Oskar Ragnarsson, C. Christofer Juhlin, David J. Torpy, Henrik Falhammar
{"title":"A clinical perspective on ectopic Cushing’s syndrome","authors":"Oskar Ragnarsson, C. Christofer Juhlin, David J. Torpy, Henrik Falhammar","doi":"10.1016/j.tem.2023.12.003","DOIUrl":"https://doi.org/10.1016/j.tem.2023.12.003","url":null,"abstract":"<p>Cushing’s syndrome (CS) refers to the clinical features of prolonged pathological glucocorticoid excess. About 10–20% of individuals with CS have ectopic CS (ECS), that is, an adrenocorticotropin (ACTH)-producing tumour outside the pituitary gland. ACTH-secreting neuroendocrine neoplasia (NENs) can arise from many organs, although bronchial NEN, small cell lung cancer (SCLC), pancreatic NEN, thymic NEN, medullary thyroid cancer (MTC), and pheochromocytoma are the most common. Patients with ECS frequently present with severe hypercortisolism. The risk of life-threatening complications is high in severe cases, unless the hypercortisolism is effectively treated. A good outcome in ECS requires a methodical approach, incorporating prompt diagnosis, tumour localization, control of cortisol excess, and resection of the primary tumour when possible.</p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138943488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Large metabolic swings: when feeding exceeds its goals","authors":"Francisco J.G. Muriana","doi":"10.1016/j.tem.2023.12.001","DOIUrl":"https://doi.org/10.1016/j.tem.2023.12.001","url":null,"abstract":"<p>Exaggerated blood excursions of nutrients and endogenous molecules in response to food intake may have health consequences if they repeatedly exceed the capacity of homeostatic mechanisms. Here, I discuss the significance of abnormally high postprandial metabolic fluctuations, the role of some influencing factors, and suggest ways to avoid them.</p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"29 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138840442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mitochondrial quality control pathways sense mitochondrial protein import","authors":"Laurie P. Lee-Glover, Timothy E. Shutt","doi":"10.1016/j.tem.2023.11.004","DOIUrl":"https://doi.org/10.1016/j.tem.2023.11.004","url":null,"abstract":"<p>Mitochondrial quality control (MQC) mechanisms are required to maintain a functional proteome, which enables mitochondria to perform a myriad of important cellular functions from oxidative phosphorylation to numerous other metabolic pathways. Mitochondrial protein homeostasis begins with the import of over 1000 nuclear-encoded mitochondrial proteins and the synthesis of 13 mitochondrial DNA-encoded proteins. A network of chaperones and proteases helps to fold new proteins and degrade unnecessary, damaged, or misfolded proteins, whereas more extensive damage can be removed by mitochondrial-derived vesicles (MDVs) or mitochondrial autophagy (mitophagy). Here, focusing on mechanisms in mammalian cells, we review the importance of mitochondrial protein import as a sentinel of mitochondrial function that activates multiple MQC mechanisms when impaired.</p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138657754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Irisin limits amyloid-β buildup in Alzheimer’s disease","authors":"Mychael V. Lourenco","doi":"10.1016/j.tem.2023.11.006","DOIUrl":"https://doi.org/10.1016/j.tem.2023.11.006","url":null,"abstract":"<p><span>Mounting evidence suggests that physical exercise protects the brain against neurodegenerative disease. In a recent paper in </span><em>Neuron</em>, <span>Kim <em>et al</em>.</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"8px\" viewbox=\"0 0 8 8\" width=\"8px\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg><span><span><span> reported that the exercise-induced hormone irisin curbs amyloid-β buildup by promoting secretion of astrocyte-derived </span>neprilysin. These findings may help explain the </span>neuroprotection by irisin and exercise in Alzheimer’s disease.</span></p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"33 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138634439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Emily M. Esquea, Riley G. Young, Mauricio J. Reginato
{"title":"Fructose promotes liver cancer via microbial acetate-induced O-GlcNAcylation","authors":"Emily M. Esquea, Riley G. Young, Mauricio J. Reginato","doi":"10.1016/j.tem.2023.12.002","DOIUrl":"https://doi.org/10.1016/j.tem.2023.12.002","url":null,"abstract":"<p><span>High dietary fructose consumption is linked to multiple disease states, including cancer. </span><span>Zhou and colleagues</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"8px\" viewbox=\"0 0 8 8\" width=\"8px\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg><span> recently reported a novel mechanism where high dietary fructose levels increase acetate production by the gut microbiome increasing post-translational modification </span><em>O</em><span>-GlcNAcylation in liver cells, which contributes to disease progression in mouse models of hepatocellular carcinoma.</span></p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138657679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Caterina Mancini, Giulia Lori, Erica Pranzini, Maria Letizia Taddei
{"title":"Metabolic challengers selecting tumor-persistent cells","authors":"Caterina Mancini, Giulia Lori, Erica Pranzini, Maria Letizia Taddei","doi":"10.1016/j.tem.2023.11.005","DOIUrl":"https://doi.org/10.1016/j.tem.2023.11.005","url":null,"abstract":"<p>Resistance to anticancer therapy still represents one of the main obstacles to cancer treatment. Numerous components of the tumor microenvironment (TME) contribute significantly to the acquisition of drug resistance. Microenvironmental pressures arising during cancer evolution foster tumor heterogeneity (TH) and facilitate the emergence of drug-resistant clones. In particular, metabolic pressures arising in the TME may favor epigenetic adaptations supporting the acquisition of persistence features in tumor cells. Tumor-persistent cells (TPCs) are characterized by high phenotypic and metabolic plasticity, representing a noticeable advantage in chemo- and radio-resistance. Understanding the crosslink between the evolution of metabolic pressures in the TME, epigenetics, and TPC evolution is significant for developing novel therapeutic strategies specifically targeting TPC vulnerabilities to overcome drug resistance.</p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138559400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The ups and downs of bone-marrow adipose tissue in space","authors":"Guy Trudel, Gerd Melkus, Tammy Liu","doi":"10.1016/j.tem.2023.11.003","DOIUrl":"https://doi.org/10.1016/j.tem.2023.11.003","url":null,"abstract":"<p>Knowledge is rapidly accumulating on basic roles and modulation of bone-marrow adipose tissue (BMAT). Among key modulators are physical forces on bones as exerted by gravity and exercise. Studying humans returning from space has revealed that, in addition to physical forces, local energetics within the bone marrow can play modulatory roles.</p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":" 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138469438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Luís Almeida, Ayesha Dhillon-LaBrooy, Tim Sparwasser
{"title":"The evolutionary tug-of-war of macrophage metabolism during bacterial infection","authors":"Luís Almeida, Ayesha Dhillon-LaBrooy, Tim Sparwasser","doi":"10.1016/j.tem.2023.11.002","DOIUrl":"https://doi.org/10.1016/j.tem.2023.11.002","url":null,"abstract":"<p>The function and phenotype of macrophages are intimately linked with pathogen detection. On sensing pathogen-derived signals and molecules, macrophages undergo a carefully orchestrated process of polarization to acquire pathogen-clearing properties. This phenotypic change must be adequately supported by metabolic reprogramming that is now known to support the acquisition of effector function, but also generates secondary metabolites with direct microbicidal activity. At the same time, bacteria themselves have adapted to both manipulate and take advantage of macrophage-specific metabolic adaptations. Here, we summarize the current knowledge on macrophage metabolism during infection, with a particular focus on understanding the ‘arms race’ between host immune cells and bacteria during immune responses.</p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"116 17","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138455756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Methylmalonic acid in aging and disease","authors":"Joanne Tejero, Felicia Lazure, Ana P. Gomes","doi":"10.1016/j.tem.2023.11.001","DOIUrl":"https://doi.org/10.1016/j.tem.2023.11.001","url":null,"abstract":"<p>Metabolic byproducts have conventionally been disregarded as waste products without functions. In this opinion article, we bring to light the multifaceted role of methylmalonic acid (MMA), a byproduct of the propionate metabolism pathway mostly commonly known as a clinical biomarker of vitamin B12 deficiency. MMA is normally present at low levels in the body, but increased levels can come from different sources, such as vitamin B12 deficiency, genetic mutations in enzymes related to the propionate pathway, the gut microbiota, and aggressive cancers. Here, we describe the diverse metabolic and signaling functions of MMA and discuss the consequences of increased MMA levels, such as during the aging process, for several age-related human pathologies.</p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"118 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138454877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Daniela G. Costa, Marisa Ferreira-Marques, Cláudia Cavadas
{"title":"Lipodystrophy as a target to delay premature aging","authors":"Daniela G. Costa, Marisa Ferreira-Marques, Cláudia Cavadas","doi":"10.1016/j.tem.2023.10.006","DOIUrl":"https://doi.org/10.1016/j.tem.2023.10.006","url":null,"abstract":"<p>Lipodystrophy syndromes are rare diseases characterized by low levels and an abnormal distribution of adipose tissue, caused by diverse genetic or acquired causes. These conditions commonly exhibit metabolic complications, including insulin resistance, diabetes, hypertriglyceridemia, nonalcoholic fatty liver disease, and adipose tissue dysfunction. Moreover, genetic lipodystrophic laminopathies exhibit a premature aging phenotype, emphasizing the importance of restoring adipose tissue distribution and function. In this opinion, we discuss the relevance of adipose tissue reestablishment as a potential approach to alleviate premature aging and age-related complications in genetic lipodystrophy syndromes.</p>","PeriodicalId":23301,"journal":{"name":"Trends in Endocrinology & Metabolism","volume":"43 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"109126866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}