Pub Date : 2026-02-03DOI: 10.1038/s41574-026-01232-1
Andreas Schäffler, Andreas Schmid, Thomas Karrasch
{"title":"Blood-brain barrier permeability of adipokines and myokines.","authors":"Andreas Schäffler, Andreas Schmid, Thomas Karrasch","doi":"10.1038/s41574-026-01232-1","DOIUrl":"https://doi.org/10.1038/s41574-026-01232-1","url":null,"abstract":"","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":" ","pages":""},"PeriodicalIF":40.0,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113639","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 : 2026-01-16DOI: 10.1038/s41574-026-01231-2
Claire Greenhill
{"title":"GPR110 as a regulator of MASH.","authors":"Claire Greenhill","doi":"10.1038/s41574-026-01231-2","DOIUrl":"https://doi.org/10.1038/s41574-026-01231-2","url":null,"abstract":"","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"19 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145986568","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 : 2026-01-15DOI: 10.1038/s41574-025-01229-2
Tobias Pischon,Katharina Nimptsch
Obesity is a risk factor for chronic diseases and early death; however, the underlying mechanisms are not fully understood. Whereas insulin resistance and inflammation are established pathways in several of these relationships, it is less clear how increases in body adipose tissue relate to these pathways and disease risk. Several adipose tissue-derived blood-based biomarkers have been identified as purported mediators, including adipokines, inflammatory cytokines and sex steroid hormones. Traditionally, these markers were discovered in animal models and their relevance in humans has then been investigated in epidemiological studies. Today, proteomics and metabolomics approaches in human observational studies are used to discover obesity biomarkers in blood, supported by Mendelian randomization studies to draw causal inferences. Here we review adipose tissue-derived blood-based obesity biomarkers and their relevance for disease risk, along with their potential role as mediators. Proteomics and metabolomics studies have partly re-identified traditional biomarkers, but more large-scale prospective analyses are needed to obtain evidence of the relevance of omics-based and traditional obesity biomarkers to disease.
{"title":"Blood-based obesity biomarkers and their relevance for disease risk.","authors":"Tobias Pischon,Katharina Nimptsch","doi":"10.1038/s41574-025-01229-2","DOIUrl":"https://doi.org/10.1038/s41574-025-01229-2","url":null,"abstract":"Obesity is a risk factor for chronic diseases and early death; however, the underlying mechanisms are not fully understood. Whereas insulin resistance and inflammation are established pathways in several of these relationships, it is less clear how increases in body adipose tissue relate to these pathways and disease risk. Several adipose tissue-derived blood-based biomarkers have been identified as purported mediators, including adipokines, inflammatory cytokines and sex steroid hormones. Traditionally, these markers were discovered in animal models and their relevance in humans has then been investigated in epidemiological studies. Today, proteomics and metabolomics approaches in human observational studies are used to discover obesity biomarkers in blood, supported by Mendelian randomization studies to draw causal inferences. Here we review adipose tissue-derived blood-based obesity biomarkers and their relevance for disease risk, along with their potential role as mediators. Proteomics and metabolomics studies have partly re-identified traditional biomarkers, but more large-scale prospective analyses are needed to obtain evidence of the relevance of omics-based and traditional obesity biomarkers to disease.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"85 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145971827","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 : 2026-01-09DOI: 10.1038/s41574-025-01228-3
Dana Goldberg,Ido Goldstein
Upon fasting, mammals undergo a fasting response in which the liver's main role is producing fuel (glucose and ketone bodies) to supply extra-hepatic tissues. Glucose is produced by glycogenolysis and gluconeogenesis, and ketone bodies are produced by ketogenesis, which is preceded by lipolysis and fatty acid oxidation. Hepatic fuel production during fasting is controlled by hormonal and metabolic cues, collectively termed here 'fasting cues'. In this Review, we discuss fasting cues that directly signal hepatocytes and whose plasma levels increase upon fasting, namely, glucagon, glucocorticoids, growth hormone, adrenaline, free fatty acids, asprosin and GP73. We outline the fasting-dependent increases in blood levels of these cues, how they regulate transcription and the metabolic consequences of these cues in hepatocytes. We put particular emphasis on their role in directing fuel production. The perception of endocrine control of fuel production is shifting from the classic 'counter-regulatory' notion that fasting cues are simply opposing insulin action, to the realization that fasting cues cooperate with each other to elicit a synergistic response and also complement each other's actions indirectly. We discuss these modes of crosstalk and cooperation between fasting cues and describe the effects of signal integration on the transcriptional and metabolic response to fasting.
{"title":"Endocrine regulation of the hepatic fasting response: cues, cooperation and consequences.","authors":"Dana Goldberg,Ido Goldstein","doi":"10.1038/s41574-025-01228-3","DOIUrl":"https://doi.org/10.1038/s41574-025-01228-3","url":null,"abstract":"Upon fasting, mammals undergo a fasting response in which the liver's main role is producing fuel (glucose and ketone bodies) to supply extra-hepatic tissues. Glucose is produced by glycogenolysis and gluconeogenesis, and ketone bodies are produced by ketogenesis, which is preceded by lipolysis and fatty acid oxidation. Hepatic fuel production during fasting is controlled by hormonal and metabolic cues, collectively termed here 'fasting cues'. In this Review, we discuss fasting cues that directly signal hepatocytes and whose plasma levels increase upon fasting, namely, glucagon, glucocorticoids, growth hormone, adrenaline, free fatty acids, asprosin and GP73. We outline the fasting-dependent increases in blood levels of these cues, how they regulate transcription and the metabolic consequences of these cues in hepatocytes. We put particular emphasis on their role in directing fuel production. The perception of endocrine control of fuel production is shifting from the classic 'counter-regulatory' notion that fasting cues are simply opposing insulin action, to the realization that fasting cues cooperate with each other to elicit a synergistic response and also complement each other's actions indirectly. We discuss these modes of crosstalk and cooperation between fasting cues and describe the effects of signal integration on the transcriptional and metabolic response to fasting.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"47 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145937875","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 : 2026-01-08DOI: 10.1038/s41574-025-01226-5
Salman Razvi
Thyroid dysfunction and diabetes mellitus frequently occur together, with evidence showing higher rates of each condition in individuals affected by the other. Beyond their statistical association, emerging research indicates shared mechanisms involving autoimmunity, obesity, ageing and insulin resistance, which might explain their bidirectional relationship. This Review synthesizes current evidence on these links, with a particular focus on how thyroid dysfunction influences glycaemic control and how antidiabetic therapies affect thyroid function. Unlike earlier reviews, we frame thyroid disorders within the broader category of non-communicable diseases (NCDs), emphasizing their public health relevance and the need for greater attention in global funding and policy agendas. By combining clinical insights with a population health perspective, this Review aims to promote earlier detection, integrated management strategies and recognition of thyroid disease as a neglected NCD priority.
{"title":"The public health burden of diabetes mellitus and thyroid disease: twin epidemics.","authors":"Salman Razvi","doi":"10.1038/s41574-025-01226-5","DOIUrl":"https://doi.org/10.1038/s41574-025-01226-5","url":null,"abstract":"<p><p>Thyroid dysfunction and diabetes mellitus frequently occur together, with evidence showing higher rates of each condition in individuals affected by the other. Beyond their statistical association, emerging research indicates shared mechanisms involving autoimmunity, obesity, ageing and insulin resistance, which might explain their bidirectional relationship. This Review synthesizes current evidence on these links, with a particular focus on how thyroid dysfunction influences glycaemic control and how antidiabetic therapies affect thyroid function. Unlike earlier reviews, we frame thyroid disorders within the broader category of non-communicable diseases (NCDs), emphasizing their public health relevance and the need for greater attention in global funding and policy agendas. By combining clinical insights with a population health perspective, this Review aims to promote earlier detection, integrated management strategies and recognition of thyroid disease as a neglected NCD priority.</p>","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":" ","pages":""},"PeriodicalIF":40.0,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145934351","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 : 2026-01-07DOI: 10.1038/s41574-025-01217-6
Alicia Diaz-Thomas,Susanne Cabrera,Rocio I Pereira,Pallavi Iyer
Diabetes mellitus is one of the fastest-growing chronic medical conditions worldwide. It disproportionately affects some minoritized populations, including certain racial and ethnic groups, migrant populations, and rural communities. Disparities in diabetes mellitus prevalence, morbidity and mortality in minoritized populations are related to longstanding structural and social inequities and are closely tied to social factors. However, current interventions to improve diabetes mellitus outcomes among people from minoritized populations have primarily focused on trying to change individual behaviour, without sufficiently addressing the root structural barriers that drive disparities. Here, we aim to describe the structural inequities in the diagnosis, management and outcomes of minoritized people with diabetes mellitus and to discuss practical measures that can ensure equitable care for people in minoritized groups who have diabetes mellitus. Using a framework to examine diabetes mellitus disparities, we will consider interventions at system levels, including public health approaches, the endocrine healthcare workforce, care quality standards, access to high-quality care (including advanced technologies) and involvement in research. We will also discuss strategies to address intermediate factors, including food insecurity and literacy, and to improve diabetes mellitus care services among migrant and refugee populations and racial and/or ethnic minority communities.
{"title":"Tailoring interventions to close gaps in diabetes mellitus care.","authors":"Alicia Diaz-Thomas,Susanne Cabrera,Rocio I Pereira,Pallavi Iyer","doi":"10.1038/s41574-025-01217-6","DOIUrl":"https://doi.org/10.1038/s41574-025-01217-6","url":null,"abstract":"Diabetes mellitus is one of the fastest-growing chronic medical conditions worldwide. It disproportionately affects some minoritized populations, including certain racial and ethnic groups, migrant populations, and rural communities. Disparities in diabetes mellitus prevalence, morbidity and mortality in minoritized populations are related to longstanding structural and social inequities and are closely tied to social factors. However, current interventions to improve diabetes mellitus outcomes among people from minoritized populations have primarily focused on trying to change individual behaviour, without sufficiently addressing the root structural barriers that drive disparities. Here, we aim to describe the structural inequities in the diagnosis, management and outcomes of minoritized people with diabetes mellitus and to discuss practical measures that can ensure equitable care for people in minoritized groups who have diabetes mellitus. Using a framework to examine diabetes mellitus disparities, we will consider interventions at system levels, including public health approaches, the endocrine healthcare workforce, care quality standards, access to high-quality care (including advanced technologies) and involvement in research. We will also discuss strategies to address intermediate factors, including food insecurity and literacy, and to improve diabetes mellitus care services among migrant and refugee populations and racial and/or ethnic minority communities.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"44 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145907661","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 : 2026-01-06DOI: 10.1038/s41574-025-01220-x
Ryan Yi Hang Loo, Xinyi Zhang, Carmen Ching, Adrian Kee Keong Teo
{"title":"Models of hyperglycaemia in diabetes mellitus and its complications","authors":"Ryan Yi Hang Loo, Xinyi Zhang, Carmen Ching, Adrian Kee Keong Teo","doi":"10.1038/s41574-025-01220-x","DOIUrl":"https://doi.org/10.1038/s41574-025-01220-x","url":null,"abstract":"","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"30 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145902541","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 : 2026-01-05DOI: 10.1038/s41574-025-01221-w
Sabrina Wangler,Marc N Jarczok,Matthew Ennis,Benedict Herhaus,Róbert Wagner,Ratika Sehgal,Martin Heni
The autonomic nervous system is a crucial mediator between the central nervous system and peripheral tissues and is essential for maintaining homeostasis. In this Review, we discuss the bidirectional communication between the autonomic nervous system and metabolic tissues in humans, focusing on the coordination of systemic glucose and lipid metabolism through autonomic signalling across changing physiological states. We also discuss the crosstalk between autonomic and immune pathways and its relevance for metabolic control. An overview of current methodologies to assess autonomic function in humans shows that quantifying organ-specific autonomic outflows remains challenging. Chronic disturbances in autonomic regulation are increasingly recognized as contributors to metabolic diseases such as obesity and type 2 diabetes mellitus. Hence, emerging therapeutic strategies targeting autonomic function could offer promising opportunities to improve metabolic health. Progress will depend on the development of tools to selectively assess autonomic input to individual metabolic organs. Addressing high inter-individual variability and capturing the temporal dynamics of organ-specific autonomic regulation will be essential for advancing mechanistic insights, ultimately enabling clinical translation.
{"title":"The autonomic nervous system in the regulation of glucose and lipid metabolism.","authors":"Sabrina Wangler,Marc N Jarczok,Matthew Ennis,Benedict Herhaus,Róbert Wagner,Ratika Sehgal,Martin Heni","doi":"10.1038/s41574-025-01221-w","DOIUrl":"https://doi.org/10.1038/s41574-025-01221-w","url":null,"abstract":"The autonomic nervous system is a crucial mediator between the central nervous system and peripheral tissues and is essential for maintaining homeostasis. In this Review, we discuss the bidirectional communication between the autonomic nervous system and metabolic tissues in humans, focusing on the coordination of systemic glucose and lipid metabolism through autonomic signalling across changing physiological states. We also discuss the crosstalk between autonomic and immune pathways and its relevance for metabolic control. An overview of current methodologies to assess autonomic function in humans shows that quantifying organ-specific autonomic outflows remains challenging. Chronic disturbances in autonomic regulation are increasingly recognized as contributors to metabolic diseases such as obesity and type 2 diabetes mellitus. Hence, emerging therapeutic strategies targeting autonomic function could offer promising opportunities to improve metabolic health. Progress will depend on the development of tools to selectively assess autonomic input to individual metabolic organs. Addressing high inter-individual variability and capturing the temporal dynamics of organ-specific autonomic regulation will be essential for advancing mechanistic insights, ultimately enabling clinical translation.","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":"4 1","pages":""},"PeriodicalIF":40.5,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145897510","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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