Pub Date : 2024-04-17DOI: 10.1038/s41574-024-00988-8
Olivia Tysoe
{"title":"A novel system for non-invasive measurement of blood levels of glucose","authors":"Olivia Tysoe","doi":"10.1038/s41574-024-00988-8","DOIUrl":"10.1038/s41574-024-00988-8","url":null,"abstract":"","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":null,"pages":null},"PeriodicalIF":40.5,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140607514","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 : 2024-04-08DOI: 10.1038/s41574-024-00973-1
Ramzi A. Ajjan, Tadej Battelino, Xavier Cos, Stefano Del Prato, Jean-Christophe Philips, Laurent Meyer, Jochen Seufert, Samuel Seidu
Although continuous glucose monitoring (CGM) devices are now considered the standard of care for people with type 1 diabetes mellitus, the uptake among people with type 2 diabetes mellitus (T2DM) has been slower and is focused on those receiving intensive insulin therapy. However, increasing evidence now supports the inclusion of CGM in the routine care of people with T2DM who are on basal insulin-only regimens or are managed with other medications. Expanding CGM to these groups could minimize hypoglycaemia while allowing efficient adaptation and escalation of therapies. Increasing evidence from randomized controlled trials and observational studies indicates that CGM is of clinical value in people with T2DM on non-intensive treatment regimens. If further studies confirm this finding, CGM could soon become a part of routine care for T2DM. In this Perspective we explore the potential benefits of widening the application of CGM in T2DM, along with the challenges that must be overcome for the evidence-based benefits of this technology to be delivered for all people with T2DM. Continuous glucose monitoring (CGM) is an effective tool in the management of diabetes mellitus. This Perspective discusses the potential benefits of widespread adoption of CGM in people with type 2 diabetes mellitus at different stages of disease progression and treatment intensification.
{"title":"Continuous glucose monitoring for the routine care of type 2 diabetes mellitus","authors":"Ramzi A. Ajjan, Tadej Battelino, Xavier Cos, Stefano Del Prato, Jean-Christophe Philips, Laurent Meyer, Jochen Seufert, Samuel Seidu","doi":"10.1038/s41574-024-00973-1","DOIUrl":"10.1038/s41574-024-00973-1","url":null,"abstract":"Although continuous glucose monitoring (CGM) devices are now considered the standard of care for people with type 1 diabetes mellitus, the uptake among people with type 2 diabetes mellitus (T2DM) has been slower and is focused on those receiving intensive insulin therapy. However, increasing evidence now supports the inclusion of CGM in the routine care of people with T2DM who are on basal insulin-only regimens or are managed with other medications. Expanding CGM to these groups could minimize hypoglycaemia while allowing efficient adaptation and escalation of therapies. Increasing evidence from randomized controlled trials and observational studies indicates that CGM is of clinical value in people with T2DM on non-intensive treatment regimens. If further studies confirm this finding, CGM could soon become a part of routine care for T2DM. In this Perspective we explore the potential benefits of widening the application of CGM in T2DM, along with the challenges that must be overcome for the evidence-based benefits of this technology to be delivered for all people with T2DM. Continuous glucose monitoring (CGM) is an effective tool in the management of diabetes mellitus. This Perspective discusses the potential benefits of widespread adoption of CGM in people with type 2 diabetes mellitus at different stages of disease progression and treatment intensification.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":null,"pages":null},"PeriodicalIF":40.5,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140534173","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}
Protein tyrosine phosphatase 1B (PTP1B), a non-transmembrane phosphatase, has a major role in a variety of signalling pathways, including direct negative regulation of classic insulin and leptin signalling pathways, and is implicated in the pathogenesis of several cardiometabolic diseases and cancers. As such, PTP1B has been a therapeutic target for over two decades, with PTP1B inhibitors identified either from natural sources or developed throughout the years. Some of these inhibitors have reached phase I and/or II clinical trials in humans for the treatment of type 2 diabetes mellitus, obesity and/or metastatic breast cancer. In this Review, we summarize the cellular processes and regulation of PTP1B, discuss evidence from in vivo preclinical and human studies of the association between PTP1B and different disorders, and discuss outcomes of clinical trials. We outline challenges associated with the targeting of this phosphatase (which was, until the past few years, viewed as difficult to target), the current state of the field of PTP1B inhibitors (and dual phosphatase inhibitors) and future directions for manipulating the activity of this key metabolic enzyme. This Review summarizes cellular processes and regulation of protein tyrosine phosphatase 1B (PTP1B), discussing evidence from in vivo preclinical and human studies. PTP1B inhibitors, which are being developed for type 2 diabetes mellitus, obesity, rare diseases (such as Rett syndrome) and some cancers, are also discussed.
蛋白酪氨酸磷酸酶 1B（PTP1B）是一种非跨膜磷酸酶，在多种信号通路中发挥着重要作用，包括直接负向调节经典的胰岛素和瘦素信号通路，并与多种心脏代谢疾病和癌症的发病机制有关。因此，二十多年来，PTP1B 一直是一个治疗靶点，多年来，从天然来源或开发的 PTP1B 抑制剂不断被发现。其中一些抑制剂已进入人类 I 期和/或 II 期临床试验阶段，用于治疗 2 型糖尿病、肥胖症和/或转移性乳腺癌。在本综述中，我们总结了 PTP1B 的细胞过程和调控，讨论了 PTP1B 与不同疾病相关的体内临床前研究和人体研究的证据，并讨论了临床试验的结果。我们概述了与靶向这种磷酸酶相关的挑战（直到过去几年，这种磷酸酶一直被视为难以靶向）、PTP1B 抑制剂（和双重磷酸酶抑制剂）领域的现状以及操纵这种关键代谢酶活性的未来方向。
{"title":"Protein tyrosine phosphatase 1B in metabolic diseases and drug development","authors":"Mirela Delibegović, Sergio Dall’Angelo, Ruta Dekeryte","doi":"10.1038/s41574-024-00965-1","DOIUrl":"10.1038/s41574-024-00965-1","url":null,"abstract":"Protein tyrosine phosphatase 1B (PTP1B), a non-transmembrane phosphatase, has a major role in a variety of signalling pathways, including direct negative regulation of classic insulin and leptin signalling pathways, and is implicated in the pathogenesis of several cardiometabolic diseases and cancers. As such, PTP1B has been a therapeutic target for over two decades, with PTP1B inhibitors identified either from natural sources or developed throughout the years. Some of these inhibitors have reached phase I and/or II clinical trials in humans for the treatment of type 2 diabetes mellitus, obesity and/or metastatic breast cancer. In this Review, we summarize the cellular processes and regulation of PTP1B, discuss evidence from in vivo preclinical and human studies of the association between PTP1B and different disorders, and discuss outcomes of clinical trials. We outline challenges associated with the targeting of this phosphatase (which was, until the past few years, viewed as difficult to target), the current state of the field of PTP1B inhibitors (and dual phosphatase inhibitors) and future directions for manipulating the activity of this key metabolic enzyme. This Review summarizes cellular processes and regulation of protein tyrosine phosphatase 1B (PTP1B), discussing evidence from in vivo preclinical and human studies. PTP1B inhibitors, which are being developed for type 2 diabetes mellitus, obesity, rare diseases (such as Rett syndrome) and some cancers, are also discussed.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":null,"pages":null},"PeriodicalIF":40.5,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140189004","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 : 2024-03-21DOI: 10.1038/s41574-024-00970-4
Robert C. Baxter
The acid-labile subunit (ALS) of the insulin-like growth factor (IGF) binding protein (IGFBP) complex, encoded in humans by IGFALS, has a vital role in regulating the endocrine transport and bioavailability of IGF-1 and IGF-2. Accordingly, ALS has a considerable influence on postnatal growth and metabolism. ALS is a leucine-rich glycoprotein that forms high-affinity ternary complexes with IGFBP-3 or IGFBP-5 when they are occupied by either IGF-1 or IGF-2. These complexes constitute a stable reservoir of circulating IGFs, blocking the potentially hypoglycaemic activity of unbound IGFs. ALS is primarily synthesized by hepatocytes and its expression is lower in non-hepatic tissues. ALS synthesis is strongly induced by growth hormone and suppressed by IL-1β, thus potentially serving as a marker of growth hormone secretion and/or activity and of inflammation. IGFALS mutations in humans and Igfals deletion in mice cause modest growth retardation and pubertal delay, accompanied by decreased osteogenesis and enhanced adipogenesis. In hepatocellular carcinoma, IGFALS is described as a tumour suppressor; however, its contribution to other cancers is not well delineated. This Review addresses the endocrine physiology and pathology of ALS, discusses the latest cell and proteomic studies that suggest emerging cellular roles for ALS and outlines its involvement in other disease states. The acid-labile subunit (ALS) of the insulin-like growth factor (IGF) binding protein complex regulates the endocrine transport and bioavailability of IGF-1 and IGF-2 and therefore influences postnatal growth and metabolism. This Review addresses the endocrine physiology and pathology of ALS, discusses the emerging cellular roles for ALS and outlines its involvement in disease states.
{"title":"Endocrine and cellular physiology and pathology of the insulin-like growth factor acid-labile subunit","authors":"Robert C. Baxter","doi":"10.1038/s41574-024-00970-4","DOIUrl":"10.1038/s41574-024-00970-4","url":null,"abstract":"The acid-labile subunit (ALS) of the insulin-like growth factor (IGF) binding protein (IGFBP) complex, encoded in humans by IGFALS, has a vital role in regulating the endocrine transport and bioavailability of IGF-1 and IGF-2. Accordingly, ALS has a considerable influence on postnatal growth and metabolism. ALS is a leucine-rich glycoprotein that forms high-affinity ternary complexes with IGFBP-3 or IGFBP-5 when they are occupied by either IGF-1 or IGF-2. These complexes constitute a stable reservoir of circulating IGFs, blocking the potentially hypoglycaemic activity of unbound IGFs. ALS is primarily synthesized by hepatocytes and its expression is lower in non-hepatic tissues. ALS synthesis is strongly induced by growth hormone and suppressed by IL-1β, thus potentially serving as a marker of growth hormone secretion and/or activity and of inflammation. IGFALS mutations in humans and Igfals deletion in mice cause modest growth retardation and pubertal delay, accompanied by decreased osteogenesis and enhanced adipogenesis. In hepatocellular carcinoma, IGFALS is described as a tumour suppressor; however, its contribution to other cancers is not well delineated. This Review addresses the endocrine physiology and pathology of ALS, discusses the latest cell and proteomic studies that suggest emerging cellular roles for ALS and outlines its involvement in other disease states. The acid-labile subunit (ALS) of the insulin-like growth factor (IGF) binding protein complex regulates the endocrine transport and bioavailability of IGF-1 and IGF-2 and therefore influences postnatal growth and metabolism. This Review addresses the endocrine physiology and pathology of ALS, discusses the emerging cellular roles for ALS and outlines its involvement in disease states.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":null,"pages":null},"PeriodicalIF":40.5,"publicationDate":"2024-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140182826","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 : 2024-03-21DOI: 10.1038/s41574-024-00977-x
Maria J. Redondo, Noel G. Morgan
{"title":"Reply to ‘Slowly progressive insulin dependent diabetes mellitus in type 1 diabetes endotype 2’","authors":"Maria J. Redondo, Noel G. Morgan","doi":"10.1038/s41574-024-00977-x","DOIUrl":"10.1038/s41574-024-00977-x","url":null,"abstract":"","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":null,"pages":null},"PeriodicalIF":40.5,"publicationDate":"2024-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41574-024-00977-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140184993","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 : 2024-03-21DOI: 10.1038/s41574-024-00981-1
Florent Sauvé, Loïc Kacimi, Vincent Prévot
Alzheimer disease has a sex bias: women are twice as likely as men to be affected. Studies have linked elevated follicle-stimulating hormone (FSH) levels to worsened Alzheimer disease pathology and cognitive decline in mice. Exploring the interaction of FSH with APOE4 has uncovered new aspects of Alzheimer disease. The therapeutic potential of FSH and gonadotropin-releasing hormone have also been highlighted.
{"title":"The hypothalamic–pituitary–gonadal axis and the enigma of Alzheimer disease sex differences","authors":"Florent Sauvé, Loïc Kacimi, Vincent Prévot","doi":"10.1038/s41574-024-00981-1","DOIUrl":"10.1038/s41574-024-00981-1","url":null,"abstract":"Alzheimer disease has a sex bias: women are twice as likely as men to be affected. Studies have linked elevated follicle-stimulating hormone (FSH) levels to worsened Alzheimer disease pathology and cognitive decline in mice. Exploring the interaction of FSH with APOE4 has uncovered new aspects of Alzheimer disease. The therapeutic potential of FSH and gonadotropin-releasing hormone have also been highlighted.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":null,"pages":null},"PeriodicalIF":40.5,"publicationDate":"2024-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140184995","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 : 2024-03-20DOI: 10.1038/s41574-024-00978-w
Stephan Petersenn, Maria Fleseriu, Shlomo Melmed
{"title":"Reply to ‘Tumour fibrosis in dopamine agonist-exposed prolactinomas is a diminishing concern’","authors":"Stephan Petersenn, Maria Fleseriu, Shlomo Melmed","doi":"10.1038/s41574-024-00978-w","DOIUrl":"10.1038/s41574-024-00978-w","url":null,"abstract":"","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":null,"pages":null},"PeriodicalIF":40.5,"publicationDate":"2024-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41574-024-00978-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140175598","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}
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