Erin E Mauney, Marsha C Wibowo, Yu-Hua Tseng, Aleksandar D Kostic
{"title":"Adipose tissue-gut microbiome crosstalk in inflammation and thermogenesis.","authors":"Erin E Mauney, Marsha C Wibowo, Yu-Hua Tseng, Aleksandar D Kostic","doi":"10.1016/j.tem.2024.10.004","DOIUrl":"10.1016/j.tem.2024.10.004","url":null,"abstract":"<p><p>Previously characterized as inert fat depots, adipocytes are now recognized as dynamic mediators of inflammatory tone, metabolic health, and nutrient homeostasis. As endocrine organs, specialized depots of adipose tissue engage in crosstalk between the gut, liver, pancreas, and brain to coordinate appetite, thermogenesis, and ultimately body weight. These functions are tightly linked to the inflammatory status of adipose tissue, which is in turn influenced by the health of the gut microbiome. Here, we review recent findings linking specific gut microbes and their secreted factors, including recently identified elements such as bacterial extracellular vesicles, to the functional status of adipocytes. We conclude that further study may generate novel approaches for treating obesity and metabolic disease.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"721-732"},"PeriodicalIF":12.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142632285","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}
{"title":"Inter-organ communication is a critical machinery to regulate metabolism and aging.","authors":"Kyohei Tokizane, Shin-Ichiro Imai","doi":"10.1016/j.tem.2024.11.013","DOIUrl":"10.1016/j.tem.2024.11.013","url":null,"abstract":"<p><p>Inter-organ communication (IOC) is a complex mechanism involved in maintaining metabolic homeostasis and healthy aging. Dysregulation of distinct forms of IOC is linked to metabolic derangements and age-related pathologies, implicating these processes as a potential target for therapeutic intervention to promote healthy aging. In this review, we delve into IOC mediated by hormonal signaling, circulating factors, organelle signaling, and neuronal networks and examine their roles in regulating metabolism and aging. Given the role of the hypothalamus as a high-order control center for aging and longevity, we particularly emphasize the importance of its communication with peripheral organs and pave the way for a better understanding of this critical machinery in metabolism and aging.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"756-766"},"PeriodicalIF":12.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856826","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}
Ke Wang, Karina Cunha E Rocha, Houji Qin, Zixuan Zeng, Wei Ying
{"title":"Host metabolic inflammation fueled by bacterial DNA.","authors":"Ke Wang, Karina Cunha E Rocha, Houji Qin, Zixuan Zeng, Wei Ying","doi":"10.1016/j.tem.2024.11.003","DOIUrl":"10.1016/j.tem.2024.11.003","url":null,"abstract":"<p><p>Metabolic diseases, characterized by chronic low-grade inflammation, exhibit a compromised gut barrier allowing the translocation of bacteria-derived products to bloodstream and distant metabolic organs. Bacterial DNA can be detected in metabolic tissues during the onset of these diseases, highlighting its role in the development of metabolic diseases. Extracellular vesicles (EVs) are involved in the delivery of bacterial DNA to the local tissues, and its sensing by the host triggers local and system inflammation. Understanding bacterial DNA translocation and its induced inflammation is crucial in deciphering metabolic disease pathways. Here, we delve into the mechanisms dictating the interaction between host physiology and bacterial DNA, focusing on its origin and delivery, host immune responses against it, and its roles in metabolic disorders.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"767-777"},"PeriodicalIF":12.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142752264","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}
Kathryn M Citrin, Balkrishna Chaube, Carlos Fernández-Hernando, Yajaira Suárez
{"title":"Intracellular endothelial cell metabolism in vascular function and dysfunction.","authors":"Kathryn M Citrin, Balkrishna Chaube, Carlos Fernández-Hernando, Yajaira Suárez","doi":"10.1016/j.tem.2024.11.004","DOIUrl":"10.1016/j.tem.2024.11.004","url":null,"abstract":"<p><p>Endothelial cells (ECs) form the inner lining of blood vessels that is crucial for vascular function and homeostasis. They regulate vascular tone, oxidative stress, and permeability. Dysfunction leads to increased permeability, leukocyte adhesion, and thrombosis. ECs undergo metabolic changes in conditions such as wound healing, cancer, atherosclerosis, and diabetes, and can influence disease progression. We discuss recent research that has revealed diverse intracellular metabolic pathways in ECs that are tailored to their functional needs, including lipid handling, glycolysis, and fatty acid oxidation (FAO). Understanding EC metabolic signatures in health and disease will be crucial not only for basic biology but can also be exploited when designing new therapies to target EC-related functions in different vascular diseases.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"744-755"},"PeriodicalIF":12.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12159263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822859","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}
Bandy Chen, David Meseguer, Stephanie Lenck, Jean-Leon Thomas, Marc Schneeberger
{"title":"Rewiring of the glymphatic landscape in metabolic disorders.","authors":"Bandy Chen, David Meseguer, Stephanie Lenck, Jean-Leon Thomas, Marc Schneeberger","doi":"10.1016/j.tem.2024.11.005","DOIUrl":"10.1016/j.tem.2024.11.005","url":null,"abstract":"<p><p>The incorporation of the glymphatic clearance system in the study of brain physiology aids in the advancement of innovative diagnostic and treatment strategies for neurological disorders. Exploring the glymphatic system across (from) neurological and (to) metabolic diseases may provide a better link between obesity and neurological disorders. Recent studies indicate the role of metabolic dysfunction as a risk factor for cognitive decline and neurological disorders through the disruption of the glymphatic system. Further investigation into how metabolic dysfunction disrupts glymphatic homeostasis and the domino effects on the neurovascular landscape, including neurovascular uncoupling, cerebral blood flow disruptions, blood-brain barrier leakage, and demyelination, can provide mechanistic insights into the link between obesity and neurological disorders.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"710-720"},"PeriodicalIF":12.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142787765","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}
{"title":"Fumarate.","authors":"Désirée Schatton, Christian Frezza","doi":"10.1016/j.tem.2024.12.010","DOIUrl":"10.1016/j.tem.2024.12.010","url":null,"abstract":"","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"778-779"},"PeriodicalIF":12.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016599","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}
{"title":"Microglial insulin resistance drives neurodegeneration.","authors":"Miao Sun, Weidong Mi","doi":"10.1016/j.tem.2025.06.006","DOIUrl":"10.1016/j.tem.2025.06.006","url":null,"abstract":"<p><p>Brain insulin resistance (BIR) contributes to neurodegenerative diseases such as Alzheimer's disease (AD). Recently, Chen et al. revealed that microglial insulin signaling loss drives neuroinflammation and amyloid-β (Aβ) accumulation, promoting AD progression. These findings provide insights for the prevention and treatment of AD and cognitive disorders.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"696-698"},"PeriodicalIF":12.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144562015","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}
Ruth Frampton, Samantha Hocking, Jennifer R Snaith, Jerry R Greenfield
{"title":"Targeting cardiometabolic risk in type 1 diabetes through incretin physiology.","authors":"Ruth Frampton, Samantha Hocking, Jennifer R Snaith, Jerry R Greenfield","doi":"10.1016/j.tem.2025.06.004","DOIUrl":"https://doi.org/10.1016/j.tem.2025.06.004","url":null,"abstract":"<p><p>People living with type 1 diabetes have significantly increased cardiovascular risk compared with the general population. Traditional risk factors include hypertension, dyslipidaemia, and obesity. However, those with type 1 diabetes contend with treatment-induced insulin resistance and pancreatic and incretin hormone dysfunction, leading to dysglycaemia, which also impacts cardiovascular risk. Here, we highlight the underlying metabolic environment in type 1 diabetes with a focus on glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and glucagon physiology. With the emergence of incretin-based therapies such as semaglutide (a GLP-1 receptor agonist) and tirzepatide (a combined GLP-1/GIP receptor agonist) targeting these receptor pathways, there is now potential to directly target metabolic deficits to address cardiometabolic risk in a type 1 diabetes population.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144562017","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}
Daniel Jimenez-Blasco, Rebeca Lapresa, Jesus Agulla, Angeles Almeida, Juan P Bolaños
{"title":"Neuronal glycolysis meets mitophagy to govern organismal wellbeing.","authors":"Daniel Jimenez-Blasco, Rebeca Lapresa, Jesus Agulla, Angeles Almeida, Juan P Bolaños","doi":"10.1016/j.tem.2025.05.005","DOIUrl":"https://doi.org/10.1016/j.tem.2025.05.005","url":null,"abstract":"<p><p>Neurons are exceptionally energy-demanding cells but have limited energy storage, relying on a constant supply of fuel and oxygen. Although glucose is the brain's main energy source, neurons reduce glycolysis under normal conditions. This surprising strategy helps to protect mitochondria by preserving nicotinamide-adenine dinucleotide (NAD<sup>+</sup>), a vital cofactor consumed by glycolysis. NAD<sup>+</sup> is needed for sirtuin-driven mitophagy, a process that removes damaged mitochondria. By saving NAD<sup>+</sup>, neurons can maintain healthy, energy-efficient mitochondria. These mitochondria then use alternative fuels such as lactate and ketone bodies from astrocytes. Here, we discuss the way in which this balance between reduced glycolysis and active mitophagy supports brain function and overall metabolic health, highlighting a sophisticated system that prioritizes mitochondrial quality for long-term cognitive performance and systemic homeostasis.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144562016","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}
{"title":"Mitochondria as sensors of intracellular pathogens.","authors":"Jose M Delgado, Lena Pernas","doi":"10.1016/j.tem.2024.10.009","DOIUrl":"10.1016/j.tem.2024.10.009","url":null,"abstract":"<p><p>Mitochondria must sense their environment to enable cells and organisms to adapt to diverse environments and survive during stress. However, during microbial infection, an evolutionary pressure since the inception of the eukaryotic cell, these organelles are traditionally viewed as targets for microbes. In this opinion we consider the perspective that mitochondria are domesticated microbes that sense and guard their 'host' cell against pathogens. We explore potential mechanisms by which mitochondria detect intracellular pathogens and induce mitochondria-autonomous responses that activate cellular defenses.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"638-644"},"PeriodicalIF":11.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142696205","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}