Rafael López-Urdiales, Nuria Vilarrasa, Susana Jiménez-Murcia, Fernando Fernández-Aranda","doi":"10.1007/s11154-026-10097-8","DOIUrl":"https://doi.org/10.1007/s11154-026-10097-8","url":null,"abstract":"<p><p>Alterations in large-scale brain networks have been reported in obesity (OB) and eating disorders (ED), but their relevance to treatment outcomes remains unclear. We reviewed evidence on neurobiological predictors of treatment outcome in ED and OB and present preliminary empirical analyses exploring baseline rsFC differences between individuals with anorexia nervosa (AN), obesity with comorbid ED (OB + ED), and obesity without ED (OB - ED) and healthy controls (HC), and examining whether these connectivity differences are associated with treatment outcome in the clinical groups. A total of 98 women (AN = 27, OB + ED = 25, OB - ED = 21, HC = 25) underwent resting-state functional magnetic resonance imaging (rs-fMRI). rsFC networks were subsequently identified using probabilistic independent component analysis (ICA), and their associations with treatment outcomes were examined within each clinical group. Both OB groups showed reduced rsFC relative to HC within a thalamic-basal ganglia network, specifically in a cluster located in the left inferior occipital cortex encompassing extrastriate visual regions. Baseline connectivity in this occipital cluster showed a positive, although non-significant, association with treatment outcome in the OB - ED group, whereas no significant associations were observed in AN or OB + ED. Given the non-significant nature of this exploratory association, the observed relationship should be considered hypothesis-generating and requires confirmation in adequately powered samples. Further work is needed to clarify the role of sensory-integrative networks in treatment response across extreme weight conditions.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224819","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":"Bone health in diabetes mellitus.","authors":"Paula Hoffmanová, David Galuška, Kateřina Kaňková, Monika Pávková Goldbergová","doi":"10.1007/s11154-026-10091-0","DOIUrl":"https://doi.org/10.1007/s11154-026-10091-0","url":null,"abstract":"<p><p>Bone health depends on a complex interplay between cellular and extracellular components that together preserve skeletal integrity, microarchitecture, and mechanical strength. Disturbance of this balance in a range of pathophysiological states, particularly in diseases such as diabetes mellitus, may substantially impair bone quality, delay fracture healing, and increase fracture risk. This review summarizes the main mechanisms linking diabetes and bone health, with emphasis on advanced glycation, oxidative stress, chronic inflammation, hormonal and osteoimmune dysregulation, microvascular impairment, and altered mesenchymal stem cell fate. We also review bone turnover markers, the skeletal effects of contemporary glucose-lowering therapies, and emerging methodological approaches, including single-cell and spatial transcriptomic analyses. A more integrated understanding of these processes may improve risk stratification, treatment decisions, and prevention of skeletal complications in diabetes.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149148541","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":"The neurobiology of binge eating disorder: a systematic review of studies using functional magnetic resonance imaging.","authors":"Jennifer J Park, Kangxin Zhang, Goeun Lee, Marc N Potenza","doi":"10.1007/s11154-026-10089-8","DOIUrl":"https://doi.org/10.1007/s11154-026-10089-8","url":null,"abstract":"<p><p>Binge eating disorder (BED) is a prevalent public health concern associated with significant medical and psychosocial burden. To better understand the mechanisms underlying this concern, the present systematic review aimed to synthesize findings from resting-state and task-based functional magnetic resonance imaging (fMRI) studies of the neurobiology of BED. PubMed, MEDLINE, PsycInfo, Embase, and Web of Science were searched, the Joanna Briggs Institute Critical Appraisal Tools were used, and the PRISMA guidelines were followed. The review identified 24 studies, comprising approximately 1,689 non-independent participants from an estimated 17 unique cohorts. These included task-based fMRI studies (n = 14), resting-state fMRI studies (n = 6), and BED treatment-outcome fMRI studies (n = 4). Key findings of the review included: (i) differences in neural responsivity to palatable food cues involving reward- and salience-related circuitry (e.g., orbitofrontal cortex, ventral striatum, and insula), alongside reduced recruitment of inhibitory-control regions during cognitive-control tasks; (ii) evidence suggesting reward-related differences in BED may be more food-specific than generalized across reward types, although some findings indicate broader frontostriatal hyporesponsivity during monetary reward processing; and, (iii) findings indicating that BED may share neurobiological overlap with, but remain distinguishable from, obesity and bulimia nervosa. However, these findings/interpretations are preliminary, given limitations in the current evidence base, including small samples, methodological heterogeneity, and the underrepresentation of males. Future neuroimaging studies should prioritize large-scale, longitudinal, efforts that include more representative (e.g., greater inclusion of males) and developmental (e.g., more children and adolescents) samples and consider socioenvironmental contexts relevant to BED. Such efforts may help inform individual-level personalized interventions.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149114377","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":"Gut dysbiosis, blood pressure regulation, and cardiometabolic risk in polyendocrine metabolic ovarian syndrome (PMOS).","authors":"Muhammad Naveed, Tao Yang, Olivia Togliatti, Bina Joe, Jennifer W Hill","doi":"10.1007/s11154-026-10085-y","DOIUrl":"https://doi.org/10.1007/s11154-026-10085-y","url":null,"abstract":"<p><p>Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), is a common endocrine-metabolic disorder associated with increased hypertension and cardiometabolic risk. Gut dysbiosis is also frequently reported in affected women, raising the question of whether microbiome-linked pathways contribute to blood pressure elevation or vascular risk in this syndrome. To evaluate and synthesize the available evidence linking gut dysbiosis, gut microbial function, and microbiome-related mechanisms to hypertension, blood pressure regulation, and cardiovascular risk in women with PMOS, we conducted a narrative review of the literature in PubMed, Scopus, Web of Science, Google Scholar, and citation tracking. Search terms included PCOS, PMOS, gut microbiota, gut dysbiosis, hypertension, blood pressure, cardiovascular risk, microbial metabolites, bile acids, intestinal permeability, inflammation, renin-angiotensin signaling, renal sodium handling, and autonomic regulation. Human studies, animal models, interventional studies, and mechanistic investigations relevant to PMOS and hypertension were reviewed according to predefined inclusion and exclusion criteria. Eligible publications were preclinical studies, human studies, English language, adult females, and peer-reviewed original or review articles. Clarifying whether gut dysbiosis contributes to hypertension in PMOS may improve understanding of the mechanisms underlying cardiometabolic risk in affected women and inform the development of microbiome-targeted diagnostic and therapeutic strategies. Achieving this goal will require well-phenotyped clinical studies integrating PMOS, blood pressure and vascular assessments with functional microbiome analyses.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149114247","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":"What is measured and what is estimated in body composition? A clarification framework for terminology and interpretation.","authors":"Francesco Campa, Henry C Lukaski, Tatiana Moro, Grant M Tinsley, Antonio Paoli, Giuseppe Coratella","doi":"10.1007/s11154-026-10071-4","DOIUrl":"10.1007/s11154-026-10071-4","url":null,"abstract":"<p><p>Body composition assessment has traditionally focused on estimating body mass components and the estimation processes required to obtain them in vivo. Within this context, the five-level model and the methodological taxonomy proposed by Wang and colleagues provided a rigorous conceptual framework that has strongly shaped the field. However, contemporary research and practice reveal persistent ambiguity in the use of terms such as direct, indirect, and doubly indirect. This ambiguity has become increasingly evident as methods such as anthropometry and bioelectrical impedance analysis are widely used not only to estimate body mass components, but also to obtain whole-body variables that are directly measured and interpreted as clinically, physiologically, or performance-relevant descriptors. Confusion often arises when directly measured outputs (e.g., skinfolds, girths, phase angle) are not clearly distinguished from model-derived estimates of body composition (e.g., fat mass, fat-free mass). Accordingly, we propose a clarification framework for in vivo body composition assessment that distinguishes: (1) directly measured whole-body variables, (2) model-derived estimates of body composition, and (3) hybrid assessment pathways combining measured and inferred outputs. In this framework, classification depends on the specific variable of interest and the estimation process linking measurement to output, rather than on assigning a fixed label to the instrument itself. The term direct refers only to an output that is measured rather than model-derived, and does not imply direct assessment of body components, greater validity, or superior methodological accuracy. The proposed framework provides a practical conceptual tool for distinguishing measured from estimated body composition outputs, thereby improving methodological transparency, interpretation, and reporting consistency across research and clinical practice.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"933-942"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148376768","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":"Exercise remodels the skeletal muscle immune microenvironment to ameliorate type 2 diabetes mellitus-induced muscle atrophy: From immunometabolism to organ crosstalk.","authors":"Fu Pengyu, Xu Huiyun, Gong Lijing","doi":"10.1007/s11154-026-10069-y","DOIUrl":"10.1007/s11154-026-10069-y","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM) complicated by muscle atrophy (diabetic sarcopenia) significantly increases mortality risk, with immunometabolic imbalance-driven disruption of the skeletal muscle microenvironment as a core mechanism. This review focuses on the immune cell-myocyte crosstalk network to elucidate the pathological mechanisms of T2DM-induced muscle atrophy, the local remodeling effects of exercise, and systemic organ crosstalk. In the T2DM state, M1/M2 imbalance and metabolic reprogramming of macrophages, dysregulated mast cell activation and histamine signaling, NLRP3 inflammasome-mediated pyroptosis, T-cell immunosenescence, and chemokine storms collectively disrupt muscle homeostasis. Exercise reverses these abnormalities by downregulating TRIB3/AKT to promote M2 polarization, restoring mast cell function, inhibiting the NLRP3/caspase-1/GSDMD pyroptosis pathway, increasing Treg infiltration, and downregulating the chemokine network, thereby shifting the local microenvironment from a \"pro-inflammatory/destructive\" to a \"reparative/regenerative\" state. Furthermore, exercise exerts systemic regulation through multiple organ axes, including adipose tissue (adipokines and inflammation), gut microbiota, liver (SIRT1/FGF21 signaling), and the brain (hypothalamic-pituitary-adrenal axis and myokines such as BDNF and CTSB for bidirectional neuroimmune regulation). In summary, exercise directly remodels the local immune crosstalk network in skeletal muscle and synergistically improves T2DM-associated muscle atrophy through multi-organ interactions, providing a theoretical basis for precise exercise interventions.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"1077-1090"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148388032","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":"Mammary adipocyte plasticity and epithelial crosstalk: roles in development, remodeling, and disease.","authors":"Peitong Chen, Yunjun Liao, Junrong Cai","doi":"10.1007/s11154-026-10065-2","DOIUrl":"10.1007/s11154-026-10065-2","url":null,"abstract":"<p><p>The mammary gland is a composite organ in which epithelial ducts and alveoli develop within a specialized adipose-rich stroma. Although mammary biology has traditionally been interpreted through an epithelium-centered framework, increasing evidence indicates that mammary adipocytes actively shape mammary development, reproductive remodeling, and disease susceptibility. Across puberty, pregnancy, lactation, and involution, mammary adipocytes undergo dynamic changes in cellular state, morphology, lipid handling, and stromal interactions, reflecting fate-related, phenotypic, and metabolic plasticity. Through adipokines, growth factors, metabolic substrates, extracellular matrix (ECM)-associated mechanical cues, and immune-inflammatory networks, mammary adipocytes influence epithelial behavior and tissue remodeling. Conversely, epithelial expansion, secretory differentiation, and post-weaning regression reshape the adipose-rich stromal niche. Dysregulation of this reciprocal adipose-epithelial ecosystem may contribute to aberrant tissue expansion, local estrogenic or inflammatory amplification, impaired adipose support, and tumor-permissive remodeling. Here, we review stage-specific epithelial-adipocyte crosstalk during mammary development, define mammary adipocyte plasticity across fate-related and functional dimensions, and discuss its relevance to benign breast disorders, tumor-associated remodeling, and disease susceptibility.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"1023-1040"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562921","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":"Association between metabolic dysfunction-associated steatotic liver disease/non-alcoholic fatty liver disease and chronic kidney disease: a systematic review and meta-analysis.","authors":"André O Soares, Davi A C Loli, Gustavo R Carvalho, Vinicius Daher Alvares Delfino, Paulo Roberto Bignardi","doi":"10.1007/s11154-026-10059-0","DOIUrl":"10.1007/s11154-026-10059-0","url":null,"abstract":"<p><p>Data from current literature have suggested a positive association between Steatotic Liver Disease (SLD) and Chronic Kidney Disease (CKD). In 2023, a consensus of experts suggested that the term metabolic associated steatotic liver disease (MASLD) be used instead of non-alcoholic fatty liver disease (NAFLD), a term that had long been used to indicate the situation of hepatic steatosis not related to alcohol consumption or secondary to another etiology. The majority of hepatologists accepted this suggestion. To critically analyze this described association and compare the impact of change in criteria, we performed a systematic review followed by meta-analysis of incidence studies that evaluated the occurrence of new cases of CKD in patients diagnosed with NAFLD and MAFLD/MASLD. We searched the PubMed, LILACS, SciELO, and Cochrane Library databases for longitudinal studies published through June 2025 that included groups with NAFLD, MAFLD, and/or MASLD, as well as a control group, in the adult population without CKD at baseline. Among 2,099 studies found, twenty met the inclusion criteria. Compared to the patient's control group, the risk ratio (RR) for incidence of CKD in the group with MAFLD, MASLD, and NAFLD was 1.29 (1.18-1.40), 1.16 (1.12-1.19) and 1.25 (1.14-1.36), respectively. In a new analysis grouping MASLD with MAFLD to assess the impact of the terminology shift, the results remained similar. This review demonstrates that SLD is associated with the risk of developing CKD, regardless of classification. However, this connection needs further elucidation of its mechanisms to comprehend it better and prevent its impact.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"999-1021"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148219480","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":"Unveiling the role of aldosterone in metabolic dysfunction-associated steatotic liver disease.","authors":"Anna Hernández-Rubio, Maria-Teresa Julián, Elena Valassi, Nuria Alonso, Manel Puig-Domingo","doi":"10.1007/s11154-026-10056-3","DOIUrl":"10.1007/s11154-026-10056-3","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasing global health challenge closely linked to obesity and the metabolic syndrome. This review explores the role of aldosterone as a central contributor to metabolic dysfunction, highlighting its association with adipose tissue dysfunction and systemic insulin resistance which can further influence MASLD development and progression. While aldosterone-related organ damage has been extensively studied in other contexts such as kidney disease, its involvement in MASLD has received less attention. Beyond classical renin-angiotensin-aldosterone system activation, aldosterone secretion can be directly stimulated by leptin and other adipogenic factors, creating a pathogenic link between obesity and metabolic impairment. Aldosterone amplifies chronic inflammation, oxidative stress and insulin resistance, primarily through mineralocorticoid receptor (MR)-dependent mechanisms. These involve both genomic actions regulating pro-inflammatory genes and rapid non-genomic signalling. Additionally, aldosterone MR-independent effects, can further contribute to oxidative stress and inflammatory responses. Significantly, the MR is expressed in liver cells, including hepatocytes, liver sinusoidal endothelial cells, Kupffer cells, and hepatic stellate cells. This expression can allow for direct aldosterone-mediated effect on hepatic inflammation, oxidative stress, and fibrosis, which can occur alongside or independently of systemic metabolic pathways. Such direct mechanisms may explain associations found in clinical studies correlating high aldosterone levels -even with low renin- with the prevalence and progression of MASLD. Recognizing aldosterone as a pleiotropic hormone that integrates metabolic and hepatic disease offers new insights into the cardio-kidney-metabolic syndrome and underscores the potential for targeted therapies.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"943-958"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148353299","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}