{"title":"Pediatric thyroid side effects of immune checkpoint inhibitors.","authors":"Cesare Morgante, Alessandra Fierabracci, Armando Grossi","doi":"10.1016/j.tem.2024.04.002","DOIUrl":"10.1016/j.tem.2024.04.002","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) are associated with multiple endocrine side effects, including thyroid disfunctions. In addition, the efficacy and safety profiles of ICIs in the pediatric population need clarification. Here, we discuss the main evidence regarding the efficacy and thyroid toxicities of ICIs in children.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"765-768"},"PeriodicalIF":11.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140869566","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":"Is the endotoxin-complement cascade the major driver in lipedema?","authors":"Ilja L Kruglikov, Philipp E Scherer","doi":"10.1016/j.tem.2024.04.004","DOIUrl":"10.1016/j.tem.2024.04.004","url":null,"abstract":"<p><p>Lipedema is a poorly understood disorder of adipose tissue characterized by abnormal but symmetrical deposition of subcutaneous white adipose tissue (WAT) in proximal extremities. Here, we propose that the underlying cause for lipedema could be triggered by a selective accumulation of bacterial lipopolysaccharides (LPS; also known as endotoxin) in gluteofemoral WAT. Together with a malfunctioning complement system, this induces low-grade inflammation in the depot and raises its uncontrollable expansion. Correspondingly, more attention should be paid in future research to the endotoxemia prevalent in patients with lipedema. We would like to propose that proper management of endotoxemia can reduce the progression and even improve the state of disease in patients with lipedema.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"769-780"},"PeriodicalIF":11.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11387139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140868822","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":"SIRTifying intestinal nucleotide metabolism.","authors":"Shweta Tiwary, Cristina D Guerena, Jenna L Jewell","doi":"10.1016/j.tem.2024.07.003","DOIUrl":"10.1016/j.tem.2024.07.003","url":null,"abstract":"<p><p>The intestine is a proliferative tissue subjected to a variety of stresses that disturb its homeostasis. A recent study by Tucker et al. demonstrated that loss of the tumor suppressor SIRT4 leads to increased cell proliferation via the de novo nucleotide biosynthesis pathway over the salvage pathway after ionizing irradiation (IR).</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"763-764"},"PeriodicalIF":11.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735676","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":"An orphan to the rescue of obesity and steatotic liver?","authors":"Shanu Jain, Arun K Shukla","doi":"10.1016/j.tem.2024.06.012","DOIUrl":"10.1016/j.tem.2024.06.012","url":null,"abstract":"<p><p>In a recent article, Leeson-Payne et al. demonstrate that GPR75 knock-out in mice results in lower body fat and reduced hepatic lipid accumulation, with an increase in physical activity and energy expenditure. Loss-of-function (LoF) GPR75 variants in the UK Biobank (UKBB) are associated with reduced liver steatosis, suggesting potential therapeutic implications in metabolic dysfunction-associated steatotic liver disease (MASLD).</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"761-762"},"PeriodicalIF":11.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141472640","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}
Elizabeth S Anaya, Evelyn L de Groot, John P Lydon, Stephanie A Pangas, Sean M Hartig
{"title":"Contributions of white adipose tissue to energy requirements for female reproduction.","authors":"Elizabeth S Anaya, Evelyn L de Groot, John P Lydon, Stephanie A Pangas, Sean M Hartig","doi":"10.1016/j.tem.2024.04.012","DOIUrl":"10.1016/j.tem.2024.04.012","url":null,"abstract":"<p><p>Body composition impacts female fertility and there are established relationships between adipose tissue and the reproductive system. Maintaining functional adipose tissue is vital for meeting the energetic demands during the reproductive process, from ovulation to delivery and lactation. White adipose tissue (WAT) shows plastic responses to daily physiology and secretes diverse adipokines that affect the hypothalamic-pituitary-ovarian axis, but many other interorgan interactions remain to be determined. This review summarizes the current state of research on the dialogue between WAT and the female reproductive system, focusing on the impact of this crosstalk on ovarian and endometrial factors essential for fecundity.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"809-820"},"PeriodicalIF":11.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11387141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140946523","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":"Selenium, diabetes, and their intricate sex-specific relationship.","authors":"Kamil Demircan, Thilo Samson Chillon, Jeyoung Bang, Vadim N Gladyshev, Lutz Schomburg","doi":"10.1016/j.tem.2024.03.004","DOIUrl":"10.1016/j.tem.2024.03.004","url":null,"abstract":"<p><p>Selenium (Se) is an essential trace element, which is inserted as selenocysteine (Sec) into selenoproteins during biosynthesis, orchestrating their expression and activity. Se is associated with both beneficial and detrimental health effects; deficient supply or uncontrolled supplementation raises concerns. In particular, Se was associated with an increased incidence of type 2 diabetes (T2D) in a secondary analysis of a randomized controlled trial (RCT). In this review, we discuss the intricate relationship between Se and diabetes and the limitations of the available clinical and experimental studies. Recent evidence points to sexual dimorphism and an association of Se deficiency with gestational diabetes mellitus (GDM). We highlight the emerging evidence linking high Se status with improved prognosis in patients with T2D and lower risk of macrovascular complications.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"781-792"},"PeriodicalIF":11.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140871931","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 M Marko, Meghan O Conn, Jonathan D Schertzer
{"title":"Intermittent fasting influences immunity and metabolism.","authors":"Daniel M Marko, Meghan O Conn, Jonathan D Schertzer","doi":"10.1016/j.tem.2024.04.014","DOIUrl":"10.1016/j.tem.2024.04.014","url":null,"abstract":"<p><p>Intermittent fasting (IF) modifies cell- and tissue-specific immunometabolic responses that dictate metabolic flexibility and inflammation during obesity and type 2 diabetes (T2D). Fasting forces periods of metabolic flexibility and necessitates increased use of different substrates. IF can lower metabolic inflammation and improve glucose metabolism without lowering obesity and can influence time-dependent, compartmentalized changes in immunity. Liver, adipose tissue, skeletal muscle, and immune cells communicate to relay metabolic and immune signals during fasting. Here we review the connections between metabolic and immune cells to explain the divergent effects of IF compared with classic caloric restriction (CR) strategies. We also explore how the immunometabolism of metabolic diseases dictates certain IF outcomes, where the gut microbiota triggers changes in immunity and metabolism during fasting.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":"821-833"},"PeriodicalIF":11.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140892451","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}
Muhammad Naveed, Kathryn Smedlund, Qi-Gang Zhou, Weikang Cai, Jennifer W Hill
{"title":"Astrocyte involvement in metabolic regulation and disease.","authors":"Muhammad Naveed, Kathryn Smedlund, Qi-Gang Zhou, Weikang Cai, Jennifer W Hill","doi":"10.1016/j.tem.2024.08.001","DOIUrl":"https://doi.org/10.1016/j.tem.2024.08.001","url":null,"abstract":"<p><p>Astrocytes, the predominant glial cell type in the mammalian brain, influence a wide variety of brain parameters including neuronal energy metabolism. Exciting recent studies have shown that obesity and diabetes can impact on astrocyte function. We review evidence that dysregulation of astrocytic lipid metabolism and glucose sensing contributes to dysregulation of whole-body energy balance, thermoregulation, and insulin sensitivity. In addition, we consider the overlooked topic of the sex-specific roles of astrocytes and their response to hormonal fluctuations that provide insights into sex differences in metabolic regulation. Finally, we provide an update on potential ways to manipulate astrocyte function, including genetic targeting, optogenetic and chemogenetic techniques, transplantation, and tailored exosome-based therapies, which may lead to improved treatments for metabolic disease.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142114736","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}
Azadeh Nasuhidehnavi, Weronika Zarzycka, Ignacy Górecki, Ying Ann Chiao, Chi Fung Lee
{"title":"Emerging interactions between mitochondria and NAD<sup>+</sup> metabolism in cardiometabolic diseases.","authors":"Azadeh Nasuhidehnavi, Weronika Zarzycka, Ignacy Górecki, Ying Ann Chiao, Chi Fung Lee","doi":"10.1016/j.tem.2024.07.010","DOIUrl":"https://doi.org/10.1016/j.tem.2024.07.010","url":null,"abstract":"<p><p>Nicotinamide adenine dinucleotide (NAD<sup>+</sup>) is an essential coenzyme for redox reactions and regulates cellular catabolic pathways. An intertwined relationship exists between NAD<sup>+</sup> and mitochondria, with consequences for mitochondrial function. Dysregulation in NAD<sup>+</sup> homeostasis can lead to impaired energetics and increased oxidative stress, contributing to the pathogenesis of cardiometabolic diseases. In this review, we explore how disruptions in NAD<sup>+</sup> homeostasis impact mitochondrial function in various cardiometabolic diseases. We discuss emerging studies demonstrating that enhancing NAD<sup>+</sup> synthesis or inhibiting its consumption can ameliorate complications of this family of pathological conditions. Additionally, we highlight the potential role and therapeutic promise of mitochondrial NAD<sup>+</sup> transporters in regulating cellular and mitochondrial NAD<sup>+</sup> homeostasis.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142094218","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":"The unexpected role of GIP in transforming obesity treatment.","authors":"Inuk Zandvakili, Diego Perez-Tilve","doi":"10.1016/j.tem.2024.07.022","DOIUrl":"https://doi.org/10.1016/j.tem.2024.07.022","url":null,"abstract":"<p><p>Despite sharing incretin activity with glucagon-like peptide 1 (GLP-1), the development of gastric inhibitory polypeptide (GIP)-based drugs has been hindered by the minor effects of native GIP on appetite and body weight and genetic studies associating loss-of-function with reduced obesity. Yet, pharmacologically optimized GIP-based molecules have demonstrated profound weight lowering benefits of GIPR agonism when combined with GLP-1-based therapies, which has re-energized deeper exploration of the molecular mechanisms and downstream signaling of GIPR. Interestingly, both GIPR agonism and antagonism offer metabolic benefits, leading to differing viewpoints on how to target GIPR therapeutically. Here we summarize the emerging evidence about the tissue-specific mechanisms that positions GIP-based therapies as important targets for the next generation of anti-obesity and metabolic therapies.</p>","PeriodicalId":54415,"journal":{"name":"Trends in Endocrinology and Metabolism","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142094219","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}