Nature Reviews Endocrinology最新文献_第6页

Highlights from ESPE-ESE 2025 ESPE-ESE 2025的亮点

IF 31 1区医学

Nature Reviews Endocrinology Pub Date : 2025-06-12 DOI: 10.1038/s41574-025-01144-6

Claire Greenhill

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Tirzepatide differentially affects body weight in mice and humans 替西帕肽对小鼠和人类体重的影响是不同的

IF 31 1区医学

Nature Reviews Endocrinology Pub Date : 2025-06-09 DOI: 10.1038/s41574-025-01139-3

Aaron Novikoff, Timo D. Müller

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Diabetes mellitus polygenic risk scores: heterogeneity and clinical translation 糖尿病多基因风险评分：异质性和临床翻译

IF 4 1区医学

Nature Reviews Endocrinology Pub Date : 2025-06-04 DOI: 10.1038/s41574-025-01132-w

Hector I. Ortega, Miriam S. Udler, Anna L. Gloyn, Seth A. Sharp

{"title":"Diabetes mellitus polygenic risk scores: heterogeneity and clinical translation","authors":"Hector I. Ortega, Miriam S. Udler, Anna L. Gloyn, Seth A. Sharp","doi":"10.1038/s41574-025-01132-w","DOIUrl":"10.1038/s41574-025-01132-w","url":null,"abstract":"Diabetes mellitus encompasses several disorders, each with differing clinical presentation, prognoses and pathophysiology. Distinct polygenic architectures underlie type 1 diabetes mellitus and type 2 diabetes mellitus, and govern numerous pathophysiological pathways that converge on dysglycaemia. Over the previous decade, polygenic risk scores (PRS) derived from large genome-wide association studies have become broadly recognized for their potential in precision medicine. PRS, and now partitioned polygenic scores generated by clustering of risk variants, can quantify individual genetic predisposition to diabetes mellitus and reveal molecular heterogeneity responsible for variation in clinical presentation and prognoses. In this Review, we examine and contrast progress in the development of type 1 diabetes mellitus PRS and type 2 diabetes mellitus PRS, and discuss paths to further methodological advances. We examine how studies in the past 10 years have harnessed PRS and novel partitioned polygenic scores to reveal insights into diabetes mellitus aetiology and characterize changes in cellular and tissue-specific disease-modifying molecular pathways. Additionally, we discuss advances and opportunities in areas of clinical translation, including improved classification of diabetes mellitus type, screening of those at risk and personalized interventions informed by PRS. Finally, we emphasize the urgent need to overcome ancestry-related challenges and highlight current progress and gaps in ensuring the equitable translation of PRS for diabetes mellitus precision medicine. In this Review, the authors discuss different methods for assessing polygenic risk of diabetes mellitus and the utility of polygenic risk scores in classifying and screening for diabetes mellitus. The current limitations of these scores and ways of overcoming these limitations are also covered.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"21 9","pages":"530-545"},"PeriodicalIF":40.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Diabetes mellitus and the key role of endoplasmic reticulum stress in pancreatic β cells 糖尿病与胰岛β细胞内质网应激的关键作用

IF 4 1区医学

Nature Reviews Endocrinology Pub Date : 2025-06-04 DOI: 10.1038/s41574-025-01129-5

Maria Lytrivi (, ), Yue Tong (, ), Enrico Virgilio, Xiaoyan Yi (, ), Miriam Cnop

{"title":"Diabetes mellitus and the key role of endoplasmic reticulum stress in pancreatic β cells","authors":"Maria Lytrivi \u0000 (, ), Yue Tong \u0000 (, ), Enrico Virgilio, Xiaoyan Yi \u0000 (, ), Miriam Cnop","doi":"10.1038/s41574-025-01129-5","DOIUrl":"10.1038/s41574-025-01129-5","url":null,"abstract":"Insufficient insulin secretion by pancreatic β cells is central to the pathogenesis of diabetes mellitus. As insulin is synthesized in the endoplasmic reticulum (ER), perturbations in ER homeostasis lead to ER stress and activate the ER stress response. Over the past two decades, considerable data have accumulated on the role of β cell ER stress in diabetes mellitus. Several monogenic forms of diabetes mellitus are caused by excessive ER stress, perturbed ER stress response signalling or impaired ER–Golgi protein trafficking. These pathways are now recognized to contribute to β cell failure in both type 1 and type 2 diabetes mellitus. This Review considers the role of β cell ER stress in common forms of diabetes mellitus and examines whether it is a cause or a consequence of these diseases. The strong genetic evidence for a causal role of ER stress in 15 monogenic forms of diabetes mellitus is summarized, and the effects of ER stress on human β cell differentiation, function and survival are described. Although definitive proof is lacking that ER stress responses can be therapeutically targeted to improve β cell function in diabetes mellitus, existing and novel treatments that aim to restore ER homeostasis are also outlined. Genetic mutations and environmental exposures cause severe endoplasmic reticulum (ER) stress in pancreatic β cells, which can culminate in diabetes mellitus. Lytrivi et al. describe the causes and consequences of ER stress for β cell development, function and survival, and debate emerging therapeutic approaches.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"21 9","pages":"546-563"},"PeriodicalIF":40.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144218868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Muscle mass loss during GLP1 receptor agonist therapy prevented with GDF8 and activin A blockade GDF8和激活素A阻断可预防GLP1受体激动剂治疗期间的肌肉质量损失

IF 31 1区医学

Nature Reviews Endocrinology Pub Date : 2025-06-04 DOI: 10.1038/s41574-025-01140-w

Olivia Tysoe

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Hyperglycaemia increases anxiety in mice by boosting neuronal CCL2 高血糖通过促进神经元CCL2增加小鼠的焦虑

IF 31 1区医学

Nature Reviews Endocrinology Pub Date : 2025-06-02 DOI: 10.1038/s41574-025-01137-5

Senegal Carty

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Hypoglycaemia exacerbates diabetic retinopathy via HIF accumulation 低血糖通过HIF积累加重糖尿病视网膜病变

IF 31 1区医学

Nature Reviews Endocrinology Pub Date : 2025-05-23 DOI: 10.1038/s41574-025-01136-6

Olivia Tysoe

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The endocrine effects of leptin on energy metabolism 瘦素对能量代谢的内分泌作用

IF 31 1区医学

Nature Reviews Endocrinology Pub Date : 2025-05-22 DOI: 10.1038/s41574-025-01135-7

Rugivan Sabaratnam

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Endocrine-disrupting chemicals and female reproductive health: a growing concern 干扰内分泌的化学物质与女性生殖健康：日益受到关注。

IF 4 1区医学

Nature Reviews Endocrinology Pub Date : 2025-05-22 DOI: 10.1038/s41574-025-01131-x

Anne-Simone Parent, Pauliina Damdimopoulou, Hanna K. L. Johansson, Nora Bouftas, Monica K. Draskau, Delphine Franssen, Julie Fudvoye, Majorie van Duursen, Terje Svingen

{"title":"Endocrine-disrupting chemicals and female reproductive health: a growing concern","authors":"Anne-Simone Parent, Pauliina Damdimopoulou, Hanna K. L. Johansson, Nora Bouftas, Monica K. Draskau, Delphine Franssen, Julie Fudvoye, Majorie van Duursen, Terje Svingen","doi":"10.1038/s41574-025-01131-x","DOIUrl":"10.1038/s41574-025-01131-x","url":null,"abstract":"Female fertility and reproductive health depend on a series of developmental steps from embryogenesis through puberty, in addition to the proper functioning of the reproductive system in adulthood. Two important steps are the establishment of the ovarian reserve and development of the hypothalamic–pituitary–ovarian axis. During reproductive years, maintaining an adequate ovarian reserve of follicles as well as balanced neuroendocrine control of reproductive organs is crucial for fertility. Dysregulation of either of these events, during development or in adulthood, can lead to reproductive disorders. Over the past five decades, human fertility rates have declined, whereas the incidence of female reproductive disorders has risen, trends partially linked to environmental factors such as exposure to endocrine-disrupting chemicals (EDCs). Here we outline epidemiological and mechanistic evidence for how EDCs affect the ovarian reserve during early development, its maintenance during adulthood and the establishment of the hypothalamic–pituitary control of puberty and ovulation. Our Review not only reveals strong support for the role of EDC exposure in the development of female reproductive disorders such as abnormal puberty, impaired fertility, premature menopause or polycystic ovarian syndrome, but also highlights knowledge gaps, including the difficulty to prove causality between exposure and human disease manifestation. This article outlines evidence pointing to an important contribution of endocrine-disrupting chemicals to increasing rates of female reproductive disorders such as abnormal puberty, impaired fertility, premature menopause or polycystic ovarian syndrome reported over the past half a century.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"21 10","pages":"593-607"},"PeriodicalIF":40.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144122120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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The inflammatory spark: how TNF rewrote the insulin resistance narrative 炎症火花：肿瘤坏死因子如何改写胰岛素抵抗的故事

IF 4 1区医学

Nature Reviews Endocrinology Pub Date : 2025-05-16 DOI: 10.1038/s41574-025-01133-9

Subhajit Dutta

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