Pub Date : 2025-10-22DOI: 10.1016/j.tem.2025.10.002
Lu Zhang,Jian Zhang,Sijun Yang
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.
{"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}
Pub Date : 2025-10-19DOI: 10.1016/j.tem.2025.09.010
Ye Cao,Josephine M Kanta,Christopher A Bishop,Bente Kiens,Andreas M Fritzen,Maximilian Kleinert
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.
{"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}
Pub Date : 2025-10-17DOI: 10.1016/j.tem.2025.09.009
Elena Levi-D'Ancona,Ava M Stendahl,Belle A Henry-Kanarek,Rebecca K Davidson,Emily M Walker,Scott A Soleimanpour
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.
{"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}
Pub Date : 2025-10-17DOI: 10.1016/j.tem.2025.09.008
Yalan Deng,Zilong Zhao,Yutong Sun,Li Ma
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.
{"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}
Pub Date : 2025-10-06DOI: 10.1016/j.tem.2025.09.006
Andrey A Parkhitko,Sudipta Pathak,Jay E Johnson,Bettina Mittendorfer,Matthew L Steinhauser
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.
{"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}
Pub Date : 2025-09-27DOI: 10.1016/j.tem.2025.09.007
Taylah L Gaynor,Camilla Scheele
Recent work by Yoneshiro et al. links brown adipose tissue (BAT) activity to environmental temperatures during conception, highlighting intergenerational influences shaping BAT function. Here we explore how these findings translate into a cardiometabolic health phenotype and discuss how it can be mediated through sperm epigenetic programming.
{"title":"Cold-season programming reinforces the brown fat-cardiometabolic health link.","authors":"Taylah L Gaynor,Camilla Scheele","doi":"10.1016/j.tem.2025.09.007","DOIUrl":"https://doi.org/10.1016/j.tem.2025.09.007","url":null,"abstract":"Recent work by Yoneshiro et al. links brown adipose tissue (BAT) activity to environmental temperatures during conception, highlighting intergenerational influences shaping BAT function. Here we explore how these findings translate into a cardiometabolic health phenotype and discuss how it can be mediated through sperm epigenetic programming.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"53 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181158","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}
Childhood development and pubertal milestones continue to be pillars of pediatric growth monitoring, but increasing trends in childhood obesity and precocious puberty indicate that existing 'normal' criteria may be misleading. Here, we suggest a shift from anthropometry-based growth references to metabolically informed benchmarks that better reflect long-term health outcomes.
{"title":"Rethinking 'normal': are pubertal milestones and growth charts obsolete?","authors":"Balaji Chinnasami,Kanimozhi Sadasivam,Aamina Hussain","doi":"10.1016/j.tem.2025.09.003","DOIUrl":"https://doi.org/10.1016/j.tem.2025.09.003","url":null,"abstract":"Childhood development and pubertal milestones continue to be pillars of pediatric growth monitoring, but increasing trends in childhood obesity and precocious puberty indicate that existing 'normal' criteria may be misleading. Here, we suggest a shift from anthropometry-based growth references to metabolically informed benchmarks that better reflect long-term health outcomes.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181160","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}
Pub Date : 2025-09-26DOI: 10.1016/j.tem.2025.09.004
Yiwei Zhu,Bishuang Cai
Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease posing a major global health concern, closely related to the rising prevalence of obesity. Liver fibrosis is the primary determinant of adverse outcomes in MASH. The increasing worldwide prevalence, economic impact, and adverse outcomes of MASH-associated fibrosis have spurred extensive research to elucidate its pathogenesis and to address its treatment. However, the intricate mechanism driving the transition from metabolic dysfunction to clinically significant fibrosis is not fully understood. Moreover, effective therapies, particularly direct antifibrotic agents, are still lacking, despite the recent approval of resmetirom and semaglutide for MASH-associated fibrosis. Here, we review current insights into the mechanism of MASH-associated fibrosis and provide a comprehensive overview of emerging therapeutic strategies.
{"title":"Mechanisms and therapeutic insights into MASH-associated fibrosis.","authors":"Yiwei Zhu,Bishuang Cai","doi":"10.1016/j.tem.2025.09.004","DOIUrl":"https://doi.org/10.1016/j.tem.2025.09.004","url":null,"abstract":"Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease posing a major global health concern, closely related to the rising prevalence of obesity. Liver fibrosis is the primary determinant of adverse outcomes in MASH. The increasing worldwide prevalence, economic impact, and adverse outcomes of MASH-associated fibrosis have spurred extensive research to elucidate its pathogenesis and to address its treatment. However, the intricate mechanism driving the transition from metabolic dysfunction to clinically significant fibrosis is not fully understood. Moreover, effective therapies, particularly direct antifibrotic agents, are still lacking, despite the recent approval of resmetirom and semaglutide for MASH-associated fibrosis. Here, we review current insights into the mechanism of MASH-associated fibrosis and provide a comprehensive overview of emerging therapeutic strategies.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181159","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}
CD8+ T cells are vital for antiviral and antitumor immunity, yet in hostile microenvironments, they experience metabolic stress, leading to mitochondrial damage, metabolic dysregulation, and chromatin remodeling that cause immune dysfunction. Aging further exacerbates these processes, with intrinsic metabolic collapse and extrinsic environmental factors jointly impairing T cell immunity. Metabolites orchestrate key epigenetic modifications, shaping transcriptional programs essential for T cell differentiation and memory formation. This review explores the interconnected metabolic and epigenetic mechanisms governing CD8+ T cell fate decisions, emphasizing how mitochondrial dysfunction, metabolic inflexibility, and nutrient competition drive CD8+ T cell exhaustion, senescence, and age-associated dysfunction. Understanding these metabolic-epigenetic circuits offers novel therapeutic avenues, including metabolic reprogramming and senescence-targeted strategies, to rejuvenate immune responses and enhance immunotherapy outcomes.
{"title":"CD8+ T cell stressors converge on shared metabolic-epigenetic networks.","authors":"Yangtao Shangguan,Jianxiang Wang,Ping-Chih Ho,Yingxi Xu","doi":"10.1016/j.tem.2025.08.009","DOIUrl":"https://doi.org/10.1016/j.tem.2025.08.009","url":null,"abstract":"CD8+ T cells are vital for antiviral and antitumor immunity, yet in hostile microenvironments, they experience metabolic stress, leading to mitochondrial damage, metabolic dysregulation, and chromatin remodeling that cause immune dysfunction. Aging further exacerbates these processes, with intrinsic metabolic collapse and extrinsic environmental factors jointly impairing T cell immunity. Metabolites orchestrate key epigenetic modifications, shaping transcriptional programs essential for T cell differentiation and memory formation. This review explores the interconnected metabolic and epigenetic mechanisms governing CD8+ T cell fate decisions, emphasizing how mitochondrial dysfunction, metabolic inflexibility, and nutrient competition drive CD8+ T cell exhaustion, senescence, and age-associated dysfunction. Understanding these metabolic-epigenetic circuits offers novel therapeutic avenues, including metabolic reprogramming and senescence-targeted strategies, to rejuvenate immune responses and enhance immunotherapy outcomes.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"61 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127209","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}
Pub Date : 2025-09-16DOI: 10.1016/j.tem.2025.09.001
Siyuan Zhang,Zhenghao Deng,Hui Xu
The molecular mechanisms underlying sex differences in acute kidney injury (AKI) remain incompletely understood. In a study recently published in Nature, Tonnus et al. reported that 17β-estradiol (E2) induces an anti-ferroptotic state in renal tubules through both genomic and non-genomic mechanisms, thereby providing renal protection against AKI.
{"title":"Hydroxyestradiol alleviates acute kidney injury via blockade of ferroptosis.","authors":"Siyuan Zhang,Zhenghao Deng,Hui Xu","doi":"10.1016/j.tem.2025.09.001","DOIUrl":"https://doi.org/10.1016/j.tem.2025.09.001","url":null,"abstract":"The molecular mechanisms underlying sex differences in acute kidney injury (AKI) remain incompletely understood. In a study recently published in Nature, Tonnus et al. reported that 17β-estradiol (E2) induces an anti-ferroptotic state in renal tubules through both genomic and non-genomic mechanisms, thereby providing renal protection against AKI.","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"77 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145077734","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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