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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>2026-05-13T03:23:45.854+00:00</pubDate>
        <ttl>60</ttl>
        <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.2026.1774997</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1774997</link>
        <title><![CDATA[Identification of candidate biomarkers for NAFLD through bioinformatics analysis and machine learning based on circulating insulin degradation-associated genes]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mingjie Guo</author><author>Wei Lou</author><author>Xin Song</author><author>Dongxin Gao</author><author>Guoan Wang</author><author>Hanyu Ma</author><author>Wenlei Wang</author><author>Yongliang Wang</author>
        <description><![CDATA[Non-alcoholic fatty liver disease (NAFLD) has become as a metabolic disorder posing a significant threat to public health, with no presently available effective treatment. Circulating insulin degradation constitutes a pivotal process regulating insulin concentration and biological activity in the bloodstream, and its capacity is closely associated with hyperinsulinaemia and hepatic lipid accumulation. Hepatic lipid accumulation represents a key pathophysiological mechanism in NAFLD. Therefore, targeting the circulating insulin degradation pathway may represent a significant therapeutic opportunity for NAFLD. This study employed a multi-omics strategy, incorporating pertinent datasets from the Gene Expression Omnibus (GEO) collection, to investigate the function of circulating insulin degradation in NAFLD. We employed systems biology informatics approaches, including weighted gene co-expression network analysis (WGCNA) and machine learning models, to identify four hub biomarkers: MYO7A, AGTR1, IL1RN, and IGFBP2. We applied Shapley Additive Explanations (SHAP) to interpret the contribution of each gene to the machine learning model. The expression patterns and potential relevance of these hub genes were further assessed in external datasets, cellular models, and animal models. Overall, this hypothesis-generating study identified four candidate genes potentially associated with NAFLD and provided additional insights into the molecular mechanisms underlying disease progression.]]></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>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1819047</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1819047</link>
        <title><![CDATA[A familial case report of 17q12 recurrent deletion syndrome: clinical and molecular characterization]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Yaroslav V. Dvoryanchikov</author><author>Rita I. Khusainova</author><author>Ildar R. Minniakhmetov</author><author>Ramil R. Salakhov</author><author>Kirill V. Smirnov</author><author>Saida A. Ibragimova</author><author>Ivan I. Golodnikov</author><author>Elena A. Sechko</author><author>Ekaterina A. Dobreva</author><author>Natalia G. Mokrysheva</author>
        <description><![CDATA[This article presents the first reported familial case of 17q12 recurrent deletion syndrome in Russia, involving a female patient with diabetes and her daughter diagnosed with atypical autism without intellectual disability. A comprehensive analysis of the molecular genetic features and intrafamilial variability of clinical manifestations was performed. In addition, clinical, laboratory, and instrumental findings were compared with those observed in a classical case of maturity-onset diabetes of the young type 5 (MODY5). Furthermore, the disease course associated with other genetic alterations affecting the 17q12 region, including 17q12 microduplications and various pathogenic variants of the HNF1B gene, was comparatively evaluated. Given the orphan nature of this condition, the present report adds to the limited existing data on the clinical and genetic characteristics of 17q12 recurrent deletion syndrome.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1783741</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1783741</link>
        <title><![CDATA[Triglyceride-glucose index and subclinical left ventricular dysfunction across cardiovascular-kidney-metabolic syndrome stages: a 7-year retrospective cohort study]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kun-Zhe Tsai</author><author>Gen-Min Lin</author><author>Chunho Yun</author><author>Kuotzu Sung</author><author>Charles Jia-Yin Hou</author><author>Hung-I Yeh</author><author>Nguyen Ngoc Khoi Truong</author><author>Chung-Lieh Hung</author>
        <description><![CDATA[BackgroundThe triglyceride-glucose (TyG) index is associated with cardiovascular disease risk, but its role in identifying subclinical myocardial dysfunction and predicting heart failure (HF) in asymptomatic adults remains unclear.ObjectivesTo assess the association between TyG index and left ventricular global longitudinal strain (GLS), define a threshold for subclinical left ventricular dysfunction (SLVD), and evaluate its link to incident HF hospitalization.MethodsIn this retrospective cohort study included, 4,784 asymptomatic adults aged 18–86 years from a Taiwan community and health check-up cohort without lipid-lowering therapy were included. SLVD was defined as GLS ≥–18%. Multivariable logistic and Cox regression analyses examined the relationship between TyG index, SLVD, and HF risk with covariates adjustment.ResultsA TyG index ≥8.64 optimally discriminated individuals with SLVD, with an area under the receiver operating characteristic curve of 0.70. The prevalence of SLVD was 4.9% (130/2,656) among those with a normal TyG index and 12.9% (268/2,067) among those with an elevated TyG index. An elevated TyG index was independently associated with SLVD [odds ratio 1.62; 95% confidence interval (CI): 1.25–2.09], with stronger associations in those with stage B HF or cardiovascular-kidney-metabolic (CKM) syndrome. The proportion of individuals with an elevated TyG index increased markedly across CKM stages, from 3.5% (23/665) at stage 0 to 14.9% (148/991) at stage 1, 62.6% (1,849/2,955) at stage 2, and 42.0% (47/112) at stage 3. Over a median follow-up of 7.43 years, 61 participants experienced HF hospitalization. Individuals with both SLVD and a high TyG index had a substantially higher risk of HF hospitalization (hazard ratio 7.26; 95% CI: 3.44–15.35) compared with those without either condition.ConclusionsTyG index is a simple, accessible marker for early myocardial dysfunction and future HF risk, particularly when combined with SLVD or early-stage HF.]]></description>
      </item><item>
        <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.2026.1823237</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1823237</link>
        <title><![CDATA[Maternal exposure to the thyroperoxidase-inhibiting pesticide amitrole induces hypothyroidism and developmental neurotoxicity in the rat brain]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Louise Ramhøj</author><author>Jacob Ardenkjær-Skinnerup</author><author>Nichlas Davidsen</author><author>Jermaine Ford</author><author>Carter Kuehn</author><author>Caroline Frädrich</author><author>Josef Köhrle</author><author>Mary Gilbert</author><author>Terje Svingen</author><author>Marta Axelstad</author>
        <description><![CDATA[Thyroid hormone (TH) system-disrupting chemicals pose significant risks to human health and the environment, highlighting the urgent need for improved toxicological testing methods. A major concern is that environmental chemicals may induce developmental neurotoxicity by compromising TH signaling during critical life stages. In this study, we evaluated the thyroidal and neurotoxic effects of two compounds that interfere with TH signaling by inhibiting TH synthesis in the thyroid gland. Methimazole (MMI) is a pharmaceutical specifically designed to treat hyperthyroidism by inhibiting thyroperoxidase (TPO), while the herbicide amitrole has unintentional TPO-inhibiting properties. Pregnant and lactating rat dams were exposed to control (corn oil), 8 or 16 mg/kg body weight/day MMI, or 25 or 50 mg/kg body weight/day amitrole from gestation day 7 to postnatal day 16. MMI and amitrole induced fetal and postnatal hypothyroidism in offspring. Both compounds induced similar reductions in serum and brain TH concentrations and induced a brain malformation, periventricular heterotopia, tied to compromised TH signaling. Our results reinforce concerns over the potential for exposure to environmental chemicals with TH system-disrupting properties to negatively impact the developing brain in vertebrates.]]></description>
      </item><item>
        <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>
      </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>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1867225</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1867225</link>
        <title><![CDATA[Correction: Fracture and mortality outcomes by osteoporosis treatment route in patients with type 2 diabetes and obesity: a propensity-matched registry study]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Vanessa Rouach</author><author>Ohad Regev</author><author>Hilary Gortler</author><author>Yona Greenman</author><author>Gabriel Chodick</author><author>Inbal Goldshtein</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1859900</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1859900</link>
        <title><![CDATA[Editorial: Maternal nutrition, gut microbiota, and endocrine programming in early life]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Gratiela Gradisteanu Pircalabioru</author><author>Mara Ioana Ionescu</author><author>Robin Bernstein</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1776904</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1776904</link>
        <title><![CDATA[Gestational diabetes mellitus–induced adipokine dysregulation and links to metabolic programming risks]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jolanta Lis‐Kuberka</author><author>Marta Berghausen‐Mazur</author>
        <description><![CDATA[IntroductionGestational diabetes mellitus (GDM) is a pregnancy−related hyperglycemic disorder with highly variable global prevalence, largely driven by differences in diagnostic criteria, maternal characteristics, and lifestyle factors, which complicates efforts to standardize screening and prevention. GDM disrupts maternal–fetal glucose homeostasis, leading to fetal exposure to hyperglycemia and hyperinsulinemia, and is associated not only with immediate obstetric complications but also with long−term metabolic risk in both mothers and offspring.ObjectiveThis study evaluated the impact of maternal hyperglycemia, classified as diet−controlled (GDM−diet) or insulin−treated (GDM-insulin), on leptin, adiponectin, soluble leptin receptor (sLeptinR), and the derived indices leptin−to−adiponectin ratio (LAR) and free leptin index (FLI) across the maternal–fetal axis.DesignThis study was a retrospective observational cohort study targeting patients with gestational diabetes mellitus. Maternal and cord blood plasma from 30 hyperglycemic and 23 normoglycemic mothers were analyzed for leptin, adiponectin, and soluble leptin receptor concentrations using immunoenzymatic assays.ResultsMaternal plasma leptin concentrations were significantly higher in the GDM-insulin group (10.05 ng/mL) than in non-GDM pregnancies (4.44 ng/mL; p = 0.033). The leptin-to-adiponectin ratio was also elevated in GDM-insulin (4.99) compared to GDM-diet (2.18; p = 0.043). No significant between-group differences were observed for adiponectin, soluble leptin receptor, or the free leptin index. In cord blood, adiponectin concentrations were higher in GDM-diet neonates (9.05 μg/mL) than in GDM-insulin (5.70 μg/mL; p = 0.010). Maternal leptin and its derived indices (LAR, FLI) were associated with maternal overweight/obesity, whereas maternal adiponectin and cord blood leptin were related to neonatal birth weight.ConclusionThese findings point to leptin, adiponectin, FLI, and LAR as possible metabolic indicators of GDM-linked insulin resistance, and low-grade inflammation. Higher maternal leptin, LAR, and FLI, alongside stable sLeptinR, signal leptin resistance, which disrupts placental nutrient transport and links maternal metabolic stress to fetal anthropometric measures. Tracking these markers could guide postnatal steps to cut long-term metabolic risks across the next generations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1802981</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1802981</link>
        <title><![CDATA[The association between maternal FT3/FT4 ratio in early pregnancy and adverse neonatal outcomes: a retrospective cohort study]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiaoyu Chen</author><author>Fuyu Yang</author><author>Fanlong Meng</author><author>Lixin Li</author><author>Zhongyang Han</author><author>Jiayue Wang</author><author>Qingliang Shao</author><author>Shuang Li</author><author>Wei Sun</author>
        <description><![CDATA[IntroductionMaternal thyroid hormone homeostasis during early gestation is fundamental for fetal growth and development, yet the specific clinical implications of the ratio between free triiodothyronine and free thyroxine, a marker of peripheral deiodinase activity and metabolic status, remain insufficiently explored regarding newborn health.MethodsThis retrospective cohort study investigated the association between the maternal free triiodothyronine to free thyroxine ratio measured during the first trimester and the risk of neonatal adverse outcomes. We analyzed data from 797 eligible mother–infant pairs, excluding those with pre-existing thyroid or immune disorders to isolate physiological variations. The primary endpoint was a composite of neonatal adverse outcomes, including respiratory, cardiovascular, and infectious complications. Multivariable logistic regression and restricted cubic spline modeling were employed to evaluate linear and non-linear associations.ResultsThe results demonstrated that mothers in the highest quartile of the thyroid hormone ratio exhibited a significantly increased risk of adverse neonatal outcomes compared to those in the lowest quartile, an association that remained robust after adjusting for potential confounders such as maternal age, body mass index, and gestational age. The relationship followed a non-linear J-shaped pattern, with risks escalating sharply beyond a specific threshold. Specifically, a higher ratio was strongly associated with neonatal anemia, patent ductus arteriosus, jaundice, and myocardial injury. Subgroup analyses revealed that this risk was particularly pronounced in nulliparous women, mothers with a normal body mass index, and female neonates.DiscussionThese findings suggest that an elevated free triiodothyronine to free thyroxine ratio in early pregnancy serves as a sensitive indicator of neonatal risk, potentially reflecting maladaptive maternal metabolic demands that impact fetal health independent of traditional obstetric risk factors.]]></description>
      </item><item>
        <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.2026.1838548</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1838548</link>
        <title><![CDATA[Association between single-point insulin sensitivity estimator and three-vessel coronary disease: a cross-sectional study]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Wei Yang</author><author>Gaoying Dai</author><author>Nanhu Quan</author><author>Qian Tong</author>
        <description><![CDATA[BackgroundThe single-point insulin sensitivity estimator (SPISE) is a novel surrogate marker for assessing insulin resistance in humans. Three-vessel coronary disease (TVD) remains a major challenge in coronary interventional therapy. However, the association between the SPISE index and TVD remains unclear. Therefore, this study aimed to evaluate the relationship between SPISE and TVD in an elderly population.MethodsGeneralized additive models (GAM) and random forest variable importance scores were applied for feature selection to identify key predictors for constructing a TVD risk model. Multivariable regression and restricted cubic spline (RCS) analyses were performed to investigate the association between SPISE and TVD. Subgroup analyses were further conducted to assess potential effect modification.ResultsGAM and random forest variable importance scores identified age and SPISE as the most important predictors. After adjustment for all covariates, SPISE was inversely associated with TVD (OR = 0.75, 95% CI: 0.68-0.83, P < 0.001). RCS and segmented regression analyses revealed a significant nonlinear relationship with a distinct inflection point. Receiver operating characteristic (ROC) analysis demonstrated that SPISE showed superior performance compared with the TyG index in predicting TVD risk (AUC: 0.718 vs. 0.701). Subgroup analyses confirmed a consistent inverse association between SPISE and TVD, with significant interactions observed across strata of sex, alcohol consumption, age, and BMI.ConclusionA higher SPISE index is independently and inversely associated with TVD and may serve as a reliable predictor of disease risk, highlighting its potential utility in cardiovascular risk assessment.]]></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.2026.1758267</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1758267</link>
        <title><![CDATA[Plasma protein GDF15 has a good predictive potential for the kidney complications of type 2 diabetes]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ming Hao</author><author>Houxing Li</author><author>Mengyu Xin</author><author>Jiatong Li</author><author>Rui Sun</author><author>Qian Liu</author><author>Yujie Zhang</author><author>Xinxin Shan</author><author>Yuting He</author><author>Borui Xu</author><author>Qiuyan Guo</author><author>Hongyu Kuang</author><author>Peng Wang</author>
        <description><![CDATA[Introduction and aimsComplications of type 2 diabetes are a primary cause of public health challenges in the field of diabetes. The emergence of metabolomics and proteomics provides a direct perspective for revealing the mechanisms of metabolic diseases. Our research aims to explore the relationship between omics components and complications, as well as their clinical predictive performance.Materials and methodsThis prospective study utilized data from the UK Biobank, including over 1,400 proteins and more than 280 metabolites, to analyze outcomes such as type 2 diabetes, microvascular complications, macrovascular complications, neurological complications, kidney complications, retinal complications, cardiovascular complications, peripheral vascular complications, metabolic disorder complications, and all-cause mortality. A total of 50,021 participants without type 2 diabetes were included in the analysis. The baseline time frame spanned from 2006 to 2010, with an average follow-up duration of 12.0 to 12.03 years. Researchers used LASSO Cox and LightGBM to search for new markers of complications, and employed SHAP methods to explain the contributions of these markers within the machine learning models. Subsequently, a comprehensive prediction model was established to reveal the potential of new markers for the early diagnosis of complications under nonlinear patterns, utilizing nine specific machine learning methods (CatBoost, LightGBM, Random Forest, XGBoost, logistic regression, multi-layer perceptron, single-layer neural network, Naive Bayes, and support vector machine). ResultsGDF15 alone is more accurate than blood glucose and HbA1c in reflecting future kidney complications, especially in differentiating those who develop the disease within the next five years (GDF15 AUC=0.94, blood glucose AUC=0.68, HbA1c AUC=0.85). Within the framework of the comprehensive prediction model, the GDF15 model improved the accuracy of early screening for kidney complications compared with models constructed using traditional indicators (5-year Max AUC=0.92, 10-year Max AUC=0.88). In conclusion, both machine learning and statistical methods support the correlation between GDF15 and kidney complications, reflecting its robustness. ConclusionsThe results highlight the association of GDF15 during the early asymptomatic stage of various complications, especially kidney complications, revealing the potential role of GDF15 at the molecular pathological level during disease progression. In distinguishing participants who developed complications after the baseline period, the comprehensive GDF15 model provides a method for the early warning of various complications, particularly kidney complications.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1796327</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1796327</link>
        <title><![CDATA[Nesfatin-1 across human reproduction and early life: implications for infertility, pregnancy complications, and lactation]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Regina Katona</author><author>Dora Filarszky</author><author>Simone Funke</author><author>Reka Anna Vass</author>
        <description><![CDATA[Nesfatin-1, a peptide derived from nucleobindin-2 (NUCB2), is a widely expressed neuroendocrine factor originally identified for its anorexigenic effects in the central nervous system. Beyond energy homeostasis, accumulating evidence implicates nesfatin-1 in the regulation of glucose metabolism, stress-axis activity, inflammation, and reproductive function. These properties make nesfatin-1 particularly relevant to human reproduction and early life, physiological states characterized by profound metabolic and endocrine adaptations. The objective of this review is to examine whether nesfatin-1 functions as an integrative endocrine signal linking metabolic, stress-related, and reproductive pathways across the reproductive life course. We synthesize current human evidence on nesfatin-1 in infertility, assisted reproductive technologies, pregnancy adaptations and complications, the maternal–fetal interface, lactation, and postpartum metabolic recovery. Nesfatin-1 has been detected in several biological compartments relevant to reproductive physiology, including maternal plasma, follicular fluid, amniotic fluid, cord blood, and human breast milk. Clinical studies investigating these compartments report heterogeneous findings, with nesfatin-1 levels described as increased, decreased, or unchanged across similar clinical conditions. This variability likely reflects the context-dependent regulation of nesfatin-1 by metabolic status, stress-axis activation, inflammatory signaling, and reproductive stage. In this review, we synthesize current human evidence on nesfatin-1 across the continuum of reproduction, pregnancy, early development, and lactation, and propose a framework to reconcile these inconsistent findings. We argue that nesfatin-1 should be viewed as a context-dependent endocrine integrator reflecting the interaction of metabolic, stress-related, inflammatory, and reproductive axes rather than as a unidirectional biomarker. We further highlight key methodological challenges, including assay variability, timing of sampling, and population heterogeneity, and discuss the potential of nesfatin-1 as a longitudinal or stratification biomarker in reproductive endocrinology. Finally, we outline priorities for future research to clarify its physiological role and translational relevance in human reproduction and early life.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1832704</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1832704</link>
        <title><![CDATA[Influence of vitamin D supplementation on ovarian reserve as reflected by anti-Müllerian hormone levels: a meta-analysis of randomized controlled trials]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Sitian Fang</author><author>Yijia Li</author><author>Xinyu Fan</author><author>Liping Zheng</author>
        <description><![CDATA[BackgroundVitamin D has been implicated in ovarian physiology, yet its effect on ovarian reserve remains controversial. We performed a meta-analysis of randomized controlled trials (RCTs) to evaluate the influence of vitamin D supplementation on ovarian reserve as indicated by serum anti-Müllerian hormone (AMH) levels.MethodsPubMed, Cochrane Library, Embase, Web of Science, Wanfang, and CNKI were searched for RCTs comparing vitamin D supplementation with placebo or no intervention on AMH in women of reproductive age. The pooled effect was summarized as standardized mean difference (SMD) using a random-effects model by incorporating the influence of potential heterogeneity.ResultsEleven RCTs with 992 women were included. Overall, vitamin D supplementation did not significantly affect serum AMH levels (SMD: −0.20; 95% CI: −0.48 to 0.08; p = 0.16), with substantial heterogeneity (I² = 77%, p < 0.001). Subgroup analysis showed no significant effect in double-blind trials but a reduction in AMH in open-label trials (p for subgroup difference = 0.02). A significant interaction was observed according to baseline AMH level (p = 0.003), with a reduction in studies where baseline AMH > 6 ng/mL (SMD: −0.55; 95% CI: −0.87 to −0.23). No significant subgroup differences were found by age, baseline 25(OH)D, vitamin D dose, treatment duration, or assay method.ConclusionsCurrent randomized evidence suggests that vitamin D supplementation was not likely to alter AMH levels in reproductive-aged women overall. The certainty of evidence was moderate, and findings should be interpreted cautiously given substantial heterogeneity.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD420261329210.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fendo.2026.1716274</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fendo.2026.1716274</link>
        <title><![CDATA[Effectiveness of acupuncture on pregnancy outcomes in patients with repeated implantation failure after IVF-ET: study protocol for a pilot randomized controlled trial]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Study Protocol</category>
        <author>Ruiwen Fan</author><author>Yang Ye</author><author>Kun Liu</author><author>Jing Xu</author><author>Yutian Zhu</author><author>Haolin Zhang</author><author>Yu Gao</author><author>Xiyan Xin</author><author>Dong Li</author>
        <description><![CDATA[ObjectiveRepeated implantation failure (RIF) in in vitro fertilization-embryo transfer (IVF-ET) remains a challenging clinical issue. Although acupuncture is increasingly used as an adjunctive therapy for RIF patients, robust evidence supporting its efficacy in improving pregnancy outcomes is still lacking. This pilot study therefore aims to estimate effect sizes to inform sample size calculations for future definitive trials and to assess key feasibility parameters.Design and methodsThis single-center, two-arm, single-blind, randomized sham-controlled trial will enroll 100 women (50 per group) with RIF aged 25~40 years. Using a parallel-group design, participants will be randomized to receive either conventional Western medicine treatment combined with acupuncture (experimental group) or the same conventional Western medicine treatment combined with sham acupuncture (control group). Acupuncture or sham acupuncture will be administered twice weekly from day 5 of the menstrual cycle until the day before embryo transfer, with a minimum of three completed sessions, targeting acupoints with standardized techniques. The primary outcome will be embryo implantation rate, and secondary outcomes will include clinical pregnancy rate and serum biomarkers (β-human chorionic gonadotropin, luteinizing hormone, progesterone, and estradiol). Safety will be monitored through adverse event reporting.DiscussionThe findings of this study will provide preliminary data to guide the design of future large-scale, multicenter randomized controlled trials. Such trials would in turn generate more definitive evidence on the efficacy of acupuncture for improving pregnancy outcomes in RIF patients undergoing IVF-ET.Clinical trial registrationhttps://itmctr.ccebtcm.org.cn/, identifier ITMCTR2025000838]]></description>
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