Pub Date : 2025-10-14DOI: 10.1038/s41574-025-01190-0
Jacqueline Jonklaas
The factors influencing the control of body weight are numerous and include many hormones. Even though levels of thyroid hormone might not always be the major factor affecting weight, in the sense that large changes in weight can occur despite a euthyroid state, there are notable changes in weight, appetite and body composition associated with excesses and deficiencies of thyroid hormone. Exploring the effect of thyroid hormone on weight is facilitated by studying the disease states of hypothyroidism and hyperthyroidism, the development and treatment of which can be associated with substantial changes in body weight. As is illustrated in the ensuing discussion, hypothyroidism is associated with modest increases in body weight and accompanying changes in body composition, with reversal of these alterations with its treatment. By contrast, hyperthyroidism can be accompanied by profound weight loss with reversal of the weight loss with restoration of euthyroidism. Using iatrogenic hyperthyroidism, whether during treatment for hypothyroidism or during off-label use in euthyroid individuals, has not proven to be an effective weight loss strategy.
{"title":"The complexity of the relationship between thyroid disease and body weight.","authors":"Jacqueline Jonklaas","doi":"10.1038/s41574-025-01190-0","DOIUrl":"https://doi.org/10.1038/s41574-025-01190-0","url":null,"abstract":"The factors influencing the control of body weight are numerous and include many hormones. Even though levels of thyroid hormone might not always be the major factor affecting weight, in the sense that large changes in weight can occur despite a euthyroid state, there are notable changes in weight, appetite and body composition associated with excesses and deficiencies of thyroid hormone. Exploring the effect of thyroid hormone on weight is facilitated by studying the disease states of hypothyroidism and hyperthyroidism, the development and treatment of which can be associated with substantial changes in body weight. As is illustrated in the ensuing discussion, hypothyroidism is associated with modest increases in body weight and accompanying changes in body composition, with reversal of these alterations with its treatment. By contrast, hyperthyroidism can be accompanied by profound weight loss with reversal of the weight loss with restoration of euthyroidism. Using iatrogenic hyperthyroidism, whether during treatment for hypothyroidism or during off-label use in euthyroid individuals, has not proven to be an effective weight loss strategy.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"91 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145288497","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}
Pub Date : 2025-10-10DOI: 10.1038/s41574-025-01198-6
Victor Martinez Leon, Rachel Hilburg, Katalin Susztak
{"title":"Author Correction: Mechanisms of diabetic kidney disease and established and emerging treatments","authors":"Victor Martinez Leon, Rachel Hilburg, Katalin Susztak","doi":"10.1038/s41574-025-01198-6","DOIUrl":"10.1038/s41574-025-01198-6","url":null,"abstract":"","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"22 1","pages":"61-61"},"PeriodicalIF":40.0,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41574-025-01198-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-10DOI: 10.1038/s41574-025-01188-8
The November 2025 issue marks 20 years since the launch of Nature Reviews Endocrinology (originally Nature Clinical Practice Endocrinology & Metabolism). Here, we reflect on the past 20 years and consider what the future holds.
{"title":"Marking 20 years of Nature Reviews Endocrinology","authors":"","doi":"10.1038/s41574-025-01188-8","DOIUrl":"10.1038/s41574-025-01188-8","url":null,"abstract":"The November 2025 issue marks 20 years since the launch of Nature Reviews Endocrinology (originally Nature Clinical Practice Endocrinology & Metabolism). Here, we reflect on the past 20 years and consider what the future holds.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"21 11","pages":"657-657"},"PeriodicalIF":40.0,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41574-025-01188-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145248861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-08DOI: 10.1038/s41574-025-01195-9
Mamta Rai, Fabio Demontis
Neurodegeneration is not merely determined by local cues but is also influenced by systemic signals, such as factors released by peripheral tissues. Muscle-to-brain communication via muscle-secreted signalling factors is increasingly recognized as an important signalling axis. Collectively, muscle-to-brain signalling could be harnessed to impede neurodegeneration and delay cognitive decline during ageing.
{"title":"Therapeutic potential of myokines and myometabolites for brain ageing and neurodegeneration","authors":"Mamta Rai, Fabio Demontis","doi":"10.1038/s41574-025-01195-9","DOIUrl":"10.1038/s41574-025-01195-9","url":null,"abstract":"Neurodegeneration is not merely determined by local cues but is also influenced by systemic signals, such as factors released by peripheral tissues. Muscle-to-brain communication via muscle-secreted signalling factors is increasingly recognized as an important signalling axis. Collectively, muscle-to-brain signalling could be harnessed to impede neurodegeneration and delay cognitive decline during ageing.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"22 1","pages":"1-2"},"PeriodicalIF":40.0,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246801","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}
Pub Date : 2025-10-06DOI: 10.1038/s41574-025-01187-9
Selim Chaib, Allyson K. Palmer, Saranya P. Wyles, Nicolas Musi, James L. Kirkland, Tamara Tchkonia
Translational research on cellular senescence has led to numerous early-phase clinical trials targeting senescent cells to treat, prevent or alleviate multiple disorders and diseases, including metabolic diseases and their comorbidities. Cellular senescence is a cell fate that occurs in response to stressors, including metabolic disruptions, and is one of the hallmarks (or pillars) of ageing. In their senescent state, cells cease proliferation and can develop a senescence-associated secretory and metabolic phenotype that contributes to the pathogenesis of metabolic dysfunction associated with obesity and ageing. Metabolic stress, which is central to the development of metabolic diseases, can trigger cellular senescence, thereby enabling a vicious cycle that exacerbates metabolic dysfunction. Therapies targeting senescent cells (senotherapeutics), either alone or in combination with other gerotherapies or lifestyle interventions, hold great promise for addressing the ongoing obesity epidemic and the need for improved therapies to prevent and treat metabolic diseases and their complications and comorbidities. In this Review, we discuss novel senotherapeutics, including challenges related to the translation of these therapies and the need to establish gerodiagnostic biomarkers to track the elimination of senescent cells, define eligibility and measure efficacy, as well as considerations for clinical trial design and execution. This Review explores the translation of senotherapeutics into clinical practice for metabolic disorders. The authors discuss the relationship between metabolic disorders and cellular senescence, current and emerging therapies, and the challenges of translating senotherapeutics into clinical practice for metabolic disorders.
{"title":"Translating cellular senescence research into clinical practice for metabolic disease","authors":"Selim Chaib, Allyson K. Palmer, Saranya P. Wyles, Nicolas Musi, James L. Kirkland, Tamara Tchkonia","doi":"10.1038/s41574-025-01187-9","DOIUrl":"10.1038/s41574-025-01187-9","url":null,"abstract":"Translational research on cellular senescence has led to numerous early-phase clinical trials targeting senescent cells to treat, prevent or alleviate multiple disorders and diseases, including metabolic diseases and their comorbidities. Cellular senescence is a cell fate that occurs in response to stressors, including metabolic disruptions, and is one of the hallmarks (or pillars) of ageing. In their senescent state, cells cease proliferation and can develop a senescence-associated secretory and metabolic phenotype that contributes to the pathogenesis of metabolic dysfunction associated with obesity and ageing. Metabolic stress, which is central to the development of metabolic diseases, can trigger cellular senescence, thereby enabling a vicious cycle that exacerbates metabolic dysfunction. Therapies targeting senescent cells (senotherapeutics), either alone or in combination with other gerotherapies or lifestyle interventions, hold great promise for addressing the ongoing obesity epidemic and the need for improved therapies to prevent and treat metabolic diseases and their complications and comorbidities. In this Review, we discuss novel senotherapeutics, including challenges related to the translation of these therapies and the need to establish gerodiagnostic biomarkers to track the elimination of senescent cells, define eligibility and measure efficacy, as well as considerations for clinical trial design and execution. This Review explores the translation of senotherapeutics into clinical practice for metabolic disorders. The authors discuss the relationship between metabolic disorders and cellular senescence, current and emerging therapies, and the challenges of translating senotherapeutics into clinical practice for metabolic disorders.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"22 2","pages":"102-115"},"PeriodicalIF":40.0,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145235893","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}
Pub Date : 2025-10-02DOI: 10.1038/s41574-025-01191-z
John C. Lin, Clara E. Tandar
{"title":"Global patterns of visceral adiposity and cardiometabolic disease","authors":"John C. Lin, Clara E. Tandar","doi":"10.1038/s41574-025-01191-z","DOIUrl":"10.1038/s41574-025-01191-z","url":null,"abstract":"","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"22 1","pages":"8-8"},"PeriodicalIF":40.0,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145209139","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}
Pub Date : 2025-09-26DOI: 10.1038/s41574-025-01180-2
Victoria J. Vieira-Potter, Gargi Mishra, Kristy L. Townsend
Menopausal women are more likely than premenopausal women to gain weight in the form of excess adipose tissue, which becomes preferentially deposited in the viscera. This body composition shift, largely driven by declining oestrogen levels, increases cardiometabolic disease risk. Oestrogens are key hormones involved in many metabolic processes, including in adipose tissue. Given the strong influence that adipose tissue health has on systemic metabolism, additional insights into mechanisms by which oestrogens affect adipose tissue phenotype and function are critical. Not only is adipose tissue affected by oestrogen signalling, adipose tissue is also a major source of circulating oestrogens, and the only appreciable source of oestrogens for men and postmenopausal women. Therefore, women with obesity have higher circulating levels of oestrogens, but whether this fact contributes to the diverse comorbidities of obesity (such as, cancer, metabolic syndrome and osteoporosis) remains unclear. Loss of the effects of oestrogen in adipose tissue later in life could underlie the tissue’s functional decline and expanded mass during menopause and beyond. In this Review, we discuss the roles of oestrogens in adipose functional health, and how these functions influence obesity and metabolic disease risk. Oestrogen is a key regulator in many metabolic processes, particularly in adipose tissue. This Review discusses the role of oestrogen in adipose tissue metabolism and its wider implications for systemic metabolic health.
{"title":"Health of adipose tissue: oestrogen matters","authors":"Victoria J. Vieira-Potter, Gargi Mishra, Kristy L. Townsend","doi":"10.1038/s41574-025-01180-2","DOIUrl":"10.1038/s41574-025-01180-2","url":null,"abstract":"Menopausal women are more likely than premenopausal women to gain weight in the form of excess adipose tissue, which becomes preferentially deposited in the viscera. This body composition shift, largely driven by declining oestrogen levels, increases cardiometabolic disease risk. Oestrogens are key hormones involved in many metabolic processes, including in adipose tissue. Given the strong influence that adipose tissue health has on systemic metabolism, additional insights into mechanisms by which oestrogens affect adipose tissue phenotype and function are critical. Not only is adipose tissue affected by oestrogen signalling, adipose tissue is also a major source of circulating oestrogens, and the only appreciable source of oestrogens for men and postmenopausal women. Therefore, women with obesity have higher circulating levels of oestrogens, but whether this fact contributes to the diverse comorbidities of obesity (such as, cancer, metabolic syndrome and osteoporosis) remains unclear. Loss of the effects of oestrogen in adipose tissue later in life could underlie the tissue’s functional decline and expanded mass during menopause and beyond. In this Review, we discuss the roles of oestrogens in adipose functional health, and how these functions influence obesity and metabolic disease risk. Oestrogen is a key regulator in many metabolic processes, particularly in adipose tissue. This Review discusses the role of oestrogen in adipose tissue metabolism and its wider implications for systemic metabolic health.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"22 2","pages":"76-91"},"PeriodicalIF":40.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153451","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}
Pub Date : 2025-09-24DOI: 10.1038/s41574-025-01186-w
Mary Saunders
{"title":"Reply to ‘Why the science on T3 and genomics is not settled’","authors":"Mary Saunders","doi":"10.1038/s41574-025-01186-w","DOIUrl":"10.1038/s41574-025-01186-w","url":null,"abstract":"","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"21 12","pages":"800-800"},"PeriodicalIF":40.0,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145134076","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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