World Journal of Diabetes最新文献

{"title":"Selection of dialysis methods for end-stage kidney disease patients with diabetes.","authors":"Yao-Hua Hu, Ya-Li Liu, Ling-Fei Meng, Yi-Xian Zhang, Wen-Peng Cui","doi":"10.4239/wjd.v15.i9.1862","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1862","url":null,"abstract":"<p><p>The increasing prevalence of diabetes has led to a growing population of end-stage kidney disease (ESKD) patients with diabetes. Currently, kidney transplantation is the best treatment option for ESKD patients; however, it is limited by the lack of donors. Therefore, dialysis has become the standard treatment for ESKD patients. However, the optimal dialysis method for diabetic ESKD patients remains controversial. ESKD patients with diabetes often present with complex conditions and numerous complications. Furthermore, these patients face a high risk of infection and technical failure, are more susceptible to malnutrition, have difficulty establishing vascular access, and experience more frequent blood sugar fluctuations than the general population. Therefore, this article reviews nine critical aspects: Survival rate, glucose metabolism disorder, infectious complications, cardiovascular events, residual renal function, quality of life, economic benefits, malnutrition, and volume load. This study aims to assist clinicians in selecting individualized treatment methods by comparing the advantages and disadvantages of hemodialysis and peritoneal dialysis, thereby improving patients' quality of life and survival rates.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1862-1873"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298994","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":"Gut microbiome: A revolution in type II diabetes mellitus.","authors":"Madhan Jeyaraman, Tejaswin Mariappan, Naveen Jeyaraman, Sathish Muthu, Swaminathan Ramasubramanian, Gabriel Silva Santos, Lucas Furtado da Fonseca, José Fábio Lana","doi":"10.4239/wjd.v15.i9.1874","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1874","url":null,"abstract":"<p><p>Type II diabetes mellitus (T2DM) has experienced a dramatic increase globally across countries of various income levels over the past three decades. The persistent prevalence of T2DM is attributed to a complex interplay of genetic and environmental factors. While numerous pharmaceutical therapies have been developed, there remains an urgent need for innovative treatment approaches that offer effectiveness without significant adverse effects. In this context, the exploration of the gut microbiome presents a promising avenue. Research has increasingly shown that the gut microbiome of individuals with T2DM exhibits distinct differences compared to healthy individuals, suggesting its potential role in the disease's pathogenesis and progression. This emerging field offers diverse applications, particularly in modifying the gut environment through the administration of prebiotics, probiotics, and fecal microbiome transfer. These inter-ventions aim to restore a healthy microbiome balance, which could potentially alleviate or even reverse the metabolic dysfunctions associated with T2DM. Although current results from clinical trials have not yet shown dramatic effects on diabetes management, the groundwork has been laid for deeper investigation. Ongoing and future clinical trials are critical to advancing our understanding of the microbiome's impact on diabetes. By further elucidating the mechanisms through which microbiome alterations influence insulin resistance and glucose metabolism, researchers can develop more targeted interventions. The potential to harness the gut microbiome in developing new therapeutic strategies offers a compelling prospect to transform the treatment landscape of T2DM, potentially reducing the disease's burden significantly with approaches that are less reliant on traditional pharmaceuticals and more focused on holistic, systemic health improvements.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1874-1888"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298984","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":"Bone marrow-derived mesenchymal stem cell-derived exosome-loaded miR-129-5p targets high-mobility group box 1 attenuates neurological-impairment after diabetic cerebral hemorrhage.","authors":"Yue-Ying Wang, Ke Li, Jia-Jun Wang, Wei Hua, Qi Liu, Yu-Lan Sun, Ji-Ping Qi, Yue-Jia Song","doi":"10.4239/wjd.v15.i9.1979","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1979","url":null,"abstract":"<p><strong>Background: </strong>Diabetic intracerebral hemorrhage (ICH) is a serious complication of diabetes. The role and mechanism of bone marrow mesenchymal stem cell (BMSC)-derived exosomes (BMSC-exo) in neuroinflammation post-ICH in patients with diabetes are unknown. In this study, we investigated the regulation of BMSC-exo on hyperglycemia-induced neuroinflammation.</p><p><strong>Aim: </strong>To study the mechanism of BMSC-exo on nerve function damage after diabetes complicated with cerebral hemorrhage.</p><p><strong>Methods: </strong>BMSC-exo were isolated from mouse BMSC media. This was followed by transfection with microRNA-129-5p (miR-129-5p). BMSC-exo or miR-129-5p-overexpressing BMSC-exo were intravitreally injected into a diabetes mouse model with ICH for <i>in vivo</i> analyses and were cocultured with high glucose-affected BV2 cells for <i>in vitro</i> analyses. The dual luciferase test and RNA immunoprecipitation test verified the targeted binding relationship between miR-129-5p and high-mobility group box 1 (HMGB1). Quantitative polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay were conducted to assess the levels of some inflammation factors, such as HMGB1, interleukin 6, interleukin 1β, toll-like receptor 4, and tumor necrosis factor α. Brain water content, neural function deficit score, and Evans blue were used to measure the neural function of mice.</p><p><strong>Results: </strong>Our findings indicated that BMSC-exo can promote neuroinflammation and functional recovery. MicroRNA chip analysis of BMSC-exo identified miR-129-5p as the specific microRNA with a protective role in neuroinflammation. Overexpression of miR-129-5p in BMSC-exo reduced the inflammatory response and neurological impairment in comorbid diabetes and ICH cases. Furthermore, we found that miR-129-5p had a targeted binding relationship with <i>HMGB1</i> mRNA.</p><p><strong>Conclusion: </strong>We demonstrated that BMSC-exo can reduce the inflammatory response after ICH with diabetes, thereby improving the neurological function of the brain.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1979-2001"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298979","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":"cNPAS2 induced β cell dysfunction by regulating KANK1 expression in type 2 diabetes.","authors":"Yan-Bin Yin, Wei Ji, Ying-Lan Liu, Qian-Hao Gao, Dong-Dong He, Shi-Lin Xu, Jing-Xin Fan, Li-Hai Zhang","doi":"10.4239/wjd.v15.i9.1932","DOIUrl":"https://doi.org/10.4239/wjd.v15.i9.1932","url":null,"abstract":"<p><strong>Background: </strong>Diabetes mellitus type 2 (T2DM) is formed by defective insulin secretion with the addition of peripheral tissue resistance of insulin action. It has been affecting over 400 million people all over the world.</p><p><strong>Aim: </strong>To explore the pathogenesis of T2DM and to develop and implement new prevention and treatment strategies for T2DM.</p><p><strong>Methods: </strong>Receiver operating characteristic (ROC) curve analysis was used to conduct diagnostic markers. The expression level of genes was determined by reverse transcription-PCR as well as Western blot. Cell proliferation assays were performed by cell counting kit-8 (CCK-8) tests. At last, T2DM mice underwent Roux-en-Y gastric bypass surgery.</p><p><strong>Results: </strong>We found that <i>NPAS2</i> was significantly up-regulated in islet β cell apoptosis of T2DM. The ROC curve revealed that <i>NPAS2</i> was capable of accurately diagnosing T2DM. <i>NPAS2</i> overexpression did increase the level of <i>KANK1</i>. In addition, the CCK-8 test revealed knocking down NPAS2 and KANK1 increased the proliferation of MIN6 cells. At last, we found that gastric bypass may treat type 2 diabetes by down-regulating <i>NPAS2</i> and <i>KANK1</i>.</p><p><strong>Conclusion: </strong>This study demonstrated that <i>NPAS2</i> induced β cell dysfunction by regulating <i>KANK1</i> expression in type 2 diabetes, and it may be an underlying therapy target of T2DM.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1932-1941"},"PeriodicalIF":4.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142298980","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":"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}