Nature Reviews Endocrinology最新文献

Global patterns of visceral adiposity and cardiometabolic disease. 内脏脂肪和心脏代谢疾病的全球模式。

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-10-02 DOI: 10.1038/s41574-025-01191-z

John C Lin,Clara E Tandar

引用次数: 0

Health of adipose tissue: oestrogen matters. 脂肪组织的健康：雌激素很重要。

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-09-26 DOI: 10.1038/s41574-025-01180-2

Victoria J Vieira-Potter,Gargi Mishra,Kristy L Townsend

{"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":"https://doi.org/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.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"42 1","pages":""},"PeriodicalIF":40.5,"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}

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Reply to 'Why the science on T3 and genomics is not settled'. 回复“为什么T3和基因组学的科学还没有解决”。

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-09-24 DOI: 10.1038/s41574-025-01186-w

Mary Saunders

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Why the science on T3 and genomics is not settled. 为什么T3和基因组学的科学还没有定论。

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-09-24 DOI: 10.1038/s41574-025-01185-x

Greta Lyons,Julia Priestley

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Negative effects of ultra-processed foods beyond increasing calories. 超加工食品的负面影响不仅仅是增加卡路里。

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-09-22 DOI: 10.1038/s41574-025-01189-7

Senegal Carty

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Leptin and melanocortin signalling in the response to infection. 瘦素和黑素皮质素在感染反应中的信号。

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-09-22 DOI: 10.1038/s41574-025-01184-y

Roger R Fan,John D Beckham,Kartik N Rajagopalan

{"title":"Leptin and melanocortin signalling in the response to infection.","authors":"Roger R Fan,John D Beckham,Kartik N Rajagopalan","doi":"10.1038/s41574-025-01184-y","DOIUrl":"https://doi.org/10.1038/s41574-025-01184-y","url":null,"abstract":"The response to infection is an energy-demanding process that bolsters cell division and protein synthesis to overcome a rapidly dividing and invasive pathogen. Paradoxically, anorexia, a conserved behavioural response to infection, sharply limits food intake during this period of high energy demand. Leptin, the release of which from adipocytes is coordinated with the immune response, signals to the hypothalamus to balance energy availability and expenditure with respect to various physiological processes. Congenital deficiency of leptin or its receptor in humans predisposes to infection. Moreover, low serum levels of leptin are associated with poor outcomes in sepsis. Leptin activates pro-opiomelanocortin neurons, which produce melanocortins, a family of peptide hormones that has diverse roles. The melanocortins have targets in many organ systems and their functions include suppressing inflammation and upregulating sympathetic tone. Here, we discuss what is known about leptin and melanocortin signalling in the response to infection, with evidence from preclinical research and human studies. We close by offering insights into how study of these pathways might be translated into therapies for infectious disease as well as new avenues for exploration.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"12 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117164","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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HDL metabolism and function in diabetes mellitus. 糖尿病患者HDL代谢与功能。

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-09-17 DOI: 10.1038/s41574-025-01176-y

Blake J Cochran,Thomas W King,Kevin Chemello,Shane R Thomas,Kerry-Anne Rye

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Antigen-specific Treg cells induce infectious tolerance 抗原特异性Treg细胞诱导感染性耐受

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-09-11 DOI: 10.1038/s41574-025-01182-0

Olivia Tysoe

{"title":"Antigen-specific Treg cells induce infectious tolerance","authors":"Olivia Tysoe","doi":"10.1038/s41574-025-01182-0","DOIUrl":"https://doi.org/10.1038/s41574-025-01182-0","url":null,"abstract":"Regulatory T (Treg) cells can induce immune tolerance, making Treg cellular therapy a promising strategy to prevent autoimmunity. Clinical trials of Treg cell therapies so far have shown limited efficacy, probably due to the use of polyclonal Treg cells, which lack antigen specificity. A study in Science Translational Medicine demonstrates that Treg cells expressing a chimeric antigen receptor (CAR) specific to the HLA-A2 antigen (A2-CAR Treg cells) were able to induce persistent tolerance in a mouse model of type 1 diabetes mellitus.Mice injected with BDC2.5 Teff cells alone experienced hyperglycaemia and autoimmune destruction of both the transplanted and native islets. Of the mice co-treated with A2-CAR Treg cells, 82% were protected from hyperglycaemia, compared with only 33% of mice treated with BDC2.5 Teff cells plus polyclonal Treg cells. As expected, the A2-CAR Treg cells prevented the autoimmune destruction of the transplanted HLA-A2+ islet graft. Surprisingly, however, HLA-A2− islets in the pancreas were also protected, which suggests that the A2-CAR Treg cells had induced systemic tolerance even without the HLA-A2 antigen.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"20 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031723","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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Cardiometabolic and renal benefits of sodium–glucose cotransporter 2 inhibitors 钠-葡萄糖共转运蛋白2抑制剂对心脏代谢和肾脏的益处

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-09-11 DOI: 10.1038/s41574-025-01170-4

Yong-ho Lee, Soo Lim, Melanie J. Davies

{"title":"Cardiometabolic and renal benefits of sodium–glucose cotransporter 2 inhibitors","authors":"Yong-ho Lee, Soo Lim, Melanie J. Davies","doi":"10.1038/s41574-025-01170-4","DOIUrl":"https://doi.org/10.1038/s41574-025-01170-4","url":null,"abstract":"The therapeutic scope of sodium–glucose cotransporter 2 (SGLT2) inhibitors has expanded beyond glycaemic regulation in the management of diabetes mellitus. Studies published in the past few years highlight their substantial effect on cardiovascular outcomes, notably in decreasing mortality and the need for heart failure-related hospitalization. These agents also lead to pronounced improvements in a range of renal outcomes. The primary actions of SGLT2 inhibition, glycosuria and natriuresis, are pivotal in enhancing glucose control, promoting weight loss and lowering blood pressure. These effects initiate a series of beneficial mechanisms: facilitating haemodynamic improvement by reducing interstitial volume, enhancing cardiac function, boosting energy efficiency through altered ketone body metabolism and mitigating inflammation and oxidative stress. Additional effects include heightened erythropoiesis, reduced hyperuricaemia and increased levels of angiotensin-converting enzyme 2 and angiotensin (1–7). SGLT2 inhibitors also attenuate sympathetic overactivity by modulating neurohumoral activation and renal afferent signalling, contributing to their cardioprotective and renoprotective profiles. This Review provides a comprehensive overview of the diverse mechanisms underpinning the cardiometabolic and renal effects of SGLT2 inhibitors, emphasizing their clinical relevance and therapeutic potential.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"53 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031775","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}

引用次数: 0

Mechanisms of diabetic kidney disease and established and emerging treatments 糖尿病肾病的机制和已建立的和新兴的治疗方法

IF 40.5 1区医学

Nature Reviews Endocrinology Pub Date : 2025-09-11 DOI: 10.1038/s41574-025-01171-3

Victor Martinez Leon, Rachel Hilburg, Katalin Susztak

{"title":"Mechanisms of diabetic kidney disease and established and emerging treatments","authors":"Victor Martinez Leon, Rachel Hilburg, Katalin Susztak","doi":"10.1038/s41574-025-01171-3","DOIUrl":"https://doi.org/10.1038/s41574-025-01171-3","url":null,"abstract":"Kidney disease is the leading cause of mortality in persons with diabetes mellitus. Diabetic kidney disease (DKD) typically presents with a reduced estimated glomerular filtration rate and, in many but not all cases, with marked proteinuria. Strict glycaemic control and blood pressure control remain foundational in managing DKD, and advances in the understanding of disease mechanisms have redefined the therapeutic landscape. Large outcome trials, such as EMPA-KIDNEY, DAPA-CKD and CREDENCE, have demonstrated that sodium–glucose cotransporter 2 inhibitors slow chronic kidney disease progression and improve cardiovascular outcomes. Glucagon-like peptide 1 receptor agonists reduce albuminuria and preserve estimated glomerular filtration rate, as shown most recently in the FLOW trial. Finerenone, a non-steroidal mineralocorticoid receptor antagonist, lowered renal and cardiovascular risk in the FIDELIO-DKD and FIGARO-DKD trials. Combination approaches (for example, sodium–glucose cotransporter 2 inhibition plus endothelin receptor type A blockade in ZENITH-CKD), aldosterone synthase inhibition, and targeted anti-inflammatory or complement-modifying agents offer additional promise. We summarize the key pathophysiological drivers (glomerular hyperfiltration, podocyte injury, tubulointerstitial inflammation and fibrosis), review established treatments and highlight emerging strategies to prevent or halt DKD.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"17 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031776","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}

引用次数: 0