World Journal of Diabetes最新文献

{"title":"Islet β-cell function preservation by different anti-diabetic treatments in Chinese elderly patients with type 2 diabetes mellitus.","authors":"Wei Ling, Yan-Chao Wang, Yi Huang, Yang-Fu Ou, Yan-Chun Jiang","doi":"10.4239/wjd.v16.i2.94976","DOIUrl":"10.4239/wjd.v16.i2.94976","url":null,"abstract":"<p><strong>Background: </strong>The preservation of islet β-cell function in elderly patients with type 2 diabetes mellitus (T2DM) is a top priority for diabetic control.</p><p><strong>Aim: </strong>To assess the preservation of islet β-cell function among elderly Chinese patients with T2DM after different anti-diabetic treatments.</p><p><strong>Methods: </strong>In this longitudinal observational study, elderly patients with T2DM treated with insulin, oral antidiabetic drugs or a combination of both were enrolled to disclose their islet β-cell function between baseline and follow-up. Islet β-cell function was determined by the plasma Homeostasis Model for β-cell function (HOMA-β), C-peptide and area under the curve (AUC) based on oral glucose tolerance test. Changes in β-cell function (decrement or increment from baseline) between different therapy groups were the outcomes.</p><p><strong>Results: </strong>In total, 745 elderly patients (≥ 60 years) with T2DM [insulin monotherapy, <i>n</i> = 105; oral anti-diabetic drugs (OAD) monotherapy, <i>n</i> = 321; insulin plus OAD, <i>n</i> = 319] had their baseline and follow-up β-cell function assessed during a median observation period of 4.5 years (range, 3.0-7.2 years). Overall, islet β-cell function (HOMA-β, fasting C-peptide, fasting insulin, AUC_c-pep, AUC_ins, AUC_c-pep/AUC_glu, AUC_ins/AUC_glu) consistently deteriorated over time regardless of the three different antidiabetic treatments. No statistical differences in decrement were observed among the three groups regarding the islet β-cell function indices. All three groups showed an increased ratio of delayed insulin secretion response after 4.5 years of observation.</p><p><strong>Conclusion: </strong>In Chinese elderly patients with T2DM, islet β-cell function progressively declines regardless of insulin supplement or insulin plus OAD treatments.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"94976"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434085","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":"DNA methylation in the association between pesticide exposures and type 2 diabetes.","authors":"Guang-Jun Zheng, Zheng-Er Fang, Bi-Ying Zhou, Lei Zuo, Xia Chen, Ming-Liang Liu, Lei Yu, Chun-Xia Jing, Guang Hao","doi":"10.4239/wjd.v16.i2.99200","DOIUrl":"10.4239/wjd.v16.i2.99200","url":null,"abstract":"<p><strong>Background: </strong>Numerous epidemiological studies have found that pesticide exposure is associated with the incidence of type 2 diabetes (T2D); however, the underlying mechanisms remain unknown. DNA methylation may play a role in this process.</p><p><strong>Aim: </strong>To identify the genes associated with pesticide exposure and T2D by reviewing the current literature.</p><p><strong>Methods: </strong>We systematically searched PubMed and Embase for relevant studies that examined the association between pesticide exposure and DNA methylation, and studies on DNA methylation and T2D through January 15, 2024.</p><p><strong>Results: </strong>We identified six genes (<i>Alu</i>, <i>CABLES1</i>, <i>CDH1, PDX1</i>, <i>PTEN</i>, <i>PTPRN2</i>) related to pesticide exposure and T2D. We also suggested future research directions to better define the role of DNA methylation in the association between pesticide exposure and T2D.</p><p><strong>Conclusion: </strong>DNA methylation of specific genes may play a vital role in the association between pesticide exposure and T2D.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"99200"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434112","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":"Insulin autoantibodies, D-dimer and microalbuminuria: A cross-sectional, case-control study of type 2 diabetes.","authors":"Lin-Shan Zhang, Peng Yu, Fei Yao, Zhi-Qiang Lu, Xiao-Mu Li, Hong Chen","doi":"10.4239/wjd.v16.i2.101501","DOIUrl":"10.4239/wjd.v16.i2.101501","url":null,"abstract":"<p><strong>Background: </strong>Type 2 diabetes mellitus (T2DM) often leads to vascular complications, such as albuminuria. The role of insulin autoantibodies (IAA) and their interaction with D-dimer in this context remains unclear.</p><p><strong>Aim: </strong>To investigate the characteristics of IAA and its effect on albuminuria in T2DM patients.</p><p><strong>Methods: </strong>We retrospectively analyzed clinical data from 115 T2DM patients with positive IAA induced by exogenous insulin, and 115 age- and sex-matched IAA-negative T2DM patients as controls. Propensity scores were calculated using multivariate logistic regression. Key variables were selected using the least absolute shrinkage and selection operator (LASSO) algorithm. We constructed a prediction model and analyzed the association between IAA and albuminuria based on demographic and laboratory parameters.</p><p><strong>Results: </strong>The IAA-positive group had significantly higher D-dimer levels [0.30 (0.19-0.55) mg/L <i>vs</i> 0.21 (0.19-0.33) mg/L, <i>P</i> = 0.008] and plasma insulin levels [39.1 (12.0-102.7) μU/mL <i>vs</i> 9.8 (5.5-17.6) μU/mL, <i>P</i> < 0.001] compared to the IAA-negative group. Increases in the insulin dose per weight ratio, diabetes duration, and urinary albumin-to-creatinine ratio (UACR) were observed but did not reach statistical significance. The LASSO model identified plasma insulin and D-dimer as key factors with larger coefficients. D-dimer was significantly associated with UACR in the total and IAA-positive groups but not in the IAA-negative group. The odds ratio for D-dimer elevation (> 0.5 g/L) was 2.88 (95% confidence interval: 1.17-7.07) in the IAA-positive group (<i>P</i> interaction < 0.05).</p><p><strong>Conclusion: </strong>D-dimer elevation is an independent risk factor for abnormal albuminuria and interacts with IAA in the development of abnormal albuminuria in T2DM patients.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"101501"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434004","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":"Associations between food insecurity with gestational diabetes mellitus and maternal outcomes mediated by dietary diversity: A cross-sectional study.","authors":"Hong-Li Hou, Gui-Xia Sun","doi":"10.4239/wjd.v16.i2.95463","DOIUrl":"10.4239/wjd.v16.i2.95463","url":null,"abstract":"<p><strong>Background: </strong>Food insecurity (FI) during pregnancy negatively impacts maternal health and raises the risk of gestational diabetes mellitus (GDM) and pregnancy-induced hypertension (PIH), resulting in adverse outcomes for both mother and baby.</p><p><strong>Aim: </strong>To investigate the relationships between FI and pregnancy outcomes, particularly GDM and PIH, while also examining the mediating role of the dietary diversity score (DDS).</p><p><strong>Methods: </strong>A cross-sectional study was undertaken to examine this relationship, involving 600 pregnant women. Participants were women aged 18 years or older who provided complete data on FI and pregnancy outcomes. The FI was measured <i>via</i> the Household Food Security Survey Module, with GDM defined as fasting plasma glucose levels of ≥ 5.1 mmol/L or a 2-hour oral glucose tolerance test value of ≥ 8.5 mmol/L. The DDS is determined by evaluating one's food consumption based on nine distinct food groups. A logistic regression model was used to explore the relationship between FI and PIH, and GDM.</p><p><strong>Results: </strong>Seventeen percent of participants reported experiencing FI during pregnancy. The study found a significant association between FI and an elevated risk of GDM [odds ratio (OR) = 3.32, 95%CI: 1.2-5.4]. Once more, food-insecure pregnant women had higher rates of PIH (OR = 0.10, 95%CI: 0.02-0.45) and they also faced a higher likelihood of neonatal complications, such as neonatal intensive care unit's admissions and the birth of infants with extremely low birth weight. The FI was further linked to metabolic disruptions, such as elevated fasting blood sugar (FBS), low-density lipoprotein cholesterol, and triglyceride levels. Our results indicate that the DDS acts as a significant mediator in the relationship between FI and the incidence of GDM. In particular, the mediation analysis showed that approximately 65% of the effect was mediated through DDS (<i>P</i> = 0.002).</p><p><strong>Conclusion: </strong>These findings underscore the serious challenges that FI presents during pregnancy and its effects on maternal and infant health. Additionally, the study explored how DDS mediates the relationship between FI and the incidence of GDM.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"95463"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434118","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":"Plantamajoside improves type 2 diabetes mellitus pancreatic β-cell damage by inhibiting endoplasmic reticulum stress through Dnajc1 up-regulation.","authors":"Duo Wang, Yuan-Song Wang, Hong-Min Zhao, Peng Lu, Meng Li, Wei Li, Huan-Tian Cui, Zhong-Yong Zhang, Shu-Quan Lv","doi":"10.4239/wjd.v16.i2.99053","DOIUrl":"10.4239/wjd.v16.i2.99053","url":null,"abstract":"<p><strong>Background: </strong>Plantamajoside (PMS) has shown potential in mitigating cell damage caused by high glucose (HG) levels. Despite this, the precise therapeutic effects of PMS on type 2 diabetes mellitus (T2DM) and the underlying regulatory mechanisms require further exploration.</p><p><strong>Aim: </strong>To investigate PMS therapeutic effects on T2DM in mice and elucidate its mechanisms of action through <i>in vivo</i> and <i>in vitro</i> experiments.</p><p><strong>Methods: </strong>An <i>in vitro</i> damage model of MIN6 cells was established using HG and palmitic acid (PA). PMS's protective effect on cell damage was assessed. Next, transcriptomics was employed to examine how PMS treatment affects gene expression of MIN6 cells. Furthermore, the effect of PMS on protein processing in endoplasmic reticulum and apoptosis pathways was validated. A T2DM mouse model was used to validate the therapeutic effects and mechanisms of PMS <i>in vivo</i>.</p><p><strong>Results: </strong>PMS intervention ameliorated cell injury in HG + PA-induced MIN6 cell damage. Transcriptomic analysis revealed that protein processing in the endoplasmic reticulum and apoptosis pathways were enriched in cells treated with PMS, with significant downregulation of the gene Dnajc1. Further validation indicated that PMS significantly inhibited the expression of apoptosis-related factors (Bax, CytC) and endoplasmic reticulum stress (ERS)-related factors [ATF6, XBP1, Ddit3 (CHOP), GRP78], while promoting the expression of Bcl-2 and Dnajc1. Additionally, the inhibitory effects of PMS on ERS and apoptosis were abolished upon Dnajc1 silencing. Furthermore, <i>in vivo</i> experiments demonstrated that PMS intervention effectively improved pancreatic damage, suppressed the expression of apoptosis-related factors (Bax, CytC), and ERS-related factors [ATF6, XBP1, Ddit3 (CHOP), GRP78], while promoting the expression of Bcl-2 and Dnajc1 in a T2DM model mice.</p><p><strong>Conclusion: </strong>PMS intervention could alleviate pancreatic tissue damage effectively. The mechanism of action involves Dnajc1 activation, which subsequently inhibits apoptosis and ERS, ameliorating damage to pancreatic β-cells.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"99053"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434099","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":"Association between body mass index and lumbar spine volumetric bone mineral density in diabetic and non-diabetic patients.","authors":"Fang Lv, Xiao-Ling Cai, Xiu-Ying Zhang, Xiang-Hai Zhou, Xue-Yao Han, Yu-Feng Li, Li-Nong Ji","doi":"10.4239/wjd.v16.i2.98085","DOIUrl":"10.4239/wjd.v16.i2.98085","url":null,"abstract":"<p><strong>Background: </strong>The association between body mass index (BMI) and bone mineral density (BMD) has shown inconsistent results, varying by sex and skeletal site. Despite normal or elevated bone mass, individuals with type 2 diabetes have an increased risk of hip and vertebral fractures.</p><p><strong>Aim: </strong>To assess lumbar spine trabecular volumetric BMD (vBMD) across different BMI categories in individuals with and without diabetes.</p><p><strong>Methods: </strong>This cross-sectional study included 966 men over 50 years old and 1001 postmenopausal women from the Pinggu Metabolic Disease Study. The vBMD of lumbar vertebrae 2 through 4 was measured using quantitative computed tomography. Total adipose tissue, subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), and lumbar skeletal muscle area were also quantified.</p><p><strong>Results: </strong>In men with obesity (<i>P</i> = 0.038) and overweight (<i>P</i> = 0.032), vBMD was significantly higher in the diabetes group compared to non-diabetic men. After adjusting for age and sex, no significant saturation effect between BMI and BMD was found in participants with diabetes or in women without diabetes. However, a BMI threshold of 22.33 kg/m² indicated a saturation point for vBMD in non-diabetic men. Independent predictors of vBMD in men included age (<i>r</i> = -0.387, <i>P</i> < 0.001), BMI (<i>r</i> = 0.130, <i>P</i> = 0.004), and VAT (<i>r</i> = -0.145, <i>P</i> = 0.001). For women, significant predictors were age (<i>r</i> = -0.594, <i>P</i> < 0.001), BMI (<i>r</i> = 0.157, <i>P</i> = 0.004), VAT (<i>r</i> = -0.112, <i>P</i> = 0.001), and SAT (<i>r</i> = -0.068, <i>P</i> = 0.035).</p><p><strong>Conclusion: </strong>The relationship between BMI and trabecular vBMD differs in individuals with and without diabetes. Overweight and obese men with diabetes exhibit higher vBMD.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"98085"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434051","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":"Dapagliflozin exerts anti-apoptotic effects by mitigating macrophage polarization <i>via</i> modulation of the phosphoinositide 3-kinase/protein kinase B signaling pathway.","authors":"Sheng-Xi Xiong, Lin-Juan Huang, Han-Shuang Liu, Xiao-Xiao Zhang, Min Li, Yu-Bing Cui, Chen Shao, Xiao-Lei Hu","doi":"10.4239/wjd.v16.i2.97287","DOIUrl":"10.4239/wjd.v16.i2.97287","url":null,"abstract":"<p><strong>Background: </strong>Macrophages are central to the orchestration of immune responses, inflammatory processes, and the pathogenesis of diabetic complications. The dynamic polarization of macrophages into M1 and M2 phenotypes critically modulates inflammation and contributes to the progression of diabetic nephropathy. Sodium-glucose cotransporter 2 inhibitors such as dapagliflozin, which are acclaimed for their efficacy in diabetes management, may influence macrophage polarization, thereby ameliorating diabetic nephropathy. This investigation delves into these mechanistic pathways, aiming to elucidate novel therapeutic strategies for diabetes.</p><p><strong>Aim: </strong>To investigate the inhibitory effect of dapagliflozin on macrophage M1 polarization and apoptosis and to explore its mechanism of action.</p><p><strong>Methods: </strong>We established a murine model of type 2 diabetes mellitus and harvested peritoneal macrophages following treatment with dapagliflozin. Concurrently, the human monocyte cell line cells were used for <i>in vitro</i> studies. Macrophage viability was assessed in a cell counting kit 8 assay, whereas apoptosis was evaluated by Annexin V/propidium iodide staining. Protein expression was examined through western blotting, and the expression levels of macrophage M1 surface markers, inflammatory cytokines, and apoptotic factors were quantified using flow cytometry, enzyme linked immunosorbent assay, and quantitative real-time polymerase chain reaction analyses.</p><p><strong>Results: </strong>Dapagliflozin attenuated M1 macrophage polarization and mitigated apoptosis in the abdominal macrophages of diabetic mice, evidenced by the downregulation of proapoptotic genes (<i>Caspase 3</i>), inflammatory cytokines [interleukin (IL)-6, tumor necrosis factor-α, and IL-1β], and M1 surface markers (inducible nitric oxide synthase, and cluster of differentiation 86), as well as the upregulation of the antiapoptotic gene <i>BCL2</i>. Moreover, dapagliflozin suppressed the expression of proteins associated with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway (PI3K, AKT, phosphorylated protein kinase B). These observations were corroborated <i>in vitro</i>, where we found that the modulatory effects of dapagliflozin were abrogated by 740Y-P, an activator of the PI3K/AKT signaling pathway.</p><p><strong>Conclusion: </strong>Dapagliflozin attenuates the polarization of macrophages toward the M1 phenotype, thereby mitigating inflammation and promoting macrophage apoptosis. These effects are likely mediated through the inhibition of the PI3K/AKT signaling pathway.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"97287"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434083","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":"Impact of setting distinct target blood glucose levels on endogenous insulin suppression and pharmacodynamics of insulin preparations.","authors":"Hui Liu, Ting Li, Xin-Lei Chen, Hong-Ling Yu, Ye-Rong Yu","doi":"10.4239/wjd.v16.i2.101779","DOIUrl":"10.4239/wjd.v16.i2.101779","url":null,"abstract":"<p><strong>Background: </strong>Insulin therapy plays a crucial role in managing diabetes. Regulatory guidelines mandate assessing the pharmacokinetics (PK) and pharmacodynamics (PD) of new insulin formulations with euglycemic clamp techniques before entry into the market. Typically, blood glucose (BG) levels are maintained at 5% below baseline to suppress endogenous insulin secretion in healthy volunteers. However, in scenarios where BG baseline is relatively low, maintaining it at 5% below baseline can increase hypoglycemic risk. Consequently, we adjusted to maintain it at 2.5% below a baseline of < 4.00 mmol/L. It remains uncertain whether this adjustment impacts endogenous insulin inhibition or the PD of study insulin.</p><p><strong>Aim: </strong>To evaluate and compare the PD and C-peptide status using two different target BG setting methods.</p><p><strong>Methods: </strong>Data came from euglycemic clamp trials assessing the PK/PD of insulin aspart (IAsp) in healthy participants. Target BG was set at 2.5% below baseline for those with a basal BG of < 4.00 mmol/L (group A), and at 5% below baseline for others (group B). The area under the curve (AUC) of IAsp (AUC_{IAsp, 0-8 h}) and GIR from 0 to 8 hours (AUC_{GIR, 0-8 h}) was used to characterize the PK and PD of IAsp, respectively. The C-peptide reduction and PK/PD of IAsp were compared between the two groups.</p><p><strong>Results: </strong>Out of 135 subjects, 15 were assigned to group A and 120 to group B; however, group B exhibited higher basal C-peptide (1.59 ± 0.36 <i>vs</i> 1.32 ± 0.42 ng/mL, <i>P</i> = 0.006). Following propensity score matching to adjust for basal C-peptide differences, 71 subjects (15 in group A and 56 in group B) were analyzed. No significant differences were observed in demographics, IAsp dosage, or clamp quality. Group B showed significantly higher baseline (4.35 ± 0.21 <i>vs</i> 3.91 ± 0.09 mmol/L, <i>P</i> < 0.001), target (4.13 ± 0.20 <i>vs</i> 3.81 ± 0.08 mmol/L, <i>P</i> < 0.001), and clamped (4.10 ± 0.17 <i>vs</i> 3.80 ± 0.06 mmol/L, <i>P</i> < 0.001) BG levels. Both groups exhibited comparable C-peptide suppression (32.5% ± 10.0% <i>vs</i> 35.6% ± 12.1%, <i>P</i> = 0.370) and similar IAsp activity (AUC_{GIR, 0-8 h}: 1433 ± 400 <i>vs</i> 1440 ± 397 mg/kg, <i>P</i> = 0.952) under nearly equivalent IAsp exposure (AUC_{IAsp, 0-8 h}: 566 ± 51 <i>vs</i> 571 ± 85 ng/mL × h, <i>P</i> = 0.840).</p><p><strong>Conclusion: </strong>Maintaining BG at 2.5% below a baseline of < 4.00 mmol/L did not compromise the endogenous insulin suppression nor alter the observed pharmacodynamic effects of the study insulin.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"101779"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433883","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":"Improving nursing care protocols for diabetic patients through a systematic review and meta-analysis of recent years.","authors":"Mónica Grande-Alonso, María Barbado García, Soledad Cristóbal-Aguado, Soledad Aguado-Henche, Rafael Moreno-Gómez-Toledano","doi":"10.4239/wjd.v16.i2.100801","DOIUrl":"10.4239/wjd.v16.i2.100801","url":null,"abstract":"<p><strong>Background: </strong>Diabetes mellitus has become one of the major pandemics of the 21^st century. In this scenario, nursing interventions are essential for improving self-care and quality of life in patients with type 2 diabetes mellitus. Nursing interventions are crucial for managing the disease and preventing complications.</p><p><strong>Aim: </strong>To analyse nursing interventions in recent years through a systematic review and meta-analysis and to propose improvements in care plans.</p><p><strong>Methods: </strong>This study conducted a systematic review and meta-analysis of the impact of nursing interventions on quantitative glycaemic variables, such as glycated haemoglobin and fasting plasma glucose.</p><p><strong>Results: </strong>After confirming that the combined effect of all studies from the past 5 years positively impacts quantitative variables, a descriptive analysis of the studies with the most significant changes was conducted. Based on this, an improvement in diabetic patient care protocols has been proposed through follow-up plans tailored to the patient's technological skills.</p><p><strong>Conclusion: </strong>The combined results obtained and the proposal for improvement developed in this manuscript could help to improve the quality of life of many people around the world.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"100801"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433884","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":"Pelvic floor dysfunction in patients with gestational diabetes mellitus.","authors":"Mustafa Arslan, Ramazan Kozan","doi":"10.4239/wjd.v16.i2.99823","DOIUrl":"10.4239/wjd.v16.i2.99823","url":null,"abstract":"<p><p>In this editorial, we comment on an article by Wang <i>et al.</i> Recent literature shows an increase in research on pelvic organ prolapse (POP). Although the true incidence of POP remains uncertain, its impact on quality of life is substantial. Anatomical studies report high incidence rates, surpassing those observed in symptom-based surveys. Weakness of the endopelvic fascia is a primary anatomical risk factor for POP. Additionally, gestational diabetes mellitus (GDM) has emerged as a growing concern, as poor glycemic control increases complications for both mother and fetus. GDM and POP are interconnected, with factors like maternal obesity, macrosomia, and hormonal changes exacerbating pelvic floor dysfunction. Modifiable risk factors, such as obesity and chronic hyperglycemia, along with multiparity, instrumental deliveries, and obstetric trauma, further increase susceptibility. For patients with GDM, gynecological exams, Pelvic Organ Prolapse Quantification staging, and pelvic floor ultrasonography are valuable diagnostics, with proctological exams and magnetic resonance defecography aiding in multi-compartment prolapse diagnoses. Imaging, though uncomfortable during pregnancy, is safe in the early postpartum period. This editorial emphasizes the need for further research on the pathophysiology of GDM-related POP and offers recommendations for improving diagnosis and clinical management of patients with GDM.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"99823"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434095","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}