{"title":"Subscription and Copyright Information","authors":"","doi":"10.1016/s1043-2760(25)00232-2","DOIUrl":"https://doi.org/10.1016/s1043-2760(25)00232-2","url":null,"abstract":"","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145434406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Beatriz Rodriguez-Cortes, Ricardo Gomez-Martínez, Rachel Spenle, Markus Schwaninger, Ruben Nogueiras, Sowmyalakshmi Rasika, Vincent Prevot
{"title":"Tanycytes: bloodhounds of the metabolic brain","authors":"Beatriz Rodriguez-Cortes, Ricardo Gomez-Martínez, Rachel Spenle, Markus Schwaninger, Ruben Nogueiras, Sowmyalakshmi Rasika, Vincent Prevot","doi":"10.1016/j.tem.2025.10.005","DOIUrl":"https://doi.org/10.1016/j.tem.2025.10.005","url":null,"abstract":"","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"24 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145411969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marica Esposito, Ida Rimauro, Vittoria Frattolillo, Gianmario Forcina, Pierluigi Marzuillo, Emanuele Miraglia del Giudice, Anna Di Sessa
{"title":"MASLD in childhood as a multisystem health challenge beyond the liver","authors":"Marica Esposito, Ida Rimauro, Vittoria Frattolillo, Gianmario Forcina, Pierluigi Marzuillo, Emanuele Miraglia del Giudice, Anna Di Sessa","doi":"10.1016/j.tem.2025.10.001","DOIUrl":"https://doi.org/10.1016/j.tem.2025.10.001","url":null,"abstract":"","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"205 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145382739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adrenalectomy is underused: a call to reduce mortality.","authors":"Tobias Carling","doi":"10.1016/j.tem.2025.10.004","DOIUrl":"https://doi.org/10.1016/j.tem.2025.10.004","url":null,"abstract":"Adrenal tumors driving hormone excess, like primary aldosteronism, Cushing syndrome, and pheochromocytoma, claim thousands of lives yearly; yet, adrenalectomy remains underused despite its lifesaving potential. Ideal surgical rates in the USA, UK, and Sweden could prevent tens of thousands of deaths, rivaling cancer operations' impact. Urgent screening reforms are needed.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"52 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145381149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Daan A Jiskoot,Jeroen L A Pennings,Willie J G M Peijnenburg,Gerard J P van Westen,Willem Jespers,Pim N H Wassenaar
{"title":"In silico prediction of endocrine activity.","authors":"Daan A Jiskoot,Jeroen L A Pennings,Willie J G M Peijnenburg,Gerard J P van Westen,Willem Jespers,Pim N H Wassenaar","doi":"10.1016/j.tem.2025.09.011","DOIUrl":"https://doi.org/10.1016/j.tem.2025.09.011","url":null,"abstract":"Endocrine-disrupting chemicals (EDCs) pose health risks; yet, conventional in vitro and in vivo testing remains slow, costly, and animal-intensive. Enhanced use of in silico approaches can contribute to earlier and increased detection of potential EDCs. This review evaluates advances in computational toxicology for early identification and prioritization of EDCs, with a focus on estrogen, androgen, thyroid, and steroidogenesis pathways. We discuss various implementations of ligand- and structure-based approaches, covering machine learning, deep learning, docking, molecular dynamics, and free energy methods, as well as their application in a regulatory setting. Moreover, we outline the future prospects necessary to advance the field and improve the in silico identification of potential EDCs.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"52 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145370628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Art breaks obesity's health information silos.","authors":"Lu Zhang,Jian Zhang,Sijun Yang","doi":"10.1016/j.tem.2025.10.002","DOIUrl":"https://doi.org/10.1016/j.tem.2025.10.002","url":null,"abstract":"Conventional obesity interventions create 'health information silos', isolating scientific knowledge from lived experience and systemic drivers. Artistic interventions can uniquely dismantle these silos by translating complex data into visceral, co-created experiences, connecting urban design, behavioral science, and community action to transform obesogenic systems into equitable health ecosystems.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"50 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ye Cao,Josephine M Kanta,Christopher A Bishop,Bente Kiens,Andreas M Fritzen,Maximilian Kleinert
{"title":"Dietary medium-chain triacylglycerols in metabolic regulation.","authors":"Ye Cao,Josephine M Kanta,Christopher A Bishop,Bente Kiens,Andreas M Fritzen,Maximilian Kleinert","doi":"10.1016/j.tem.2025.09.010","DOIUrl":"https://doi.org/10.1016/j.tem.2025.09.010","url":null,"abstract":"Dietary medium-chain triacylglycerols (MCTs; C8:0-C12:0) are absorbed and utilized differently compared with long-chain fats. They directly enter the portal vein as free medium-chain fatty acids, most of which are converted to ketone bodies in the liver, with a significant proportion entering the circulation. Accumulating evidence links MCT intake to improved glucose homeostasis; increased energy expenditure and satiety with concomitant modest weight loss; and chain length-dependent modulation of circulating lipoprotein profiles and liver metabolism. Emerging data also suggest direct benefits for cardiac contractility, hinting at a broader cardiometabolic advantage. Here, we synthesize the current evidence, outlining how MCTs influence cardiometabolic health. We further discuss mechanistic insights, from cellular substrate partitioning and mitochondrial dynamics to gut-liver signaling to propose mechanisms of MCT action.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145331802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elena Levi-D'Ancona,Ava M Stendahl,Belle A Henry-Kanarek,Rebecca K Davidson,Emily M Walker,Scott A Soleimanpour
{"title":"Mitophagy in the adaptation to pancreatic β cell stress in diabetes.","authors":"Elena Levi-D'Ancona,Ava M Stendahl,Belle A Henry-Kanarek,Rebecca K Davidson,Emily M Walker,Scott A Soleimanpour","doi":"10.1016/j.tem.2025.09.009","DOIUrl":"https://doi.org/10.1016/j.tem.2025.09.009","url":null,"abstract":"Mitophagy is a crucial quality control process that preserves metabolic efficiency by selectively targeting damaged mitochondria for removal. Given the high metabolic demand of pancreatic β cells' insulin secretion, disruption of mitophagy contributes to the mitochondrial dysfunction and β cell failure that are a common feature of both type 1 and type 2 diabetes (T1D and T2D). We review the impact of mitophagy on β cell responses to (patho)physiologic stressors that underlie the development of T1D and T2D. We examine how β cells engage mitophagy in the adaptive response to metabolic, inflammatory, and oxidative damage. We also dissect the importance of ubiquitin- and receptor-mediated mitophagy, methodological advances to quantify mitophagy in β cells, and ongoing efforts to pharmacologically target mitophagy to preserve β cell health and improve glycemic control.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"44 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Systemic and metabolic control of liver regeneration.","authors":"Yalan Deng,Zilong Zhao,Yutong Sun,Li Ma","doi":"10.1016/j.tem.2025.09.008","DOIUrl":"https://doi.org/10.1016/j.tem.2025.09.008","url":null,"abstract":"The liver possesses a unique regenerative capacity, driven by mechanisms that extend beyond classical growth factor signaling. Recent studies underscore the importance of metabolic reprogramming, mitochondrial adaptation, and signaling metabolites in promoting tissue injury repair. Dynamic crosstalk between hepatocytes, non-parenchymal cells, and other organs governs the regenerative process. Spatial compartmentalization within the liver and systemic cues from adipose tissue, the pancreas, the gut, the brain, skeletal muscle, and other organs play critical roles in shaping regenerative outcomes. In this review we discuss how the liver's tissue microenvironment and inter-organ communication networks regulate liver regeneration, providing new insights into the complex biology underlying tissue repair.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"43 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Andrey A Parkhitko,Sudipta Pathak,Jay E Johnson,Bettina Mittendorfer,Matthew L Steinhauser
{"title":"Methionine restriction and mimetics to ameliorate human aging and disease.","authors":"Andrey A Parkhitko,Sudipta Pathak,Jay E Johnson,Bettina Mittendorfer,Matthew L Steinhauser","doi":"10.1016/j.tem.2025.09.006","DOIUrl":"https://doi.org/10.1016/j.tem.2025.09.006","url":null,"abstract":"Methionine restriction (MetR) attenuates the severity of numerous age-related diseases and extends lifespan across multiple species. Implementing MetR in humans remains challenging due to the low palatability of MetR diets, unfavorable side effects associated with continuous dietary MetR, and interindividual variation in factors that can diminish its efficacy, including microbiota activity, compensatory effects from cysteine, and methionine transfer from neighboring cells. Several novel approaches that target methionine metabolism have been developed - including small molecules, synthetic biotics, and xenotopic tools - with some already translated into early-stage clinical trials. In this review, we discuss a variety of approaches that either produce or mimic MetR, as well as their potential applications for human healthspan improvement.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"22 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145235895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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