Hormones (Athens, Greece)最新文献

{"title":"Antidiabetic medications in the pipeline.","authors":"Zoe A Efstathiadou, Apostolos I Gogakos, Efstathios Divaris, Georgios Kostopoulos, Evangelia Makri","doi":"10.1007/s42000-026-00780-5","DOIUrl":"https://doi.org/10.1007/s42000-026-00780-5","url":null,"abstract":"<p><p>There is an extensive pipeline of therapies for diabetes mellitus. It has been known for the past three decades that obesity is a key pathophysiological player, involving inflammation, insulin resistance and metabolic dysfunction leading to type 2 diabetes and to significant cardiovascular, renal and hepatic complications, all central to the metabolic syndrome. On the basis of this knowledge and the disposition of drugs with multiple effects on different disease components, the diabetes therapeutic paradigm has shifted from merely glucocentric to multitargeted against these interconnected pathways.Much more recently, incretin-based multi-agonists have been developed that deliver unprecedented glycemic and weight benefits as well as weekly insulins and oral GLP-1 agonists that are able to reduce the burden of injectable therapies. An antibody-peptide conjugate that acts as a dual GLP-1/GIP receptor modulator has also shown promising results. Today, novel insulin sensitizers are modulating metabolic pathways towards higher energy expenditure with fewer side effects. Adjunctive agents for type 1 diabetes are improving glucose control while reducing hypoglycemia risk. Finally, drugs designed to restrain the inevitable muscle mass loss caused by antiobesity treatments are being tested. The diabetes pipeline is rich and there is hope that in the next few years, the therapeutic landscape will be further transformed with even more efficacious and individualized treatments.</p>","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning and penalized logistic regression-based models for the identification of potential characteristic genes in primary hyperparathyroidism.","authors":"Tianze Wang, Qila Sa, Boyuan Nan, Wei Zhang","doi":"10.1007/s42000-026-00832-w","DOIUrl":"https://doi.org/10.1007/s42000-026-00832-w","url":null,"abstract":"<p><strong>Purpose: </strong>Primary hyperparathyroidism (PHPT) is an endocrine disorder in which one or more parathyroid glands oversecrete parathyroid hormone, leading to hypercalcemia and potential complications such as kidney stones, bone fractures, and other systemic issues. Machine learning (ML) is extensively applied to diagnose medical diseases due to its high accuracy and ease of implementation.</p><p><strong>Methods: </strong>The microarray expression dataset (GSE83421) was selected from the Gene Expression Omnibus Database (GEO) for analysis. Differential expression analysis was performed with false discovery rate (FDR) correction. Weighted gene co-expression network analysis (WGCNA) identified correlated gene modules. Consensus feature selection using six algorithms (LASSO, SVM-RFE, random forest, Boruta, XGBoost, and decision tree) was applied to identify robust biomarkers and mitigate overfitting. A penalized logistic regression model was developed and evaluated using leave-one-out cross-validation (LOOCV).</p><p><strong>Results: </strong>Ten candidate genes were identified by intersecting 24 DEGs with the WGCNA red module. Consensus ML selected five hub genes (LOC51092, KIAA1479, PRO2214, TBX4, and ZNF361). T. The LOOCV-validated penalized logistic regression model effectively distinguished PHPT from normal controls.</p><p><strong>Conclusion: </strong>Our analysis identified a 5-gene signature (LOC51092, KIAA1479, PRO2214, TBX4, and ZNF361) with diagnostic potential for PHPT. The model was internally validated using LOOCV. However, without nested feature selection or external validation, the reported performance likely represents an optimistic estimate. Given the limited sample size, these findings represent preliminary hypotheses for PHPT diagnosis, requiring validation in independent cohorts.</p>","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How much is enough - surgical extent of initial parathyroidectomy and long-term outcomes in MEN1-related primary hyperparathyroidism.","authors":"Kosmas Daskalakis, Konstantinos Ntalaperas, Nektaria Papadopoulou, Marina Tsoli, Anna Angelousi, Eva Kassi, Gregory Kaltsas","doi":"10.1007/s42000-026-00828-6","DOIUrl":"https://doi.org/10.1007/s42000-026-00828-6","url":null,"abstract":"<p><strong>Context: </strong>Multiple endocrine neoplasia type 1 (MEN1)-associated primary hyperparathyroidism (pHPT) is typically multiglandular, which contributes to both persistent and recurrent disease following surgery. The optimal extent of initial parathyroidectomy in MEN1 remains debated.</p><p><strong>Objective: </strong>To evaluate long-term outcomes of subtotal parathyroidectomy (SPTX) and total parathyroidectomy with autotransplantation (TPTX-AT) versus less-than-subtotal parathyroidectomy (LSPTX) in MEN1-related pHPT, specifically regarding persistence, recurrence, permanent hypoparathyroidism, and need for reoperation.</p><p><strong>Methods: </strong>A retrospective cohort study was conducted including 65 MEN1 patients who underwent initial parathyroidectomy and were followed at a single tertiary referral center. Patients were stratified according to surgical extent (LSPTX vs SPTX/TPTX-AT). Recurrence was analyzed only among patients who had documented initial postoperative normocalcemia and evaluable follow-up; Kaplan-Meier curves were constructed for recurrence-free survival. Multivariable Cox regression was applied to identify independent predictors of adverse outcomes.</p><p><strong>Results: </strong>The median follow-up was 133.1 months (range 2.4-442.2 months). Nineteen patients underwent LSPTX and 46 underwent SPTX/TPTX-AT. Among patients evaluable for recurrence, recurrent pHPT occurred in 13/19 (68.4%) after LSPTX versus 16/45 (35.6%) after SPTX/TPTX-AT (Fisher's exact test, p = .027). Permanent hypoparathyroidism at last follow-up occurred in 2/17 (11.8%) and 10/45 (22.2%), respectively (p = 0.484). Recurrence-free survival was significantly shorter after LSPTX (log-rank p<0.001). In a parsimonious Cox model adjusted for age at surgery, LSPTX remained associated with shorter recurrence-free survival compared with SPTX/TPTX-AT (HR 6.11 (95% CI 2.64-14.17).</p><p><strong>Conclusion: </strong>In MEN1-related pHPT, limited parathyroidectomy (LSPTX) is associated with significantly higher recurrence rates and shorter recurrence-free survival. Although the risk of permanent hypoparathyroidism appeared lower after LSPTX, this difference did not reach statistical significance. These findings support subtotal parathyroidectomy as the preferred initial surgical strategy in most MEN1 patients, while emphasizing lifelong biochemical surveillance.</p>","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149122743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of calcitriol (1,25(OH)₂D₃) on endothelial-derived factors implicated in atheromatous plaque vulnerability.","authors":"Narjes Nasiri-Ansari, Aspasia Rizou, Christina-Maria Flessa, Manpal S Randeva, Eliana Spilioti, Maria-Eleni Chondrogianni, Lisa Dannenberg, Athanasios G Papavassiliou, Eva Kassi","doi":"10.1007/s42000-026-00831-x","DOIUrl":"https://doi.org/10.1007/s42000-026-00831-x","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis progresses from endothelial dysfunction to arterial plaque vulnerability, rupture, erosion, and calcification. Vitamin D deficiency is an independent cardiovascular risk factor associated with advanced atherosclerotic disease. This study investigated whether calcitriol (1,25(OH)₂D₃), the active hormonal form of vitamin D, modulates the expression of MMP-2, MMP-9, TIMP-1, TIMP-2, MCP-1, RANK, RANKL, and OPG in human aortic endothelial cells (HAECs).</p><p><strong>Methods: </strong>Cells were treated with calcitriol alone or in combination with TNF-α. Gene expression was assessed by qPCR, MCP-1 and OPG protein levels were measured by ELISA, and MMP activity by zymography.</p><p><strong>Results: </strong>Calcitriol did not significantly affect basal MMP-2, MMP-9, TIMP-1, or TIMP-2 expression but reduced MCP-1 mRNA at 10⁻⁸ M. In TNF-α-activated cells, pre-incubation of cells with calcitriol decreased MMP-9 and MCP-1 expression, restored TIMP-2 levels, elevated the pro-/active-MMP-2 ratio and increased OPG mRNA expression, although this transcriptional effect was not accompanied by a corresponding increase in OPG protein levels.</p><p><strong>Conclusion: </strong>The effects of calcitriol on human aortic endothelial cells suggest that calcitriol modulates inflammatory and extracellular matrix-remodeling markers in TNF-α-stimulated human aortic endothelial cells. Whether these changes contribute to plaque stability requires confirmation in more complex experimental models.</p>","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149122709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Weekday-weekend sleep patterning and testosterone outcomes in US men: a cross-sectional analysis of NHANES 2011-2014.","authors":"Renjie Huang, Miao Huang, Rui Zhang","doi":"10.1007/s42000-026-00833-9","DOIUrl":"https://doi.org/10.1007/s42000-026-00833-9","url":null,"abstract":"<p><strong>Purpose: </strong>Weekday-weekend differences in sleep duration are common, but their associations with testosterone and the specificity of corrected weekend catch-up sleep (CUS) as a sleep-pattern measure remain uncertain. We examined corrected CUS and related weekday-weekend sleep-pattern measures in relation to low and continuous total testosterone in US men.</p><p><strong>Methods: </strong>This cross-sectional analysis included 3,042 men aged ≥ 20 years from NHANES 2011-2014. Corrected CUS was defined as max (mean weekend sleep duration - mean weekday sleep duration, 0). Survey-weighted logistic and linear regression models examined biochemically low total testosterone and continuous total testosterone, with multiple imputation for missing covariates.</p><p><strong>Results: </strong>Low total testosterone was present in 883 participants (weighted prevalence, 28.0%). Compared with CUS = 0, only the highest positive corrected-CUS category (> 1.346 h) was associated with low total testosterone (OR 1.37, 95% CI 1.06-1.77) and lower continuous testosterone (- 28.90 ng/dL, 95% CI - 46.96 to - 10.84). The categorical low-testosterone association was not retained in complete-case, strict valid-night, or upper-tail-excluded analyses, whereas the corresponding continuous-testosterone contrast remained evident in the strict and upper-tail-excluded cohorts. Directional weekday-weekend and sleep-irregularity analyses did not support an association specific to weekend sleep extension.</p><p><strong>Conclusion: </strong>Corrected CUS showed modest cross-sectional associations with testosterone outcomes, but the broader pattern of results did not establish specificity to weekend sleep extension. Corrected CUS may instead reflect weekday-weekend sleep-pattern mismatch or broader sleep irregularity. These findings do not establish causality or support clinical use.</p>","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149066308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipodystrophies and female reproduction: pathophysiology, clinical spectrum, and management across the reproductive lifespan.","authors":"Dimitrios Pappas, Ifigenia Kostoglou-Athanassiou, Georgios Troupis, George Mastorakos","doi":"10.1007/s42000-026-00824-w","DOIUrl":"https://doi.org/10.1007/s42000-026-00824-w","url":null,"abstract":"<p><strong>Background: </strong>Lipodystrophies represent a heterogeneous group of rare disorders characterized by partial or generalized loss of adipose tissue, leading to severe metabolic derangements and endocrine dysfunction. In women, these disorders are frequently accompanied by reproductive abnormalities ranging from hypogonadotropic amenorrhea to hyperandrogenism and polycystic ovary syndrome-like phenotypes.</p><p><strong>Objective: </strong>To summarize current knowledge linking adipose-tissue dysfunction and female reproductive health, focusing on mechanistic pathways, clinical manifestations, fertility outcomes, contraception, pregnancy complications, and therapeutic perspectives including leptin replacement.</p><p><strong>Methods: </strong>A comprehensive review of PubMed and guideline literature (1996-2025) was performed, prioritizing official recommendations, registry data, and recent mechanistic and clinical studies.</p><p><strong>Results: </strong>Profound leptin deficiency in generalized lipodystrophy leads to hypothalamic suppression of gonadotropin-releasing hormone (GnRH) and amenorrhea, whereas hyperinsulinemia and androgen excess dominate partial forms, producing anovulation and infertility. Metreleptin therapy restores ovulatory cycles in leptin-deficient women and improves metabolic control, while pregnancy carries heightened risks of gestational diabetes, pre-eclampsia, and pancreatitis. Oral estrogens exacerbate hypertriglyceridemia; thus, progestin-only or non-hormonal contraception is preferred, and transdermal estrogen may be considered for hormone replacement.</p><p><strong>Conclusions: </strong>Female reproductive dysfunction in lipodystrophy results from complex interactions between leptin, insulin, and gonadal steroid pathways. A multidisciplinary approach is required to optimize metabolic and reproductive outcomes, while prospective data on fertility and pregnancy under metreleptin remain crucial for future practice.</p>","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149043122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond insulin resistance: insights into the clinical utility of TyG and TG/HDL-C in hospitalized patients.","authors":"Rafailia Gidari, Marina Ioannidou, Iraklis Leonidis, Djordje S Popovic, Theocharis Koufakis","doi":"10.1007/s42000-026-00830-y","DOIUrl":"https://doi.org/10.1007/s42000-026-00830-y","url":null,"abstract":"<p><strong>Background: </strong>The triglyceride-glucose (TyG) index and triglyceride-to-high-density lipoprotein cholesterol (TG/HDL-C) ratio are established surrogate markers of insulin resistance and cardiometabolic risk, but their interpretation in hospitalized patients remains unclear.</p><p><strong>Methods: </strong>In this cross-sectional study, we evaluated associations of TyG and TG/HDL-C with clinical characteristics, laboratory parameters, and cause of admission in 101 consecutive internal medicine inpatients.</p><p><strong>Results: </strong>Both indices correlated strongly with triglycerides (TyG: ρ = 0.765, p < 0.001; TG/HDL-C: ρ = 0.861, p < 0.001) and were associated with renal dysfunction (urea: TyG ρ = 0.391, p < 0.001; TG/HDL-C ρ = 0.300, p = 0.002). Urea remained independently associated with TyG (β = 0.003, p = 0.033) and TG/HDL-C (β = 0.006, p = 0.003). Hematological (β=-0.815, p = 0.007) and infectious/fever of unknown origin admissions (β=-0.663, p = 0.039) were independently associated with lower TyG values.</p><p><strong>Conclusions: </strong>In hospitalized patients, TyG and TG/HDL-C reflect a broader cardiometabolic-inflammatory-renal profile, warranting cautious interpretation and further study.</p>","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149033045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic modifications in type 2 diabetes mellitus.","authors":"Marina Spaho, Fotios Karytis, Stavros P Papadakos, Antonios Chatzigeorgiou","doi":"10.1007/s42000-026-00829-5","DOIUrl":"https://doi.org/10.1007/s42000-026-00829-5","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM) develops through the interplay of insulin resistance and progressive beta-cell dysfunction. Beyond genetic predisposition, epigenetic regulation provides a mechanistic link between environmental exposures (e.g., overnutrition, physical inactivity, inflammation) and durable changes in gene expression in pancreatic islets and insulin-sensitive tissues (skeletal muscle, adipose tissue, and liver). Accordingly, this review aims to synthesize current evidence on the epigenetic mechanisms underlying T2DM and its complications, with a particular focus on epigenetically targeted therapeutic strategies. We summarize major epigenetic processes, including DNA and RNA methylation, histone post-translational modifications, and non-coding RNAs, and discuss how these alterations remodel chromatin and transcriptional programs under metabolic stress. A key concept is \"metabolic memory,\" whereby transient hyperglycemia or lipotoxicity can induce persistent epigenetic signatures that sustain dysfunctional cellular phenotypes, partly shaped by mitochondrial metabolism and Krebs cycle intermediates regulating chromatin-modifying enzymes. Importantly, several epigenetic alterations demonstrate partial reversibility following lifestyle modification, metabolic surgery, or pharmacological intervention (e.g., DNA methyltransferase inhibition), underscoring their therapeutic relevance. Finally, we address translational challenges, including limited access to human tissues and inadequate modeling of chronic metabolic stress, which currently constrain clinical exploitation of epigenetic targets in T2DM.</p>","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149026811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hormonal target validation based on biochemical shifts in gender-affirming hormone therapy.","authors":"Jeroen Vervalcke, Lorenzo Marinelli, Dorte Glintborg, Louise Lehmann Christensen, Martin den Heijer, Alessandra Fisher, Konstantina Barouti, Guy T'Sjoen","doi":"10.1007/s42000-026-00822-y","DOIUrl":"https://doi.org/10.1007/s42000-026-00822-y","url":null,"abstract":"<p><strong>Background: </strong>Hormonal targets for gender-affirming hormone therapy (GAHT) remain largely unvalidated in gender-diverse individuals, with no clinical markers to assess dosing adequacy. We hypothesize that a biochemical shift towards the hormonal profile of the identified sex correlates with appropriate dosing.</p><p><strong>Methods: </strong>A data-subset from the National Health and Nutrition Examination Survey (NHANES), comprising 5,433 assumed-cisgender individuals (47.2% male) aged < 52 years, was used to train and validate a random forest model to predict sex-registered-at-birth, incorporating platelet count, high-density lipoprotein cholesterol percentage, sex hormone-binding globulin (SHBG), creatinine, and hematocrit. The model was subsequently run in 174 transgender men (TM) and 135 transgender women (TW) from the European Network for the Investigation of Gender Incongruence (ENIGI) Ghent cohort. Blood samples were collected at 0, 3, 12, 18, 24, and 36 months after GAHT-initiation. Hormonal profiles were compared based on predicted sex-registered-at-birth.</p><p><strong>Results: </strong>The model achieved 91% accuracy in NHANES, with baseline accuracy of 81.5% in ENIGI, declining to 10.7% at 36 months. Median estradiol (E2) concentrations in TW-predicted males-assigned-at-birth (59.0 ng/L, interquartile range, IQR: 45.3-73.3) were significantly lower (p < 0.0001) than in TW-predicted females-assigned-at-birth with a fully feminized biochemical signature (78.5 ng/L, IQR: 53.1-107.4). Difference in testosterone concentrations in TM-classified female-assigned-at-birth and predicted male-assigned-at-birth did not reach significance. Classification according to sex-at-birth seemed less likely to occur at higher E2 concentrations in TW.</p><p><strong>Conclusion: </strong>The innate sexual dimorphism of biochemical parameters might provide a framework for GAHT target validation. Significantly different hormonal profiles can be seen in people depending on the biochemical shift experienced during GAHT.</p>","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucagon-like peptide-1 receptor agonists and cognitive function: beyond the metabolic effects.","authors":"Stergios A Polyzos, Michael Doulberis, Nikolaos Zervogiannis, Christos-Alexandros Batakoias, Jannis Kountouras","doi":"10.1007/s42000-026-00827-7","DOIUrl":"https://doi.org/10.1007/s42000-026-00827-7","url":null,"abstract":"","PeriodicalId":520640,"journal":{"name":"Hormones (Athens, Greece)","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148972997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}