Saja Al-rubaye, Moisés Rodríguez-Mañero, José Ramón González-Juanatey, Sonia Eiras
Type 2 diabetes mellitus (T2DM) is present in 25% of patients with atrial fibrillation (AF), the most prevalent arrhythmia in the world. This concomitant disorder enhances thromboembolic events, length of hospital stay after AF ablation, renal impairment after anticoagulation, heart rate variability after glucose-lowering treatment, and cardiac mortality. These patients accumulate inflamed epicardial fat (EAT) with paracrine consequences on β-oxidation of mitochondria, cytosolic Ca2+ fluxes, and sarcomere shortening. Knowing these specific targets will improve the efficacy of personalised preventive and curative therapies since AF leads to AF and EAT accumulation. This review tries to clarify the interplay among epicardial fat accumulation and macrophages with concomitant T2DM and AF to provide a summary of current known mechanisms and therapeutic strategies.
{"title":"Concomitant Diabetes and Atrial Fibrillation: Epicardial Fat and Macrophage-Related Mechanisms","authors":"Saja Al-rubaye, Moisés Rodríguez-Mañero, José Ramón González-Juanatey, Sonia Eiras","doi":"10.1002/dmrr.70065","DOIUrl":"https://doi.org/10.1002/dmrr.70065","url":null,"abstract":"<p>Type 2 diabetes mellitus (T2DM) is present in 25% of patients with atrial fibrillation (AF), the most prevalent arrhythmia in the world. This concomitant disorder enhances thromboembolic events, length of hospital stay after AF ablation, renal impairment after anticoagulation, heart rate variability after glucose-lowering treatment, and cardiac mortality. These patients accumulate inflamed epicardial fat (EAT) with paracrine consequences on β-oxidation of mitochondria, cytosolic Ca<sup>2+</sup> fluxes, and sarcomere shortening. Knowing these specific targets will improve the efficacy of personalised preventive and curative therapies since AF leads to AF and EAT accumulation. This review tries to clarify the interplay among epicardial fat accumulation and macrophages with concomitant T2DM and AF to provide a summary of current known mechanisms and therapeutic strategies.</p>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 5","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70065","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144520156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Diabetic bone disease, a form of secondary osteoporosis, is characterised by reduced bone strength and increased fracture risk, particularly in patients with type 2 diabetes (T2D). Over 35% of T2D patients experience bone loss, with approximately 20% meeting diagnostic criteria for osteoporosis. This review highlights the complex mechanisms underlying diabetic bone disease, emphasising the need to reduce fracture risk and improve clinical outcomes. Key factors such as hyperglycemia, insulin resistance, insulin-like growth factors (IGFs), advanced glycation end products (AGEs), and proinflammatory cytokines disrupt bone turnover by impairing osteoblast and osteoclast function, leading to imbalanced bone formation and resorption. We explore the role of bone turnover and mineralisation in both cortical and trabecular bone, and the impact of microvascular complications on bone microarchitecture. Gut hormones, including Glucagon-like peptide-1 (GLP-1), Glucose-dependent insulinotropic polypeptide (GIP), and Parathyroid hormone (PTH), and the gut microbiota also play crucial roles in the pathogenesis of diabetic bone disease. Specific bacterial species, such as Akkermansia muciniphila and Bacteroides fragilis, are implicated in modulating the gut-bone axis through short-chain fatty acids (SCFAs) and other signalling pathways. These changes, along with altered gut hormone responses, affect bone density, microstructure, and material properties. Despite normal or increased bone mineral density (BMD) in some T2D patients, the material quality of bone is compromised, leading to greater fragility. This review integrates current knowledge of molecular, hormonal, and microbial interactions that contribute to diabetic bone disease, offering insights into potential therapeutic strategies and improving patient care.
{"title":"Diabetes and Bone Health: A Comprehensive Review of Impacts and Mechanisms","authors":"Prabhat Upadhyay, Sudhir Kumar","doi":"10.1002/dmrr.70062","DOIUrl":"https://doi.org/10.1002/dmrr.70062","url":null,"abstract":"<p>Diabetic bone disease, a form of secondary osteoporosis, is characterised by reduced bone strength and increased fracture risk, particularly in patients with type 2 diabetes (T2D). Over 35% of T2D patients experience bone loss, with approximately 20% meeting diagnostic criteria for osteoporosis. This review highlights the complex mechanisms underlying diabetic bone disease, emphasising the need to reduce fracture risk and improve clinical outcomes. Key factors such as hyperglycemia, insulin resistance, insulin-like growth factors (IGFs), advanced glycation end products (AGEs), and proinflammatory cytokines disrupt bone turnover by impairing osteoblast and osteoclast function, leading to imbalanced bone formation and resorption. We explore the role of bone turnover and mineralisation in both cortical and trabecular bone, and the impact of microvascular complications on bone microarchitecture. Gut hormones, including Glucagon-like peptide-1 (GLP-1), Glucose-dependent insulinotropic polypeptide (GIP), and Parathyroid hormone (PTH), and the gut microbiota also play crucial roles in the pathogenesis of diabetic bone disease. Specific bacterial species, such as <i>Akkermansia muciniphila</i> and <i>Bacteroides fragilis</i>, are implicated in modulating the gut-bone axis through short-chain fatty acids (SCFAs) and other signalling pathways. These changes, along with altered gut hormone responses, affect bone density, microstructure, and material properties. Despite normal or increased bone mineral density (BMD) in some T2D patients, the material quality of bone is compromised, leading to greater fragility. This review integrates current knowledge of molecular, hormonal, and microbial interactions that contribute to diabetic bone disease, offering insights into potential therapeutic strategies and improving patient care.</p>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 5","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70062","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144473235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}