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        <title>Frontiers in Endocrinology | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/endocrinology</link>
        <description>RSS Feed for Frontiers in Endocrinology | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-13T08:31:28.121+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1833684</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1833684</link>
        <title><![CDATA[Comparative effectiveness of high-intensity interval training versus moderate-intensity continuous training in patients with type 2 diabetes mellitus: a systematic review and meta-analysis]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Pengbo Ren</author><author>Jian Zhang</author><author>Shi Li</author><author>Tingwen Li</author>
        <description><![CDATA[ObjectiveTo systematically evaluate and compare the effects of High-Intensity Interval Training (HIIT) and Moderate-Intensity Continuous Training (MICT) on key glycemic indicators and related metabolic parameters in patients with Type 2 Diabetes Mellitus (T2DM).MethodsDatabases including PubMed, Web of Science, Cochrane Library, CNKI, and Wanfang were searched to collect randomized controlled trials (RCTs) published up to October 2025 on HIIT and MICT in T2DM. Two researchers independently screened the literature, extracted data, and assessed the risk of bias in the included studies. A meta-analysis was then performed using RevMan 5.4.ResultsA total of 21 RCTs involving 831 T2DM patients were included. The meta-analysis results showed that compared to a normal control group, both HIIT and MICT significantly reduced fasting blood glucose (FBG) and increased patients’ VO2max levels. HIIT significantly reduced patients’ glycated hemoglobin (HbA1c) levels, body mass index (BMI), and significantly increased high-density lipoprotein (HDL) levels. Compared to MICT, HIIT was more effective in reducing FBG and provided a greater increase in maximal oxygen uptake (VO2max). Both HIIT and MICT effectively reduced HbA1c in T2DM patients, although there was no significant difference in the effect between the two modalities. Regarding BMI, low-density lipoprotein (LDL), and HDL, the two exercise modalities did not show statistically significant differences.ConclusionIn the management of T2DM, HIIT offers greater advantages in improving FBG and enhancing VO2max, providing a basis for the scientific and effective management of T2DM. However, due to the limitations in the number and quality of the included studies, the above conclusions require verification through more high-quality research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1872081</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1872081</link>
        <title><![CDATA[Correction: Pancreatic islet cell calcium ion imaging at single-cell resolution: functional identification of first responder, highly connected (“hub”), and leader beta-cells]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Frontiers Production Office </author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1805525</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1805525</link>
        <title><![CDATA[Impact of gestational diabetes mellitus and hypertensive disorders of pregnancy on adverse pregnancy outcomes: a retrospective cohort study]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Junjia Shao</author><author>Xia Li</author><author>Lifeng Wang</author><author>Bo Dong</author>
        <description><![CDATA[ObjectiveTo investigate the independent and joint effects of gestational diabetes mellitus (GDM) and hypertensive disorders of pregnancy (HDP) on adverse pregnancy outcomes, evaluate their potential interaction, and explore the nonlinear dose–response relationships between blood glucose and blood pressure levels and composite adverse outcomes using a restricted cubic spline (RCS) model.MethodsThis retrospective cohort study included 240 women who delivered at Dongyang Maternal and Child Health Hospital between January 2020 and December 2024. Participants were categorized into four groups according to the presence of GDM and/or HDP: control, GDM only, HDP only, and comorbid GDM + HDP. The primary outcome was a composite of adverse pregnancy outcomes, including preterm birth, Apgar score < 7, neonatal intensive care unit (NICU) admission, and fetal growth abnormalities. Multivariable logistic regression models were applied to estimate adjusted odds ratios (aORs) and 95% confidence intervals (CIs). Additive interaction indices—relative excess risk due to interaction (RERI) and attributable proportion (AP)—were calculated to assess synergistic effects. Nonlinear dose–response associations between mean fasting glucose, systolic blood pressure (SBP).ResultsCompared with the control group, HDP was independently associated with a higher risk of composite adverse outcomes (aOR = 3.30, 95% CI: 1.41–7.70, P = 0.006), while comorbid GDM + HDP showed a substantially elevated risk (aOR = 9.25, 95% CI: 2.63–32.45, P < 0.001). Additive interaction analysis demonstrated a significant positive interaction between GDM and HDP (RERI = 5.62; AP = 0.61), suggesting that over half of the excess risk was attributable to their joint effect. Specifically, the risks of preterm birth and small-for-gestational-age infants increased markedly in the HDP and comorbid groups, whereas GDM alone was primarily associated with large-for-gestational-age outcomes. RCS analysis revealed a nonlinear positive relationship between mean SBP and composite adverse outcomes, with the risk increasing sharply beyond approximately 135 mmHg and accelerating above 160 mmHg.ConclusionBoth GDM and HDP independently increase the risk of adverse pregnancy outcomes, and their coexistence exerts a synergistic effect that amplifies maternal and neonatal risk. The nonlinear dose–response pattern between SBP and adverse outcomes highlights that even mild elevations in blood pressure can have detrimental effects.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1758519</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1758519</link>
        <title><![CDATA[Glucose cotransporter-2 inhibitors on mortality and hospitalization in heart failure patients: a comprehensive meta-analysis]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiang Mao</author><author>Wenhua Liu</author><author>Bingqian Hu</author><author>Enguo Xu</author>
        <description><![CDATA[BackgroundHeart failure (HF) remains a major global health challenge, with high rates of hospitalization and mortality despite advances in therapy. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, originally developed as antidiabetic agents, have demonstrated significant cardiovascular and renal benefits across a wide range of patients.ObjectiveThis study aims to evaluate the impact of SGLT2 inhibitors on all-cause mortality, heart failure hospitalization, and secondary outcomes, including NT-proBNP levels, left ventricular (LV) systolic function, and diuretic efficiency in patients with heart failure, irrespective of ejection fraction or diabetes status.MethodsA systematic review and a meta-analysis were conducted according to PRISMA 2020 guidelines. Electronic databases (PubMed, Embase, Cochrane CENTRAL, Scopus, and Web of Science) were searched for randomized controlled trials (RCTs) published between January 2017 and November 2025. A total of 15 eligible RCTs encompassing 28,484 participants were included. Data were extracted on clinical and functional outcomes, and pooled estimates were calculated using a DerSimonian–Laird random-effects model. Heterogeneity was assessed using the I² statistic, and publication bias was evaluated using Egger’s and Begg’s tests.ResultsSGLT2 inhibitor therapy was associated with a 14% reduction in all-cause mortality (HR = 0.86, 95% CI: 0.79–0.92; p < 0.001) and a 26% reduction in heart failure hospitalization (HR = 0.74, 95% CI: 0.68–0.81; p < 0.001). Heterogeneity was low for mortality (I² = 18%) and moderate for hospitalization (I² = 39%). SGLT2 inhibitors also significantly decreased the NT-proBNP levels (mean difference −168.4 pg/mL, 95% CI: −245.6 to −91.2; p < 0.001) and improved the LV systolic function (LVEF + 3.8%, 95% CI: +2.4 to +5.2; p < 0.001). Diuretic efficiency improved by an average of 480 mL/day (95% CI: +290 to +640; p = 0.002). The benefits were consistent across subgroups, including patients with HFrEF and HFpEF, with or without diabetes, and across individual SGLT2 inhibitors (empagliflozin, dapagliflozin, and sotagliflozin). No significant publication bias was detected.ConclusionsSGLT2 inhibitors significantly reduce the mortality and heart failure hospitalizations while improving the biomarker and cardiac function parameters, independent of diabetes status or heart failure phenotype. The consistency and magnitude of benefit confirm a class effect and support SGLT2 inhibitors as foundational therapy for heart failure across all ejection fraction categories.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1838301</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1838301</link>
        <title><![CDATA[Impact of diabetes mellitus on mortality in patients with acute exacerbation of chronic obstructive Pulmonary disease: a meta-analysis and systematic review]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Dongmei Zhang</author><author>Hongbo Zhou</author><author>Xiujuan Yang</author><author>Dajian Xia</author>
        <description><![CDATA[BackgroundAs one of the most prevalent comorbidities in chronic obstructive pulmonary disease (COPD), diabetes mellitus has drawn growing attention for its potential impact on clinical outcomes in acute exacerbation of COPD (AECOPD). However, the association between diabetes and mortality risk in AECOPD remains controversial. This meta-analysis synthesized available evidence to quantify the effect of diabetes on mortality among AECOPD patients, aiming to provide an evidence-based foundation for clinical risk stratification and individualized intervention.MethodsWe systematically searched PubMed, Embase, Cochrane Library, Web of Science, CNKI, and Wanfang databases up to March 2026 for cohort or case-control studies investigating the association between diabetes and mortality in AECOPD patients. Two researchers independently conducted literature screening, data extraction and quality evaluation. The Newcastle-Ottawa Scale (NOS) was used to assess risk of bias. Meta-analysis was performed using Stata 14.0 software. The hazard rations (HR) was used to combine the effect size, and corresponding 95% confidence interval (CI) was computed.ResultsA total of 9 studies were included, involving 23,883 participants. In the univariate model, diabetes increased the mortality risk of patients with AECOPD (HR = 1.45, 95%CI (1.19,1.77), P < 0.0001), whereas no significant association was observed in multivariate analysis (HR = 1.50, 95% CI (0.45, 5.00), P = 0.513). Subgroup analysis showed that diabetes increased mortality risk in hospitalized AECOPD patients but not in those admitted to intensive care units. A significant association was found in case-control studies but not in cohort studies, and in studies with a sample size > 1000 but not in smaller studies.ConclusionsThis meta-analysis demonstrates inconsistent associations between diabetes and mortality in AECOPD patients, which may be confounded by methodological factors and study design. Current evidence does not support diabetes as an independent risk factor for mortality in AECOPD. Further well-designed, adequately powered prospective cohort studies with rigorous adjustment for confounders are warranted to clarify the true prognostic impact of diabetes on AECOPD patients.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1764227</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1764227</link>
        <title><![CDATA[Timing of dexamethasone initiation during controlled ovarian stimulation and live birth after IVF/ICSI: a retrospective cohort study]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ling Zhang</author><author>Bin Tang</author><author>Yaqian Qin</author><author>Xuan Lu</author><author>Jia Tang</author><author>Ailing Peng</author>
        <description><![CDATA[BackgroundDexamethasone (DXM) is used as an empirical adjuvant in IVF/ICSI, but evidence for its benefit remains inconsistent, and the clinical importance of initiation timing during controlled ovarian stimulation (COS) is unclear.MethodsWe retrospectively analyzed 644 COS cycles at a tertiary reproductive center. Cycles were classified as no DXM (n = 185), early-follicular DXM (stimulation days 0-4; n = 296), mid-follicular DXM (days 5-7; n = 69), or late/trigger-day DXM (day ≥8 or hCG day; n = 94). DXM was prescribed at the treating physician’s discretion, mainly for cycles considered at increased risk of premature progesterone elevation, and was administered as oral dexamethasone acetate once daily at 0.75-1.125 mg/day, predominantly 0.75 mg/day. Ovarian response, embryo development, and total usable embryos were analyzed in the full COS cohort. Pregnancy outcomes were analyzed among post-transfer cycles, and neonatal outcomes among deliveries. Multivariable logistic regression, propensity score-based inverse probability of treatment weighting, and mediation analysis were used to assess associations and address confounding.ResultsMid- and late/trigger DXM cycles generated more transferable and frozen embryos and more total usable embryos than cycles without DXM. In the post-transfer cohort, early- and mid-follicular DXM were associated with higher live-birth rates than no DXM, whereas late/trigger DXM showed no clear live-birth advantage. Adjusted and propensity score-weighted models produced consistent estimates. Mediation analysis did not show significant evidence that total usable embryos mediated the association between early DXM and live birth. Neonatal outcomes, including gestational age, birthweight, preterm birth, low birthweight, and congenital malformations, did not differ significantly by DXM timing.ConclusionsIn this retrospective cohort, DXM timing was associated with distinct reproductive outcomes. Early- and mid-follicular DXM were associated with higher live birth after transfer, whereas late/trigger DXM did not show clear clinical benefit. These findings should be interpreted cautiously given the clinically selected nature of DXM use.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1865319</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1865319</link>
        <title><![CDATA[Editorial: Advancing reproductive outcomes: integrating molecular, metabolic, and endocrine insights into oocyte maturation]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Konstantinos Dafopoulos</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1791850</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1791850</link>
        <title><![CDATA[Integrated RNA-seq and sQTL analysis reveal immune and splicing regulatory features underlying relapse and remission after treatment of Graves’ disease]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yang Wu</author><author>Jie Liu</author><author>Yu Yang</author><author>Kun Chen</author><author>Fei Hua</author><author>Kun Wang</author>
        <description><![CDATA[IntroductionGraves' disease (GD) is a classical autoimmune disorder caused by interactions between genetic susceptibility and immune dysregulation. However, the transcriptomic mechanisms underlying disease relapse and remission, particularly those involving alternative splicing (AS), remain poorly understood.MethodsWe performed an integrative RNA-seq analysis of peripheral blood samples from 33 GD patients in remission, 31 GD patients in relapse, and 30 normal controls (NC). Gene expression, transcript usage, alternative splicing events (ASEs), RNA-binding protein (RBP) regulation, and splicing quantitative trait loci (sQTLs) were systematically analyzed to characterize transcriptomic alterations associated with different disease states.ResultsCompared with NC, relapse-associated differentially expressed genes (DEGs) were mainly enriched in antimicrobial humoral immunity and suppression of TNF signaling, whereas remission-associated DEGs were associated with metabolic homeostasis and apoptosis regulation. Notably, 74 DEGs were consistently upregulated in both disease states. Transcriptomic analysis identified 234,595 transcripts, including 17.1% novel isoforms, and detected 352 and 387 differentially expressed transcripts (DETs) in relapse and remission, respectively. Transcript-level alterations frequently occurred independently of gene-level expression changes, indicating extensive isoform-specific regulation, as exemplified by isoform switching of HELZ2. In addition, 858 relapse-associated and 670 remission-associated aberrant ASEs (AASEs) were identified. RBP-AASE regulatory network analysis suggested that key RBPs, including APOBEC3C, may contribute to stage-specific splicing remodeling. sQTL analysis further identified 4,507 significant SNP-ASE associations, with affected genes enriched in immune-related pathways, including Th1/Th2/Th17 cell differentiation and TNF signaling. Among these, 12 splicing-related genes also exhibited aberrant AS patterns, while DDX5 and PKM showed sustained upregulation in both relapse and remission phases.DiscussionThese findings demonstrate that GD relapse and remission are closely associated with genetically and RBP-mediated alternative splicing regulation. Our study provides new insights into the molecular mechanisms underlying immune imbalance in GD and highlights potential transcriptomic biomarkers associated with disease relapse.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1736419</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1736419</link>
        <title><![CDATA[Association of sleep variability and irregularity with gestational metabolic syndrome: a birth cohort study]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Haiyan Gao</author><author>Libo Xu</author><author>Wenjuan Liu</author><author>Haibo Li</author><author>Bin Sun</author><author>Wei Li</author><author>Zhengqin Wu</author><author>Beihong Zheng</author><author>Yibing Zhu</author>
        <description><![CDATA[BackgroundPregnant women exhibit a high prevalence of sleep disturbances; however, the relationships between sleep variability, sleep irregularity, and gestational metabolic syndrome (GMS) remain poorly understood. This study aimed to investigate prospective associations of sleep variability and irregularity with the odds of GMS and its individual components.MethodsFour sub-cohorts of pregnant women were established based on data from the Fujian Birth Cohort Study (FJBCS) collected from 2019 to 2021. Logistic regression models were adopted to assess the associations between sleep variability and irregularity during pregnancy and the occurrence of GMS and its components. Stratified analyses examined potential modification of effects by demographic factors. Restricted cubic spline (RCS) models were used to evaluate potential non-linear relationships.ResultsGreater sleep variability was significantly associated with increased odds of GMS (aOR 1.348; 95% CI: 1.136-1.559) and dyslipidemia (aOR 1.086; 95% CI: 1.019-1.159), although no significant associations were found for hyperglycemia or hypertension. Sleep irregularity exhibited no significant association with GMS or its components. Subgroup analyses revealed increased vulnerability in women of advanced maternal age compared to younger age groups (aOR: 1.536 vs. 1.279). Those with a history of two or more prior pregnancies and natural pregnancies were more susceptible. RCS modeling confirmed the absence of nonlinear associations.ConclusionsHigher sleep variability is prospectively associated with an increased odds of GMS and dyslipidemia, with potential modulation by maternal age, conception method, and gravidity. No significant association was found between sleep irregularity and GMS or its components.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1816340</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1816340</link>
        <title><![CDATA[Phenotype-driven protocol switching is associated with improved ART outcomes under constant gonadotropin dosage: a self-controlled analysis of 4,632 cycles]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jie Gao</author><author>Yiran Li</author>
        <description><![CDATA[BackgroundManaging failure after an initial assisted reproductive technology (ART) cycle remains a significant clinical challenge. Clinicians often face a dilemma between repeating the index protocol, escalating gonadotropin (Gn) dosages, or switching to an alternative strategy. We aimed to evaluate whether phenotype-driven protocol switching, specifically addressing issues like over-suppression or poor embryo quality, is more effective than repeating the same protocol.MethodsThis large-scale, retrospective, self-controlled study involved 4,632 patients who underwent two consecutive ART cycles between January 2010 and December 2025. Patients were stratified into four pathways based on their second-cycle strategy: (i) Releasing Suppression (Long-to-Antagonist, n=1,412); (ii) Boosting Quantity (Mild-to-Antagonist, n=220); (iii) Improving Quality (Antagonist-to-Mild, n=829); and (iv) Reference (Antagonist-to-Antagonist, n=2,171). The primary outcome was the cumulative live birth rate (CLBR). Statistical analysis employed the Wilcoxon signed-rank test for paired continuous data and multivariable logistic regression to identify independent predictors of success.ResultsIn the Reference group, repeating the same protocol under identical Gn dosages significantly increased the CLBR (9.9% to 51.9%, P < 0.001). Beyond this baseline, individualised switching yielded distinct benefits. The Long-to-Antagonist switch significantly increased the median oocyte retrieval (8.0 [5.0–12.0] vs 9.0 [6.0–13.0], P < 0.001). The Mild-to-Antagonist switch successfully expanded the oocyte cohort in low responders (2.0 [1.0–4.0] vs 3.0 [2.0–5.2], P < 0.001). Conversely, the Antagonist-to-Mild switch did not increase oocyte yield (P = 0.642) but significantly improved the good embryo rate (median 0.0% vs 16.7%, P < 0.001). Multivariable regression confirmed that while age and anti-Müllerian hormone remained dominant prognostic factors, appropriate protocol triage neutralised risks without requiring dose escalation (P > 0.05 for protocol switch strategies).ConclusionsPhenotype-driven “quantity” or “quality” rescue is associated with significant clinical improvements following ART failure while keeping Gn dosages constant. While tactical switching is effective, a substantial proportion of the success in a second attempt is driven by natural biological variation (regression to the mean).”]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1815903</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1815903</link>
        <title><![CDATA[Case Report: Twenty years of metreleptin therapy in congenital generalized lipodystrophy type 1: the longest reported follow-up to date]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Elise Van der Borght</author><author>Bart Van der Schueren</author><author>Roman Vangoitsenhoven</author><author>David Cassiman</author><author>Baris Akinci</author><author>Rebecca J. Brown</author><author>Elif A. Oral</author><author>Ann Mertens</author><author>Pieter-Jan Martens</author>
        <description><![CDATA[Congenital generalized lipodystrophy (CGL) is a rare disorder marked by near-total loss of adipose tissue and severe metabolic disturbances due to leptin deficiency and the inability to store nutrients in adipose tissue effectively. Metreleptin is the only approved leptin replacement therapy for this condition. Here we present the >20-year follow-up of two sisters with CGL type 1 (AGPAT2 deficiency, OMIM# 608594), enrolled in early metreleptin trials. Clinical outcomes, adherence, immunogenicity, and pregnancies were assessed. Both cases showed rapid and sustained metabolic improvement after metreleptin initiation, allowing insulin discontinuation and triglyceride normalization. Menstrual cycles resumed within six months; allowing both to carry successful pregnancies while continuing metreleptin. Both cases experienced reduced treatment adherence over time, linked to psychological distress. One case developed both anti-drug antibodies and neutralizing activity through immune based assay after 14 years, but without significant clinical impact. In conclusion, these cases highlight both the sustained metabolic benefits of therapy and the complex challenges that may arise over time, such as antibody formation and difficulties in maintaining long-term adherence. Documentation of unmet medical needs can provide guidance and impetus for improved therapeutic approaches to achieve optimum quality of life.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1836392</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1836392</link>
        <title><![CDATA[Proteins at the intersection of circadian rhythms and metabolic dysfunction-associated steatotic liver disease: an 18-protein panel as a novel predictive biomarker set]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yiyi Wang</author><author>Qilong Zhai</author><author>Xuemei Lian</author><author>Lei Zhao</author>
        <description><![CDATA[Disruption of circadian rhythmicity is highly prevalent in modern society and contributes to the epidemic of metabolic disorders. However, the relationship between circadian rhythm disorder and Metabolic Dysfunction-Associated Steatotic Liver (MASLD) remained poorly elucidated. Relative amplitude (RA), a metric quantifying the degree of disruption in rest–activity circadian rhythms, was calculated based on accelerometry data from UK Biobank. Basic characteristic analysis and multivariable logistic regression was used to analyze the association between RA and MASLD. Mediation analysis, functional enrichment analysis (Kyoto Encyclopedia of Genes and Genomes, KEGG) and Protein–Protein Interaction (PPI) network analysis and multiple machine learning algorithms, including Random Forest, XGBoost, logistic regression, and Support Vector Machine (SVM), were employed to identify potential protein biomarkers and construct a predictive model for RA-related MASLD risk assessment. Among 81,430 UK Biobank participants with valid accelerometry, RA was lower in individuals with MASLD versus those without (P < 0.001). Lower RA was associated to higher prevalence of MASLD (crude OR = 2.61; 95% CI [2.42, 2.81]; P < 0.001), and the association remained significant in a fully adjusted model (adjusted OR = 1.15; 95% CI [1.02,1.31]; P = 0.026), demonstrating RA as a factor independently associated with MASLD. Furthermore, 18 candidate proteins were identified as potential biomarkers for predicting RA-related MASLD. The 18-protein model demonstrated excellent predictive performance across multiple machine learning methods, with high Area Under the Curve (AUC) values in Receiver Operating Characteristic (ROC) analysis: Random Forest (AUC = 0.944), XGBoost (AUC = 0.946), Logistic Regression (AUC = 0.946), and SVM (AUC = 0.947). The model also exhibited superior discriminatory ability in predictive probability distribution, indicating strong predictive potential. Additionally, an online predictive tool based on this model has been contributed. Lower RA is independently associated with MASLD. We highlight 18 overlapping plasma proteins linked to both RA and MASLD as potential biomarkers for predicting RA-associated MASLD and as candidate therapeutic targets.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1775998</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1775998</link>
        <title><![CDATA[Elevated lactate dehydrogenase-to-albumin ratio: a novel and independent predictor of ventricular aneurysm in STEMI patients]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Dong Hu</author><author>Ting Huang</author><author>Dongyang Wu</author><author>Qinshuo Zhao</author><author>Kai Zhang</author><author>Yuanlin Zou</author><author>Xin Guo</author><author>Yi Zhou</author>
        <description><![CDATA[BackgroundLeft ventricular aneurysm (LVA) is a major mechanical complication following acute ST-segment elevation myocardial infarction (STEMI). This study aimed to evaluate the predictive ability of the lactate dehydrogenase to albumin ratio (LAR) for the risk of LVA among STEMI patients.MethodsThe study was conducted from July 2018 to 2025 across three medical centers in China. The study cohort comprised STEMI patients who underwent primary percutaneous coronary intervention across three medical centers. Multivariate logistic regression analysis and Restricted cubic spline plots were employed to assess the association between different LAR levels and LVA risk. Subgroup analyses were conducted to assess the consistency of the result.ResultsThe study included 551, 471, and 1384 eligible participants from the first, second, and third cohort, respectively. After adjusting for potential confounders, individuals in the highest quartile of LAR (Q4) demonstrated a significantly elevated risk of developing LVA compared to those in the lowest quartile (Q1) across all cohorts (First cohort: OR = 3.63, 95% CI = 1.65 - 7.96, P = 0.001; Second cohort: OR = 6.01, 95% CI = 2.22 - 16.26, P< 0.001; Third cohort: OR = 2.41, 95% CI = 1.47 - 3.96, P< 0.001). RCS analysis revealed a positive linear association between LAR and the risk of LVA across the three cohorts (overall P> 0.05). The predictive capacity of LAR for assessing LVA risk exceeded that of both lactate dehydrogenase and albumin (P< 0.05). Subgroup analyses further reinforced the robustness of these findings.ConclusionAn elevated LAR was independently associated with an increased risk of LVA development in patients with STEMI who underwent primary PCI.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1843370</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1843370</link>
        <title><![CDATA[Comparison of effectiveness and safety of bexagliflozin and other sodium-glucose cotransporter 2 inhibitors for type 2 diabetes mellitus in adults: systematic review and network meta-analysis of randomized controlled trials]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Shan Gao</author><author>Fuyong Zhang</author><author>Xingxing Xie</author><author>Ling Fan</author>
        <description><![CDATA[BackgroundBexagliflozin exerts definite efficacy in the treatment of type 2 diabetes mellitus (T2DM). However, whether this novel sodium-glucose cotransporter 2 (SGLT2) inhibitor is superior to other SGLT2 inhibitors remains to be elucidated. We therefore performed this network meta-analysis (NMA) to compare bexagliflozin with other SGLT2 inhibitors and establish an efficacy hierarchy in T2DM management.MethodsWe systematically searched PubMed, Embase, Web of Science and the ClinicalTrials.gov registry for eligible randomized controlled trials (RCTs) published up to January 2026. Statistical analysis was conducted using Stata 14.0. Risk of bias was assessed by the Cochrane tool, evidence certainty was evaluated using the Confidence in Network Meta-Analysis (CINeMA) approach, and intervention ranking was performed using surface under the cumulative ranking curve (SUCRA) values.ResultsThis NMA included 48 studies with 26,838 patients. Bexagliflozin significantly reduced HbA1c, fasting plasma glucose (FPG), body weight, systolic blood pressure (SBP) and diastolic blood pressure (DBP) compared with placebo. For HbA1c reduction, canagliflozin (300 mg, 100 mg) and empagliflozin 25 mg were more effective than bexagliflozin, while bexagliflozin was comparable to other SGLT2 inhibitors. For FPG reduction, canagliflozin 300 mg and empagliflozin 25 mg showed slightly greater effects than bexagliflozin, with no significant differences between bexagliflozin and other comparators. Bexagliflozin was superior to dapagliflozin 5 mg but slightly inferior to canagliflozin 300 mg for weight loss, while showing comparable efficacy to other SGLT2 inhibitors. It achieved similar SBP and DBP reduction to other SGLT2 inhibitors, with a significantly greater DBP-lowering effect than empagliflozin 10 mg. Bexagliflozin had a lower incidence of urinary tract infection than dapagliflozin (5 mg, 10 mg), with comparable safety to other agents and placebo. Canagliflozin 300 mg showed the best efficacy for HbA1c, FPG and weight control.ConclusionBexagliflozin demonstrates comparable efficacy to most SGLT2 inhibitors in T2DM patients, with a relatively prominent benefit in body weight reduction and a similar safety profile. Canagliflozin 300 mg provides more effective glycemic and weight control.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1825381</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1825381</link>
        <title><![CDATA[A novel marker for predicting malignancy in patients with thyroid nodules diagnosed as AUS on initial cytology: thyroid hormone sensitivity]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Puren Gokbulut</author><author>Cagatay Emir Onder</author><author>Serife Mehlika Kuskonmaz</author><author>Huseyin Yagcı</author><author>Cavit Culha</author><author>Gonul Koc</author>
        <description><![CDATA[PurposeThis study aimed to evaluate the predictive value of thyroid hormone sensitivity indices and hematological inflammatory markers, in addition to ultrasonographic features, for malignancy in thyroid nodules initially classified as atypia of undetermined significance (AUS).MethodsData from 415 thyroid nodules initially diagnosed as Bethesda category III (AUS) on fine-needle aspiration biopsy (FNAB) were retrospectively analyzed. Nodules with benign histopathology or benign cytology on repeat FNAB were classified as the benign group, whereas those with malignant histopathology were classified as the malignant group. The groups were compared in terms of ultrasonographic features, baseline hematological parameters, and thyroid hormone sensitivity indices.ResultsA total of 185 patients with thyroid nodules initially classified as Bethesda category III (AUS) were included, and 30.8% of surgically treated cases were malignant. A family history of thyroid cancer was more frequent in the malignant group (26.3% vs 10.9%, p=0.008). Malignant nodules were more likely to be solid, hypoechoic, and associated with microcalcifications, irregular margins, intranodular vascularity, and higher EU-TIRADS categories (all p<0.05). TSH and thyroid hormone sensitivity indices (TT4RI, TSHI, TFQI) were significantly higher in malignant nodules. In multivariable analysis, suspicious EU-TIRADS classification, family history of thyroid cancer, intranodular vascularity, PLR-to-PDW ratio, and thyroid hormone sensitivity indices remained independent predictors of malignancy. ROC analysis demonstrated moderate diagnostic performance for TSHI and TT4RI.ConclusionThyroid hormone sensitivity indices may serve as adjunctive markers for malignancy risk stratification in Bethesda category III thyroid nodules and may complement ultrasonographic assessment in clinical decision-making.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1819985</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1819985</link>
        <title><![CDATA[Zinc oxide nanoparticles mitigate insulin resistance in a D-galactose-induced C57BL/6 mouse model]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kanagavalli Ramasubbu</author><author>Devi Rajeswari V.</author>
        <description><![CDATA[D-galactose promotes insulin resistance (IR) and neurodegeneration through hyperglycemia, advanced glycation end products (AGEs), oxidative stress, amyloid-β accumulation, and disruption of the insulin signalling pathway, leading to neuroinflammation and neuroapoptosis. The purpose of this study was to investigate the insulin signalling pathway and efficacy of ZnO nanoparticles (ZnO NPs) in alleviating brain IR and neurodegeneration via regulating IRS/PI3K/AGER/APP signalling. In this study, bioinformatic analysis of hub genes and PIP network revealed the interconnection between PI3K/Akt signalling pathway and neuroinflammation pathway leading to neurodegeneration. Further, in vivo analysis on 4-month-old C57BL/6 mice was randomised into control (NC), 50 mg/kg of D-galactose (DC), D-galactose + 450 μg/Kg of ZnO NPs (Z1), D-galactose + 650 μg/Kg of ZnO NPs (Z2), and D-galactose + 20 mg/kg of metformin (MF). Blood glucose, Amadori products, conjugated dienes, amyloid-β deposition, and gene and protein expression of the IRS/PI3K/AGER/APP signalling pathway were analysed. Our findings illustrated that ZnO NPs (Z1) alleviated hyperglycemia, cleared amyloid-β accumulation, maintained neural integrity, lessened fat deposition in the liver, and altered the expression of irs2, pi3k, ager, and app genes. Thus, ZnO NPs offer a therapeutic strategy for managing IR and neurodegeneration.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1832788</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1832788</link>
        <title><![CDATA[Association between circadian rhythm disruption and the risk of malignancy in patients with thyroid nodules: a propensity score-matched study]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Pengfei Gu</author><author>Beibei Zhang</author><author>Ziliang Ding</author><author>Yukun Wei</author><author>Yahui Sun</author><author>Pengzhao Song</author><author>Weiwei Zou</author><author>Yong Han</author><author>Fengli Guo</author>
        <description><![CDATA[BackgroundThe rising incidence of thyroid cancer (TC) underscores the need to identify modifiable risk factors for malignancy in patients with thyroid nodules. The role of circadian rhythm disruption (CRD), a pervasive modern lifestyle factor, in TC is poorly understood. We aimed to investigate the association between cumulative CRD and the risk of malignancy and aggressiveness in patients with thyroid nodules.MethodsWe conducted a hospital-based, propensity score-matched study involving 2,541 patients who underwent thyroidectomy for thyroid nodules between 2016 and 2019. A novel cumulative circadian rhythm disruption index (cCRDI), integrating sleep insufficiency, shift work history, chronotype/mid-sleep timing, and dietary irregularity, was calculated from preoperative questionnaires. The primary outcome was the definitive postoperative histopathological diagnosis (benign vs. malignant). Propensity score matching (PSM) (1:1) was performed to balance baseline confounders (e.g., age, sex, BMI, TSH levels, and autoimmune status), yielding a cohort of 850 matched pairs (1,700 patients). Conditional logistic regression was used to assess the association between cCRDI and malignancy.ResultsIn the matched cohort, a strong, dose-dependent relationship was observed. Compared to the No CRD group, the adjusted odds ratios (aOR) for malignancy were 1.58 (95% CI: 1.15–2.15) for Low CRD, 1.85 (95% CI: 1.30–2.62) for Moderate CRD, and 2.95 (95% CI: 2.05–4.25) for High CRD (P for trend < 0.001). Restricted cubic splines confirmed a non-linear association with accelerating risk at higher cCRDI scores (P for non-linearity = 0.008). Crucially, increasing CRD severity was independently associated with aggressive clinicopathological features, including multifocality, extrathyroidal extension (ETE), and a dramatic increase in lymph node metastasis (LNM) (69.4% in High CRD vs. 29.3% in No CRD, P < 0.001). High CRD remained the strongest independent predictor for LNM in multivariable analysis (aOR = 4.21, 95% CI: 2.90–6.10, P < 0.001).ConclusionCumulative CRD is independently associated with both the presence of malignancy and the aggressive progression of TC in patients with thyroid nodules. Assessing a patient’s circadian health might have potential utility as a novel, modifiable factor for risk stratification and may underscore the importance of lifestyle interventions in the clinical management of thyroid nodules.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1764330</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1764330</link>
        <title><![CDATA[Drosophila FMRFa neuropeptide signaling modulates systemic glycogen metabolism and fitness in a diet-dependent manner]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Tetsuya Miyamoto</author><author>Veronika Mojik</author><author>Hubert Amrein</author>
        <description><![CDATA[Glycogen is the major carbohydrate reserve in animals, mainly in the muscle and liver. It is mobilized via glycogenolysis to liberate glucose, which is used for glycolysis/mitochondrial respiration in the muscle to produce ATP, or released into the blood to maintain sugar homeostasis especially when nutrients are scarce. Although glycogen homeostasis is critical for animal physiology, the mechanisms controlling glycogen storage and utilization remain poorly understood. We recently showed that Drosophila FMRFa neuropeptide signaling is required for glycogen homeostasis in the jump muscle, a major tissue of FMRFa receptor (FMRFaR) expression. Here, we report that glycogen accumulation in the flight muscle and fat body also depends on FMRFa signaling, despite the absence of FMRFaR expression in these tissues. In vivo glucose imaging revealed that neither FMRFa nor FMRFaR mutants show deficits in intracellular glucose levels, consistent with a defect in glycogen synthesis or breakdown. Lastly, mutant flies exhibit reduced lifespan when kept on normal or protein-only food, but not on sugar-only food. These findings reveal that Drosophila FMRFa-FMRFaR signaling is a key modulator of systemic glycogen metabolism, thereby influencing survival and fitness in a diet-dependent manner.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1845611</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1845611</link>
        <title><![CDATA[Metabolomic signatures mediate the association between physical frailty and metabolic dysfunction-associated steatotic liver disease: a prospective cohort study]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Doudou Li</author><author>Yacong Bo</author><author>Yao Chen</author><author>Zhitian Guo</author><author>Li Li</author><author>Wenjie Zhang</author><author>Mingyi Xue</author><author>Yongjian Zhu</author><author>Liuhang Ren</author><author>Tingting Li</author><author>Zhan Gao</author>
        <description><![CDATA[BackgroundPhysical frailty is linked to metabolic dysfunction-associated steatotic liver disease (MASLD), but the underlying metabolic mechanisms remain unclear. This study aimed to identify a frailty-related metabolic signature and examine its association with incident MASLD and its mediating role in the frailty-MASLD relationship.MethodsWe analysed data from 244,187 UK Biobank participants. Frailty was assessed using the Fried Frailty Phenotype. Incident MASLD was ascertained via hospital records and death registries. An elastic net regression model identified frailty-associated metabolites to construct a weighted metabolic signature. Cox proportional hazards models estimated associations with MASLD risk, and mediation analysis quantified the signature’s contribution.ResultsOver a median follow-up of 13.7 years, 3,408 incident MASLD cases occurred. A 96-metabolite signature was identified. Each 1-standard deviation increase in the signature was associated with a 21% higher MASLD risk (HR = 1.21, 95% CI: 1.16-1.25). Compared with robust participants, pre-frail and frail individuals had HRs of 1.51 (95% CI: 1.40-1.63) and 2.22 (95% CI: 1.97-2.50), respectively. The metabolic signature mediated 4.25% of the frailty-MASLD association.ConclusionFrailty and its associated metabolic signature are independently associated with increased incident MASLD risk. The signature partially mediates this relationship, suggesting metabolic dysregulation links physical frailty to hepatic steatosis. Identifying this signature may enable earlier MASLD detection in frail individuals.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1827041</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1827041</link>
        <title><![CDATA[Efficacy of intraovarian autologous platelet-rich plasma in women with poor ovarian reserve or ovarian insufficiency: a meta-analysis of randomized controlled trials]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Yuan Fang</author><author>Chunhua Liu</author><author>Zixin He</author><author>Yongfei Zheng</author><author>Ling Zhu</author><author>Zhi Ye</author>
        <description><![CDATA[BackgroundPoor ovarian reserve and ovarian insufficiency pose major challenges in reproductive medicine, with limited effective therapeutic options. Intraovarian autologous platelet-rich plasma (PRP) has shown potential benefits, but its efficacy remains uncertain based on current randomized controlled trials (RCTs).MethodsThis review followed PRISMA guidelines and was registered in PROSPERO (CRD420251233432). We systematically searched PubMed, Cochrane Central, Embase, CNKI, VIP, and Wanfang up to November 22, 2025, for randomized controlled trials of intraovarian autologous PRP in women with diminished ovarian reserve or ovarian insufficiency. Meta-analyses were performed using Stata 16, with heterogeneity assessed by the I² statistic. Risk of bias and study quality were evaluated using the Cochrane RoB 2 tool and the PEDro scale. Primary outcomes included serum anti-Müllerian hormone (AMH), follicle-stimulating hormone (FSH), antral follicle count (AFC), and pregnancy rates.Result(s)This meta-analysis included seven RCTs involving 422 women with poor ovarian reserve or ovarian insufficiency/failure. PRP treatment was associated with significant improvements in several ovarian reserve-related parameters: AFC increased (MD = 0.81, 95% CI 0.31 to 1.30; I² = 41.63%), AMH increased (SMD = 0.91, 95% CI 0.41 to 1.42; I² = 54.32%), FSH decreased (MD = -5.72, 95% CI -7.03 to -4.41; I² = 0.00%), and estradiol increased (MD = 26.03, 95% CI 19.53 to 32.53; I² = 0.22%). However, PRP treatment did not significantly improve pregnancy rates compared with controls.ConclusionsThis meta-analysis suggests that intraovarian PRP may improve ovarian reserve-related markers in women with poor ovarian reserve or ovarian insufficiency/failure, but it does not appear to increase pregnancy rates significantly. These findings should be interpreted cautiously because of the limited number of studies and heterogeneity in treatment protocols, and current evidence remains insufficient to define the optimal PRP regimen or the patient subgroups most likely to benefit.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420251233432, identifier  CRD420251233432.]]></description>
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