World Journal of Diabetes最新文献

{"title":"New therapy for metabolic syndrome: Gut microbiome supplementation.","authors":"Waseem Qureshi, Maqsood Ahmad Dar, Mohd Younis Rather","doi":"10.4239/wjd.v15.i9.1833","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1833","url":null,"abstract":"<p><p>The gut microbiota is important in the development and progression of metabolic illnesses such type 2 diabetes, cardiovascular disease (CVD), and obesity. This diverse community of microorganisms controls a variety of physiological functions, including metabolism, inflammation, and immune response. Understanding these interactions has resulted in novel therapeutic options, including microbiome supplementation. The gut microbiome is extremely susceptible to dietary changes, which can alter its makeup and function, influencing metabolite synthesis that affects host health. Certain metabolites, such as butyrate and propionate, have been proven to protect against metabolic illnesses, whereas trimethylamine has been linked to CVD. Prebiotics, probiotics, synbiotics, and postbiotics are being investigated by researchers as ways to change the gut microbiome and boost metabolic health. Despite advances in therapy and lifestyle adjustments, the prevalence of metabolic syndrome is increasing, emphasizing the need for new medicines.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1833-1836"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372646/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet indices as predictors of poor glucoregulation in type 2 diabetes mellitus adults at Bishoftu General Hospital, Ethiopia.","authors":"Dereje Abebe Regassa, Gebeyaw Arega Berihun, Bisrat Fikadu Habtu, Woyesa Beyene Haile, Rahel Shumi Nagaash, Girum Tesfaye Kiya","doi":"10.4239/wjd.v15.i9.1889","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1889","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Diabetes is a chronic metabolic syndrome that has become a global public health problem with significant morbidity and mortality. It is a pro-inflammatory and pro-thrombotic condition characterized by increased platelet activation and alterations in platelet indices. However, the use of platelet indices as predictors of poor glucoregulation has not been fully evaluated in this context, and evidence for their role as predictors of poor glycemic status in diabetic patients is limited.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Aim: &lt;/strong&gt;To evaluate platelet indices and determine their prognostic significance in relation to inadequate glucoregulation among individuals diagnosed with type 2 diabetes at Bishoftu General Hospital in Ethiopia, from June 15 to August 12, 2022.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A comparative cross-sectional study was conducted in 261 participants including 174 individuals with type 2 diabetes mellitus (T2DM) and 87 non-diabetic controls. The systematic random sampling technique was used to select par-ticipants. Data were collected using structured questionnaires, physical measurements, checklists, and laboratory tests. Platelet parameters and fasting blood glucose levels were determined from blood samples using Sysmex-XN550 and CobasC311 analyzers, respectively. The hematology analyzer output was checked and participants were also screened for malaria parasites using a prepared blood smear. Collected data were entered into Epi-data version 3.1 and exported to SPSS version 25 for analysis. The &lt;i&gt;χ&lt;/i&gt; &lt;sup&gt;2&lt;/sup&gt; test, Mann-Whitney &lt;i&gt;U&lt;/i&gt; test, Kruskal-Wallis test, &lt;i&gt;post hoc&lt;/i&gt; test, Spearman correlation, and receiver operating characteristic curve were used for analysis. A &lt;i&gt;P&lt;/i&gt; value &lt; 0.05 was considered statistically significant.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The results of our study indicate that diabetic patients have significantly higher levels of platelet distribution width (PDW), mean platelet volume (MPV), platelet large cell ratio (PLCR), and plateletcrit (PCT) compared to healthy individuals (&lt;i&gt;P&lt;/i&gt; &lt; 0.001). Furthermore, these indices were found to be significantly elevated in individuals with poor glycemic control in T2DM compared to those with good glycemic control and healthy controls. We also observed significant correlations between these indices and various anthropometric and clinical variables. Our findings suggest that PDW, with a cut-off value of 15.75 fL and an area under the curve (AUC) of 0.803, MPV, with a cut-off value of 12.25 fL and an AUC of 0.774, PLCR, with a cut-off value of 36.3% and an AUC of 0.775, and PCT, with a cut-off value of 0.24% and an AUC of 0.761, can serve as predictors of poor glycemic control in patients with diabetes mellitus.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;The observed correlation between diabetic patients and a significant increase in platelet indices has highlighted their potential as predictors of poor glycemic control in diabetes. Therefore, regu","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1889-1902"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rapid correction of chronic hyperglycemia and bone remodeling, warning against overdoing.","authors":"Dured Dardari, Beatrice Segurens","doi":"10.4239/wjd.v15.i9.1858","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1858","url":null,"abstract":"<p><p>It is widely recognized that chronic hyperglycemia decreases bone quality, although little is known about the impact of the rapid correction of chronic hyperglycemia on the quality of bone remodeling. This spotlight article explores this correlation by focusing on the stages of bone remodeling linked to glucose levels.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1858-1861"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corilagin alleviates podocyte injury in diabetic nephropathy by regulating autophagy <i>via</i> the SIRT1-AMPK pathway.","authors":"Yu Lou, Yu-Ting Luan, Wen-Qing Rong, Yun Gai","doi":"10.4239/wjd.v15.i9.1916","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1916","url":null,"abstract":"<p><strong>Background: </strong>Diabetic nephropathy (DN) is the most frequent chronic microvascular consequence of diabetes, and podocyte injury and malfunction are closely related to the development of DN. Studies have shown that corilagin (Cor) has hepatoprotective, anti-inflammatory, antibacterial, antioxidant, anti-hypertensive, anti-diabetic, and anti-tumor activities.</p><p><strong>Aim: </strong>To explore the protective effect of Cor against podocyte injury in DN mice and the underlying mechanisms.</p><p><strong>Methods: </strong>Streptozotocin and a high-fat diet were combined to generate DN mice models, which were then divided into either a Cor group or a DN group (<i>n</i> = 8 in each group). Mice in the Cor group were intraperitoneally injected with Cor (30 mg/kg/d) for 12 wk, and mice in the DN group were treated with saline. Biochemical analysis was used to measure the blood lipid profiles. Hematoxylin and eosin staining was used to detect pathological changes in kidney tissue. Immunohistochemistry and Western blotting were used to assess the protein expression of nephrin and podocin. Mouse podocyte cells (MPC5) were cultured and treated with glucose (5 mmol/L), Cor (50 μM), high glucose (HG) (30 mmol/L), and HG (30 mmol/L) plus Cor (50 μM). Real-time quantitative PCR and Western blotting were performed to examine the effects of Cor on podocyte autophagy.</p><p><strong>Results: </strong>Compared with the control group, the DN mice models had increased fasting blood glucose, glycosylated hemoglobin, triglycerides, and total cholesterol, decreased nephrin and podocin expression, increased apoptosis rate, elevated inflammatory cytokines, and enhanced oxidative stress. All of the conditions mentioned above were alleviated after intervention with Cor. In addition, Cor therapy improved SIRT1 and AMPK expression (<i>P</i> < 0.001), inhibited reactive oxygen species and oxidative stress, and elevated autophagy in HG-induced podocytes (<i>P</i> < 0.01).</p><p><strong>Conclusion: </strong>Cor alleviates podocyte injury by regulating autophagy <i>via</i> the SIRT1-AMPK pathway, thereby exerting its protective impact on renal function in DN mice.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1916-1931"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372637/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-630: A potential guardian against inflammation in diabetic kidney disease.","authors":"Ashraf Al Madhoun","doi":"10.4239/wjd.v15.i9.1837","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1837","url":null,"abstract":"<p><p>In this editorial, we comment on the article by Wu <i>et al</i> published \"MicroRNA-630 alleviates inflammatory reactions in rats with diabetic kidney disease by targeting toll-like receptor 4\". Diabetic kidney disease (DKD) stands as a significant complication occurring from diabetes mellitus, which contributes substantially to the morbidity and mortality rates worldwide. Renal tubular epithelial cell da-mage, often accompanied by inflammatory responses and mesenchymal trans-differentiation, plays a pivotal role in the progression of DKD. Despite extensive research, the intricate molecular mechanisms underlying these processes remain to be determined. Wu <i>et al</i> remarkable work identifies microRNA-630 (miR-630) as an emerging potential regulator of cell migration, apoptosis, and autophagy, prompting investigation into its association with DKD pathogenesis. This study endeavors to elucidate the impact of miR-630 on TEC injury and the inflammatory response in DKD rats. The role of miR-630 in human DKD will be of interest for future studies.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1837-1841"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372643/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-linear relationship between age and subfoveal choroidal thickness in Chinese patients with proliferative diabetic retinopathy.","authors":"Chun-Yan Lei, Jiang-Ying Xie, Qi-Bo Ran, Mei-Xia Zhang","doi":"10.4239/wjd.v15.i9.1903","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1903","url":null,"abstract":"<p><strong>Background: </strong>No study has investigated the change regularity between age and subfoveal choroidal thickness (SFCT) in proliferative diabetic retinopathy (PDR).</p><p><strong>Aim: </strong>To investigate the relationship between the SFCT and age in Chinese patients with PDR.</p><p><strong>Methods: </strong>This was a cross-sectional retrospective study. The participants were hospitalized individuals with type 2 diabetes who underwent vitrectomy for PDR. Con-tralateral eyes that met the criteria were included in the study. All necessary laboratory tests were performed at the time of admission. Central macular thickness (CMT) and SFCT were two quantitative assessments made using enhanced depth imaging optical coherence tomography. CMT was measured automatically and SFCT was measured manually with digital calipers provided by the Heidelberg Eye Explorer software.</p><p><strong>Results: </strong>The final analysis included a total of 234 individuals with PDR. The average age was 55.60 years old ± 10.03 years old, and 57.69% of the population was male. Univariate analysis revealed a significant negative connection between age and SFCT in patients with PDR [β = -2.44, 95% confidence interval (95%CI): -3.46 to -1.42; <i>P</i> < 0.0001]. In the fully adjusted model, the correlation between SFCT and age remained steady (β = -1.68, 95%CI: -2.97 to -0.39; <i>P</i> = 0.0117). Spline smoothing showed that the relationship between SFCT and age in patients with PDR was non-linear, with an inflection point at 54 years of age.</p><p><strong>Conclusion: </strong>Our findings suggest that age is a key determinant of choroidal thickness. The non-linear link between SFCT and age in PDR patients should be taken into account.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1903-1915"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dexmedetomidine ameliorates diabetic intestinal injury by promoting the polarization of M2 macrophages through the MMP23B pathway.","authors":"Man Lu, Xiao-Wen Guo, Fang-Fang Zhang, Dan-Hong Wu, Di Xie, Feng-Qin Luo","doi":"10.4239/wjd.v15.i9.1962","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1962","url":null,"abstract":"<p><strong>Background: </strong>Diabetes is often associated with gastrointestinal dysfunctions, which can lead to hypoglycemia. Dexmedetomidine (DEX) is a commonly used sedative in perioperative diabetic patients and may affect gastrointestinal function.</p><p><strong>Aim: </strong>To investigate whether sedative doses of DEX alleviate diabetes-caused intestinal dysfunction.</p><p><strong>Methods: </strong>Sedation/anesthesia scores and vital signs of streptozotocin (STZ)-induced diabetic mice under DEX sedation were observed. Diabetic mice were divided into saline and DEX groups. After injecting sedatives intraperitoneally, tight junctions (TJs) and apoptotic levels were evaluated 24 hours later to assess the intestinal barrier function. The role of DEX was validated using Villin-MMP23B flox/flox mice with intestinal epithelial deletion. <i>In vitro</i>, high glucose and hyperosmolarity were used to culture Caco-2 monolayer cells with STZ inter-vention. Immunofluorescence techniques were used to monitor the barrier and mitochondrial functions.</p><p><strong>Results: </strong>MMP23B protein levels in the intestinal tissue of STZ-induced diabetic mice were significantly higher than those in the intestinal tissue of control mice, with the DEX group displaying decreased MMP23B levels. Diabetes-mediated TJ dis-ruption, increased intestinal mucosal permeability, and systemic inflammation in wild-type mice might be reversed by DEX. In Caco-2 cells, MMP23B was associated with increased reactive oxygen species accumulation, mitochondrial membrane potential depolarization, and TJ disruption.</p><p><strong>Conclusion: </strong>DEX reduces MMP23B, which may potentially contribute to STZ-induced intestinal barrier dysfunction, affecting TJ modification through mitochondrial dysfunction.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1962-1978"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory markers, oxidative stress, and mitochondrial dynamics: Repercussions on coronary artery disease in diabetes.","authors":"José Carlos Tatmatsu-Rocha, Luan Santos Mendes-Costa","doi":"10.4239/wjd.v15.i9.1853","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1853","url":null,"abstract":"<p><p>Inflammatory markers and mediators that affect the development of car-diovascular diseases have been the focus of recent scientific work. Thus, the purpose of this editorial is to promote a critical debate about the article titled \"Nε-carboxymethyl-lysine and inflammatory cytokines, markers, and mediators of coronary artery disease progression in diabetes\", published in the <i>World Journal of Diabetes</i> in 2024. This work directs us to reflect on the role of advanced glycation end products, which are pro-inflammatory products arising from the metabolism of fatty acids and sugars whose main marker in tissues is Nε-carboxymethyl-lysine (NML). Recent studies have linked high levels of pro-inflammatory agents with the development of coronary artery disease (CAD), especially tumor necrosis factor alpha, interleukins, and C-reactive protein. These inflammatory agents increase the production of reactive oxygen species (ROS), of which people with diabetes are known to have an increased production. The increase in ROS promotes lipid peroxidation, which causes damage to myocytes, promoting myocardial damage. Furthermore, oxidative stress induces the binding of NML to its receptor RAGE, which in turn activates the nuclear factor-kB, and conse-quently, inflammatory cytokines. These inflammatory cytokines induce endo-thelial dysfunction, with increased expression of adhesion molecules, changes in endothelial permeability and changes in the expression of nitric oxide. In this sense, the therapeutic use of monoclonal antibodies (inflammatory reducers such as statins and sodium-glucose transport inhibitors) has demonstrated positive results in the regression of atherogenic plaques and consequently CAD. On the other hand, many studies have demonstrated a relationship between mito-chondrial dynamics, diabetes, and cardiovascular diseases. This link occurs since ROS have their origin in the imbalance in glucose metabolism that occurs in the mitochondrial matrix, and this imbalance can have its origin in inadequate diet as well as some pathologies. Photobiomodulation (PBM) has recently been considered a possible therapeutic agent for cardiovascular diseases due to its effects on mitochondrial dynamics and oxidative stress. In this sense, therapies such as PBM that act on pro-inflammatory mediators and mitochondrial modulation could benefit those with cardiovascular diseases.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1853-1857"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372642/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the genetic basis of childhood monogenic diabetes.","authors":"Debmalya Sanyal","doi":"10.4239/wjd.v15.i9.1829","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1829","url":null,"abstract":"<p><p>Monogenic diabetes is caused by one or even more genetic variations, which may be uncommon yet have a significant influence and cause diabetes at an early age. Monogenic diabetes affects 1% to 5% of children, and early detection and genetically focused treatment of neonatal diabetes and maturity-onset diabetes of the young can significantly improve long-term health and well-being. The etiology of monogenic diabetes in childhood is primarily attributed to genetic variations affecting the regulatory genes responsible for beta-cell activity. In rare instances, mutations leading to severe insulin resistance can also result in the development of diabetes. Individuals diagnosed with specific types of monogenic diabetes, which are commonly found, can transition from insulin therapy to sulfonylureas, provided they maintain consistent regulation of their blood glucose levels. Scientists have successfully devised materials and methodologies to distinguish individuals with type 1 or 2 diabetes from those more prone to monogenic diabetes. Genetic screening with appropriate findings and interpretations is essential to establish a prognosis and to guide the choice of therapies and management of these interrelated ailments. This review aims to design a comprehensive literature summarizing genetic insights into monogenetic diabetes in children and adolescents as well as summarizing their diagnosis and management.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1829-1832"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Link between periodontitis and diabetic retinopathy: Inflammatory pathways and clinical implications.","authors":"Yu Zhao, Quan-Quan Shen","doi":"10.4239/wjd.v15.i9.1842","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1842","url":null,"abstract":"<p><p>The bidirectional relationship between periodontitis and type 2 diabetes mellitus has been well-established. However, the underlying molecular mechanisms remain unclear. Diabetic retinopathy (DR) is an important complication of diabetes, but there are few studies on the relationship between DR and periodontitis, especially on the intrinsic inflammatory pathway mechanism. This article reviews the latest clinical data on how diabetes promotes susceptibility to periodontitis from the epidemiological and molecular perspectives, with a special focus on the key roles of systemic inflammation and endothelial dysfunction in the interplay between DR and periodontitis. Comprehension of the intertwined pathogenesis of DR and periodontitis can better guide the development of comprehensive management strategies for glycemic control and periodontal health, with the aim of mitigating the progression of DR and enhancing overall well-being.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1842-1846"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}