BACKGROUND Diabetic kidney disease (DKD) is the primary cause of end-stage renal disease. The Astragalus -Coptis drug pair is frequently employed in the management of DKD. However, the precise molecular mechanism underlying its therapeutic effect remains elusive. AIM To investigate the synergistic effects of multiple active ingredients in the Astragalus-Coptis drug pair on DKD through multiple targets and pathways. METHODS The ingredients of the Astragalus -Coptis drug pair were collected and screened using the TCMSP database and the SwissADME platform. The targets were predicted using the SwissTargetPrediction database, while the DKD differential gene expression analysis was obtained from the Gene Expression Omnibus database. DKD targets were acquired from the GeneCards, Online Mendelian Inheritance in Man database, and DisGeNET databases, with common targets identified through the Venny platform. The protein-protein interaction network and the “disease-active ingredient-target” network of the common targets were constructed utilizing the STRING database and Cytoscape software, followed by the analysis of the interaction relationships and further screening of key targets and core active ingredients. Gene Ontology (GO) function and Kyoto Ency-clopedia of Genes and Genomes (KEGG) pathway enrichments were performed using the DAVID database. The tissue and organ distributions of key targets were evaluated. PyMOL and AutoDock software validate the molecular docking between the core ingredients and key targets. Finally, molecular dynamics (MD) simulations were conducted to simulate the optimal complex formed by interactions between core ingredients and key target proteins. RESULTS A total of 27 active ingredients and 512 potential targets of the Astragalus -Coptis drug pair were identified. There were 273 common targets between DKD and the Astragalus -Coptis drug pair. Through protein-protein interaction network topology analysis, we identified 9 core active ingredients and 10 key targets. GO and KEGG pathway enrichment analyses revealed that Astragalus -Coptis drug pair treatment for DKD involves various biological processes, including protein phosphorylation, negative regulation of apoptosis, inflammatory response, and endoplasmic reticulum unfolded protein response. These pathways are mainly associated with the advanced glycation end products (AGE)-receptor for AGE products signaling pathway in diabetic complications, as well as the Lipid and atherosclerosis. Molecular docking and MD simulations demonstrated high affinity and stability between the core active ingredients and key targets. Notably, the quercetin-AKT serine/threonine kinase 1 (AKT1) and quercetin-tumor necrosis factor (TNF) protein complexes exhibited exceptional stability. CONCLUSION This study demonstrated that DKD treatment with the Astragalus -Coptis drug pair involves multiple ingredients, targets, and signaling pathways. We propose a novel approach for investigating the
{"title":"Network pharmacology and molecular dynamics study of the effect of the Astragalus-Coptis drug pair on diabetic kidney disease","authors":"Mo-Yan Zhang, Shu-Qin Zheng","doi":"10.4239/wjd.v15.i7.1562","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1562","url":null,"abstract":"BACKGROUND\u0000 Diabetic kidney disease (DKD) is the primary cause of end-stage renal disease. The Astragalus -Coptis drug pair is frequently employed in the management of DKD. However, the precise molecular mechanism underlying its therapeutic effect remains elusive.\u0000 AIM\u0000 To investigate the synergistic effects of multiple active ingredients in the Astragalus-Coptis drug pair on DKD through multiple targets and pathways.\u0000 METHODS\u0000 The ingredients of the Astragalus -Coptis drug pair were collected and screened using the TCMSP database and the SwissADME platform. The targets were predicted using the SwissTargetPrediction database, while the DKD differential gene expression analysis was obtained from the Gene Expression Omnibus database. DKD targets were acquired from the GeneCards, Online Mendelian Inheritance in Man database, and DisGeNET databases, with common targets identified through the Venny platform. The protein-protein interaction network and the “disease-active ingredient-target” network of the common targets were constructed utilizing the STRING database and Cytoscape software, followed by the analysis of the interaction relationships and further screening of key targets and core active ingredients. Gene Ontology (GO) function and Kyoto Ency-clopedia of Genes and Genomes (KEGG) pathway enrichments were performed using the DAVID database. The tissue and organ distributions of key targets were evaluated. PyMOL and AutoDock software validate the molecular docking between the core ingredients and key targets. Finally, molecular dynamics (MD) simulations were conducted to simulate the optimal complex formed by interactions between core ingredients and key target proteins.\u0000 RESULTS\u0000 A total of 27 active ingredients and 512 potential targets of the Astragalus -Coptis drug pair were identified. There were 273 common targets between DKD and the Astragalus -Coptis drug pair. Through protein-protein interaction network topology analysis, we identified 9 core active ingredients and 10 key targets. GO and KEGG pathway enrichment analyses revealed that Astragalus -Coptis drug pair treatment for DKD involves various biological processes, including protein phosphorylation, negative regulation of apoptosis, inflammatory response, and endoplasmic reticulum unfolded protein response. These pathways are mainly associated with the advanced glycation end products (AGE)-receptor for AGE products signaling pathway in diabetic complications, as well as the Lipid and atherosclerosis. Molecular docking and MD simulations demonstrated high affinity and stability between the core active ingredients and key targets. Notably, the quercetin-AKT serine/threonine kinase 1 (AKT1) and quercetin-tumor necrosis factor (TNF) protein complexes exhibited exceptional stability.\u0000 CONCLUSION\u0000 This study demonstrated that DKD treatment with the Astragalus -Coptis drug pair involves multiple ingredients, targets, and signaling pathways. We propose a novel approach for investigating the","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141645916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUND Skeletal muscle handles about 80% of insulin-stimulated glucose uptake and become the major organ occurring insulin resistance (IR). Many studies have confirmed the interactions between macrophages and skeletal muscle regulated the inflammation and regeneration of skeletal muscle. However, despite of the decades of research, whether macrophages infiltration and polarization in skeletal muscle under high glucose (HG) milieus results in the development of IR is yet to be elucidated. C2C12 myoblasts are well-established and excellent model to study myogenic regulation and its responses to stimulation. Further exploration of macrophages' role in myoblasts IR and the dynamics of their infiltration and polarization is warranted. AIM To evaluate interactions between myoblasts and macrophages under HG, and its effects on inflammation and IR in skeletal muscle. METHODS We detected the polarization status of macrophages infiltrated to skeletal muscles of IR mice by hematoxylin and eosin and immunohistochemical staining. Then, we developed an in vitro co-culture system to study the interactions between myoblasts and macrophages under HG milieus. The effects of myoblasts on macrophages were explored through morphological observation, CCK-8 assay, Flow Cytometry, and enzyme-linked immunosorbent assay. The mediation of macrophages to myogenesis and insulin sensitivity were detected by morphological observation, CCK-8 assay, Immunofluorescence, and 2-NBDG assay. RESULTS The F4/80 and co-localization of F4/80 and CD86 increased, and the myofiber size decreased in IR group (P < 0.01, g = 6.26). Compared to Mc group, F4/80+CD86+CD206- cells, tumor necrosis factor-α (TNFα), inerleukin-1β (IL-1β) and IL-6 decreased, and IL-10 increased in McM group (P < 0.01, g > 0.8). In McM + HG group, F4/80+CD86+CD206- cells, monocyte chemoattractant protein 1, TNFα, IL-1β and IL-6 were increased, and F4/80+CD206+CD86- cells and IL-10 were decreased compared with Mc + HG group and McM group (P < 0.01, g > 0.8). Compered to M group, myotube area, myotube number and E-MHC were increased in MMc group (P < 0.01, g > 0.8). In MMc + HG group, myotube area, myotube number, E-MHC, GLUT4 and glucose uptake were decreased compared with M + HG group and MMc group (P < 0.01, g > 0.8). CONCLUSION Interactions between myoblasts and macrophages under HG milieus results in inflammation and IR, which support that the macrophage may serve as a promising therapeutic target for skeletal muscle atrophy and IR.
{"title":"Interactions between myoblasts and macrophages under high glucose milieus result in inflammatory response and impaired insulin sensitivity","authors":"Wei Luo, Yue Zhou, Li-Ying Wang, Lei Ai","doi":"10.4239/wjd.v15.i7.1589","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1589","url":null,"abstract":"BACKGROUND\u0000 Skeletal muscle handles about 80% of insulin-stimulated glucose uptake and become the major organ occurring insulin resistance (IR). Many studies have confirmed the interactions between macrophages and skeletal muscle regulated the inflammation and regeneration of skeletal muscle. However, despite of the decades of research, whether macrophages infiltration and polarization in skeletal muscle under high glucose (HG) milieus results in the development of IR is yet to be elucidated. C2C12 myoblasts are well-established and excellent model to study myogenic regulation and its responses to stimulation. Further exploration of macrophages' role in myoblasts IR and the dynamics of their infiltration and polarization is warranted.\u0000 AIM\u0000 To evaluate interactions between myoblasts and macrophages under HG, and its effects on inflammation and IR in skeletal muscle.\u0000 METHODS\u0000 We detected the polarization status of macrophages infiltrated to skeletal muscles of IR mice by hematoxylin and eosin and immunohistochemical staining. Then, we developed an in vitro co-culture system to study the interactions between myoblasts and macrophages under HG milieus. The effects of myoblasts on macrophages were explored through morphological observation, CCK-8 assay, Flow Cytometry, and enzyme-linked immunosorbent assay. The mediation of macrophages to myogenesis and insulin sensitivity were detected by morphological observation, CCK-8 assay, Immunofluorescence, and 2-NBDG assay.\u0000 RESULTS\u0000 The F4/80 and co-localization of F4/80 and CD86 increased, and the myofiber size decreased in IR group (P < 0.01, g = 6.26). Compared to Mc group, F4/80+CD86+CD206- cells, tumor necrosis factor-α (TNFα), inerleukin-1β (IL-1β) and IL-6 decreased, and IL-10 increased in McM group (P < 0.01, g > 0.8). In McM + HG group, F4/80+CD86+CD206- cells, monocyte chemoattractant protein 1, TNFα, IL-1β and IL-6 were increased, and F4/80+CD206+CD86- cells and IL-10 were decreased compared with Mc + HG group and McM group (P < 0.01, g > 0.8). Compered to M group, myotube area, myotube number and E-MHC were increased in MMc group (P < 0.01, g > 0.8). In MMc + HG group, myotube area, myotube number, E-MHC, GLUT4 and glucose uptake were decreased compared with M + HG group and MMc group (P < 0.01, g > 0.8).\u0000 CONCLUSION\u0000 Interactions between myoblasts and macrophages under HG milieus results in inflammation and IR, which support that the macrophage may serve as a promising therapeutic target for skeletal muscle atrophy and IR.","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141647050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In this paper, we concentrate on updating the clinical research on sodium-glucose cotransporter inhibitors (SGLTis) for patients with type 2 diabetes who have heart failure with a preserved injection fraction, acute heart failure, atrial fibrillation, primary prevention of atherosclerotic cardiovascular disease/cardiovascular disease, and acute myocardial infarction. We searched the data of randomized controlled trials and meta-analyses of SGLTis in patients with diabetes from PubMed between January 1, 2020 and April 6, 2024 for our review. According to our review, certain SGLTis (empagliflozin, dapagliflozin, canagliflozin, and tofogliflozin), but not sodium-glucose cotransporter 1 inhibitor (SGLT1i), exhibit relatively superior clinical safety and effectiveness for treating the abovementioned diseases. Proper utilization of SGLTis in these patients can foster clinical improvement and offer an alternative medication option. However, clinical trials involving SGLTis for certain diseases have relatively small sample sizes, brief intervention durations, and conclusions based on weak evidence, necessitating additional data. These findings are significant and valuable for providing a more comprehensive reference and new possibilities for the clinical utilization and scientific exploration of SGLTis.
{"title":"Update on evidence-based clinical application of sodium-glucose cotransporter inhibitors: Insight to uncommon cardiovascular disease scenarios in diabetes","authors":"Shibing Tao, Xi Lu, Zi-Wei Ye, Nan-Wei Tong","doi":"10.4239/wjd.v15.i7.1461","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1461","url":null,"abstract":"In this paper, we concentrate on updating the clinical research on sodium-glucose cotransporter inhibitors (SGLTis) for patients with type 2 diabetes who have heart failure with a preserved injection fraction, acute heart failure, atrial fibrillation, primary prevention of atherosclerotic cardiovascular disease/cardiovascular disease, and acute myocardial infarction. We searched the data of randomized controlled trials and meta-analyses of SGLTis in patients with diabetes from PubMed between January 1, 2020 and April 6, 2024 for our review. According to our review, certain SGLTis (empagliflozin, dapagliflozin, canagliflozin, and tofogliflozin), but not sodium-glucose cotransporter 1 inhibitor (SGLT1i), exhibit relatively superior clinical safety and effectiveness for treating the abovementioned diseases. Proper utilization of SGLTis in these patients can foster clinical improvement and offer an alternative medication option. However, clinical trials involving SGLTis for certain diseases have relatively small sample sizes, brief intervention durations, and conclusions based on weak evidence, necessitating additional data. These findings are significant and valuable for providing a more comprehensive reference and new possibilities for the clinical utilization and scientific exploration of SGLTis.","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141644391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Atrial fibrillation (AF) and prediabetes share common pathophysiological mechanisms with endothelial dysfunction and inflammation playing a key role. The resultant vicious cycle which sets in culminates in a higher atherogenicity and thermogenicity of the vascular system resulting in increased major adverse cardiac or cerebrovascular event (MACCE) events. However, the same has not convincingly been verified in real-world settings. In the recent retrospective study by Desai et al amongst AF patients being admitted to hospitals following MACCE, prediabetes emerged as an independent risk factor for MACCE after adjusting for all confounding variables. However, certain questions like the role of metformin, quantifying the risk for MACCE amongst prediabetes compared to diabetes, the positive impact of reversion to normoglycemia remain unanswered. We provide our insights and give future directions for dedicated research in this area to clarify the exact relationship between the two.
{"title":"Atrial fibrillation and prediabetes: A liaison that merits attention!","authors":"Akash Batta, Juniali Hatwal","doi":"10.4239/wjd.v15.i7.1645","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1645","url":null,"abstract":"Atrial fibrillation (AF) and prediabetes share common pathophysiological mechanisms with endothelial dysfunction and inflammation playing a key role. The resultant vicious cycle which sets in culminates in a higher atherogenicity and thermogenicity of the vascular system resulting in increased major adverse cardiac or cerebrovascular event (MACCE) events. However, the same has not convincingly been verified in real-world settings. In the recent retrospective study by Desai et al amongst AF patients being admitted to hospitals following MACCE, prediabetes emerged as an independent risk factor for MACCE after adjusting for all confounding variables. However, certain questions like the role of metformin, quantifying the risk for MACCE amongst prediabetes compared to diabetes, the positive impact of reversion to normoglycemia remain unanswered. We provide our insights and give future directions for dedicated research in this area to clarify the exact relationship between the two.","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141645710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The surge in type 2 diabetes mellitus (T2DM) is tightly linked to obesity, leading to ectopic fat accumulation in internal organs. Weight management has become a cornerstone of T2DM treatment, with evidence suggesting that significant weight loss can induce remission. Remission, defined as sustained hemoglobin (HbA1c) below 6.5% for at least 3 months without medication, can be achieved through various approaches, including lifestyle, medical, and surgical interventions. Metabolic bariatric surgery offers significant remission rates, particularly for patients with severe obesity. Intensive lifestyle modifications, including low-calorie diets and exercise, have also demonstrated significant potential. Medications like incretin-based agents show robust results in improving beta-cell function, achieving glycemic control, and promoting weight loss. While complete remission without medication may not be attainable for everyone, especially those with severe insulin resistance or deficiency, early and aggressive glycemic control remains a crucial strategy. Maintaining HbA1c below 6.5% from the time of diagnosis reduces the risk of long-term complications and mortality. Moreover, considering a broader definition of remission, encompassing individuals with sustained control on medication, could offer a more comprehensive and inclusive approach to managing this chronic disease.
{"title":"Remission of type 2 diabetes mellitus","authors":"A. Nakhleh, Elya Halfin, Naim Shehadeh","doi":"10.4239/wjd.v15.i7.1384","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1384","url":null,"abstract":"The surge in type 2 diabetes mellitus (T2DM) is tightly linked to obesity, leading to ectopic fat accumulation in internal organs. Weight management has become a cornerstone of T2DM treatment, with evidence suggesting that significant weight loss can induce remission. Remission, defined as sustained hemoglobin (HbA1c) below 6.5% for at least 3 months without medication, can be achieved through various approaches, including lifestyle, medical, and surgical interventions. Metabolic bariatric surgery offers significant remission rates, particularly for patients with severe obesity. Intensive lifestyle modifications, including low-calorie diets and exercise, have also demonstrated significant potential. Medications like incretin-based agents show robust results in improving beta-cell function, achieving glycemic control, and promoting weight loss. While complete remission without medication may not be attainable for everyone, especially those with severe insulin resistance or deficiency, early and aggressive glycemic control remains a crucial strategy. Maintaining HbA1c below 6.5% from the time of diagnosis reduces the risk of long-term complications and mortality. Moreover, considering a broader definition of remission, encompassing individuals with sustained control on medication, could offer a more comprehensive and inclusive approach to managing this chronic disease.","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141644892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jian-Ping Wen, Shuanji Ou, Jia-bao Liu, Wei Zhang, Yudun Qu, Jia-xuan Li, Chang Xia, Yang Yang, Y. Qi, Changpeng Xu
BACKGROUND Diabetic foot ulcers (DFUs) are one of the most severe and popular complications of diabetes. The persistent non-healing of DFUs is the leading cause of ampu-tation, which causes significant mental and financial stress to patients and their families. Macrophages are critical cells in wound healing and perform essential roles in all phases of wound healing. However, no studies have been carried out to systematically illustrate this area from a scientometric point of view. Although there have been some bibliometric studies on diabetes, reports focusing on the investigation of macrophages in DFUs are lacking. AIM To perform a bibliometric analysis to systematically assess the current state of research on macrophage-related DFUs. METHODS The publications of macrophage-related DFUs from January 1, 2004, to December 31, 2023, were retrieved from the Web of Science Core Collection on January 9, 2024. Four different analytical tools: VOSviewer (v1.6.19), CiteSpace (v6.2.R4), HistCite (v12.03.07), and Excel 2021 were used for the scientometric research. RESULTS A total of 330 articles on macrophage-related DFUs were retrieved. The most published countries, institutions, journals, and authors in this field were China, Shanghai Jiao Tong University of China, Wound Repair and Regeneration, and Aristidis Veves. Through the analysis of keyword co-occurrence networks, historical direct citation networks, thematic maps, and trend topics maps, we synthesized the prevailing research hotspots and emerging trends in this field. CONCLUSION Our bibliometric analysis provides a comprehensive overview of macrophage-related DFUs research and insights into promising upcoming research.
{"title":"Global trends in publications regarding macrophages-related diabetic foot ulcers in the last two decades","authors":"Jian-Ping Wen, Shuanji Ou, Jia-bao Liu, Wei Zhang, Yudun Qu, Jia-xuan Li, Chang Xia, Yang Yang, Y. Qi, Changpeng Xu","doi":"10.4239/wjd.v15.i7.1627","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1627","url":null,"abstract":"BACKGROUND\u0000 Diabetic foot ulcers (DFUs) are one of the most severe and popular complications of diabetes. The persistent non-healing of DFUs is the leading cause of ampu-tation, which causes significant mental and financial stress to patients and their families. Macrophages are critical cells in wound healing and perform essential roles in all phases of wound healing. However, no studies have been carried out to systematically illustrate this area from a scientometric point of view. Although there have been some bibliometric studies on diabetes, reports focusing on the investigation of macrophages in DFUs are lacking.\u0000 AIM\u0000 To perform a bibliometric analysis to systematically assess the current state of research on macrophage-related DFUs.\u0000 METHODS\u0000 The publications of macrophage-related DFUs from January 1, 2004, to December 31, 2023, were retrieved from the Web of Science Core Collection on January 9, 2024. Four different analytical tools: VOSviewer (v1.6.19), CiteSpace (v6.2.R4), HistCite (v12.03.07), and Excel 2021 were used for the scientometric research.\u0000 RESULTS\u0000 A total of 330 articles on macrophage-related DFUs were retrieved. The most published countries, institutions, journals, and authors in this field were China, Shanghai Jiao Tong University of China, Wound Repair and Regeneration, and Aristidis Veves. Through the analysis of keyword co-occurrence networks, historical direct citation networks, thematic maps, and trend topics maps, we synthesized the prevailing research hotspots and emerging trends in this field.\u0000 CONCLUSION\u0000 Our bibliometric analysis provides a comprehensive overview of macrophage-related DFUs research and insights into promising upcoming research.","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141644960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUND The glycemic control of children with type 1 diabetes (T1D) may be influenced by the economic status of their parents. AIM To investigate the association between parental economic status and blood glucose levels of children with T1D using a mobile health application. METHODS Data from children with T1D in China's largest T1D online community, Tang-TangQuan®. Blood glucose levels were uploaded every three months and parental economic status was evaluated based on annual household income. Children were divided into three groups: Low-income (< 30000 Yuan), middle-income (30000-100000 Yuan), and high-income (> 100000 yuan) (1 Yuan = 0.145 United States Dollar approximately). Blood glucose levels were compared among the groups and associations were explored using Spearman’s correlation analysis and multivariable logistic regression. RESULTS From September 2015 to August 2022, 1406 eligible children with T1D were included (779 female, 55.4%). Median age was 8.1 years (Q1-Q3: 4.6-11.6) and duration of T1D was 0.06 years (0.02-0.44). Participants were divided into three groups: Low-income (n = 320), middle-income (n = 724), and high-income (n = 362). Baseline hemoglobin A1c (HbA1c) levels were comparable among the three groups (P = 0.072). However, at month 36, the low-income group had the highest HbA1c levels (P = 0.036). Within three years after registration, glucose levels increased significantly in the low-income group but not in the middle-income and high-income groups. Parental economic status was negatively correlated with pre-dinner glucose (r = -0.272, P = 0.012). After adjustment for confounders, parental economic status remained a significant factor related to pre-dinner glucose levels (odds ratio = 13.02, 95%CI: 1.99 to 126.05, P = 0.002). CONCLUSION The blood glucose levels of children with T1D were negatively associated with parental economic status. It is suggested that parental economic status should be taken into consideration in the management of T1D for children.
{"title":"Association between glucose levels of children with type 1 diabetes and parental economic status in mobile health application","authors":"Wen-Hao Zhang, Chao-Fan Wang, Hao Wang, Jie Tang, Hong-Qiang Zhang, Jiang-Yu Zhu, Xue-Ying Zheng, Si-Hui Luo, Yu Ding","doi":"10.4239/wjd.v15.i7.1477","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1477","url":null,"abstract":"BACKGROUND\u0000 The glycemic control of children with type 1 diabetes (T1D) may be influenced by the economic status of their parents.\u0000 AIM\u0000 To investigate the association between parental economic status and blood glucose levels of children with T1D using a mobile health application.\u0000 METHODS\u0000 Data from children with T1D in China's largest T1D online community, Tang-TangQuan®. Blood glucose levels were uploaded every three months and parental economic status was evaluated based on annual household income. Children were divided into three groups: Low-income (< 30000 Yuan), middle-income (30000-100000 Yuan), and high-income (> 100000 yuan) (1 Yuan = 0.145 United States Dollar approximately). Blood glucose levels were compared among the groups and associations were explored using Spearman’s correlation analysis and multivariable logistic regression.\u0000 RESULTS\u0000 From September 2015 to August 2022, 1406 eligible children with T1D were included (779 female, 55.4%). Median age was 8.1 years (Q1-Q3: 4.6-11.6) and duration of T1D was 0.06 years (0.02-0.44). Participants were divided into three groups: Low-income (n = 320), middle-income (n = 724), and high-income (n = 362). Baseline hemoglobin A1c (HbA1c) levels were comparable among the three groups (P = 0.072). However, at month 36, the low-income group had the highest HbA1c levels (P = 0.036). Within three years after registration, glucose levels increased significantly in the low-income group but not in the middle-income and high-income groups. Parental economic status was negatively correlated with pre-dinner glucose (r = -0.272, P = 0.012). After adjustment for confounders, parental economic status remained a significant factor related to pre-dinner glucose levels (odds ratio = 13.02, 95%CI: 1.99 to 126.05, P = 0.002).\u0000 CONCLUSION\u0000 The blood glucose levels of children with T1D were negatively associated with parental economic status. It is suggested that parental economic status should be taken into consideration in the management of T1D for children.","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141645773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUND Islets of Langerhans beta cells diminish in autoimmune type 1 diabetes mellitus (T1DM). Teplizumab, a humanized anti-CD3 monoclonal antibody, may help T1DM. Its long-term implications on clinical T1DM development, safety, and efficacy are unknown. AIM To assess the effectiveness and safety of teplizumab as a therapeutic intervention for individuals with T1DM. METHODS A systematic search was conducted using four electronic databases (PubMed, Embase, Scopus, and Cochrane Library) to select publications published in peer-reviewed journals written in English. The odds ratio (OR) and risk ratio (RR) were calculated, along with their 95%CI. We assessed heterogeneity using Cochrane Q and I 2 statistics and the appropriate P value. RESULTS There were 8 randomized controlled trials (RCTs) in the current meta-analysis with a total of 1908 T1DM patients from diverse age cohorts, with 1361 patients receiving Teplizumab and 547 patients receiving a placebo. Teplizumab was found to have a substantial link with a decrease in insulin consumption, with an OR of 4.13 (95%CI: 1.72 to 9.90). Teplizumab is associated with an improved C-peptide response (OR 2.49; 95%CI: 1.62 to 3.81) and a significant change in Glycated haemoglobin A1c (HbA1c) levels in people with type 1 diabetes [OR 1.75 (95%CI: 1.03 to 2.98)], and it has a RR of 0.71 (95%CI: 0.53 to 0.95). CONCLUSION In type 1 diabetics, teplizumab decreased insulin consumption, improved C-peptide response, and significantly changed HbA1c levels with negligible side effects. Teplizumab appears to improve glycaemic control and diabetes management with good safety and efficacy.
{"title":"Evaluation of teplizumab's efficacy and safety in treatment of type 1 diabetes mellitus: A systematic review and meta-analysis","authors":"Xiao-Lan Ma, Dan Ge, Xue-Jian Hu","doi":"10.4239/wjd.v15.i7.1615","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1615","url":null,"abstract":"BACKGROUND\u0000 Islets of Langerhans beta cells diminish in autoimmune type 1 diabetes mellitus (T1DM). Teplizumab, a humanized anti-CD3 monoclonal antibody, may help T1DM. Its long-term implications on clinical T1DM development, safety, and efficacy are unknown.\u0000 AIM\u0000 To assess the effectiveness and safety of teplizumab as a therapeutic intervention for individuals with T1DM.\u0000 METHODS\u0000 A systematic search was conducted using four electronic databases (PubMed, Embase, Scopus, and Cochrane Library) to select publications published in peer-reviewed journals written in English. The odds ratio (OR) and risk ratio (RR) were calculated, along with their 95%CI. We assessed heterogeneity using Cochrane Q and I 2 statistics and the appropriate P value.\u0000 RESULTS\u0000 There were 8 randomized controlled trials (RCTs) in the current meta-analysis with a total of 1908 T1DM patients from diverse age cohorts, with 1361 patients receiving Teplizumab and 547 patients receiving a placebo. Teplizumab was found to have a substantial link with a decrease in insulin consumption, with an OR of 4.13 (95%CI: 1.72 to 9.90). Teplizumab is associated with an improved C-peptide response (OR 2.49; 95%CI: 1.62 to 3.81) and a significant change in Glycated haemoglobin A1c (HbA1c) levels in people with type 1 diabetes [OR 1.75 (95%CI: 1.03 to 2.98)], and it has a RR of 0.71 (95%CI: 0.53 to 0.95).\u0000 CONCLUSION\u0000 In type 1 diabetics, teplizumab decreased insulin consumption, improved C-peptide response, and significantly changed HbA1c levels with negligible side effects. Teplizumab appears to improve glycaemic control and diabetes management with good safety and efficacy.","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141644989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This editorial focuses on the relationship between nonalcoholic fatty pancreas disease (NAFPD) and the development and remission of type 2 diabetes (T2D). NAFPD is characterized by intrapancreatic fatty deposition associated with obesity and not associated with alcohol abuse, viral infections, and other factors. Ectopic fat deposition in the pancreas is associated with the development of T2D, and the underlying mechanism is lipotoxic β-cell dysfunction. However, the results on the relationship between intrapancreatic fat deposition (IPFD) and β-cell function are conflicting. Regardless of the therapeutic approach, weight loss improves IPFD, glycemia, and β-cell function. Pancreatic imaging is valuable for clinically monitoring and evaluating the management of T2D.
{"title":"Diabetes remission and nonalcoholic fatty pancreas disease","authors":"Wen-Jun Wu","doi":"10.4239/wjd.v15.i7.1390","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1390","url":null,"abstract":"This editorial focuses on the relationship between nonalcoholic fatty pancreas disease (NAFPD) and the development and remission of type 2 diabetes (T2D). NAFPD is characterized by intrapancreatic fatty deposition associated with obesity and not associated with alcohol abuse, viral infections, and other factors. Ectopic fat deposition in the pancreas is associated with the development of T2D, and the underlying mechanism is lipotoxic β-cell dysfunction. However, the results on the relationship between intrapancreatic fat deposition (IPFD) and β-cell function are conflicting. Regardless of the therapeutic approach, weight loss improves IPFD, glycemia, and β-cell function. Pancreatic imaging is valuable for clinically monitoring and evaluating the management of T2D.","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141647212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Diabetes mellitus (DM) and Alzheimer's disease (AD) are two major health concerns that have seen a rising prevalence worldwide. Recent studies have indicated a possible link between DM and an increased risk of developing AD. Insulin, while primarily known for its role in regulating blood sugar, also plays a vital role in protecting brain functions. Insulin resistance (IR), especially prevalent in type 2 diabetes, is believed to play a significant role in AD's development. When insulin signalling becomes dysfunctional, it can negatively affect various brain functions, making individuals more susceptible to AD's defining features, such as the buildup of beta-amyloid plaques and tau protein tangles. Emerging research suggests that addressing insulin-related issues might help reduce or even reverse the brain changes linked to AD. This review aims to explore the rela-tionship between DM and AD, with a focus on the role of IR. It also explores the molecular mechanisms by which IR might lead to brain changes and assesses current treatments that target IR. Understanding IR's role in the connection between DM and AD offers new possibilities for treatments and highlights the importance of continued research in this interdisciplinary field.
糖尿病（DM）和阿尔茨海默病（AD）是全球发病率不断上升的两大健康问题。最近的研究表明，糖尿病与阿兹海默症发病风险增加之间可能存在联系。胰岛素的主要作用是调节血糖，但它在保护大脑功能方面也发挥着重要作用。胰岛素抵抗（IR）在 2 型糖尿病中尤为普遍，被认为在注意力缺失症的发病中起着重要作用。当胰岛素信号功能失调时，会对大脑的各种功能产生负面影响，使人更容易出现注意力缺失症的特征，如β-淀粉样蛋白斑块和tau蛋白缠结的堆积。新近的研究表明，解决胰岛素相关问题可能有助于减少甚至逆转与注意力缺失症相关的大脑变化。本综述旨在探讨 DM 与 AD 之间的关系，重点关注 IR 的作用。它还探讨了IR可能导致大脑变化的分子机制，并评估了目前针对IR的治疗方法。了解IR在DM和AD之间联系中的作用为治疗提供了新的可能性，并强调了在这一跨学科领域继续开展研究的重要性。
{"title":"Insulin resistance as the molecular link between diabetes and Alzheimer's disease","authors":"Mona Mohamed Ibrahim Abdalla","doi":"10.4239/wjd.v15.i7.1430","DOIUrl":"https://doi.org/10.4239/wjd.v15.i7.1430","url":null,"abstract":"Diabetes mellitus (DM) and Alzheimer's disease (AD) are two major health concerns that have seen a rising prevalence worldwide. Recent studies have indicated a possible link between DM and an increased risk of developing AD. Insulin, while primarily known for its role in regulating blood sugar, also plays a vital role in protecting brain functions. Insulin resistance (IR), especially prevalent in type 2 diabetes, is believed to play a significant role in AD's development. When insulin signalling becomes dysfunctional, it can negatively affect various brain functions, making individuals more susceptible to AD's defining features, such as the buildup of beta-amyloid plaques and tau protein tangles. Emerging research suggests that addressing insulin-related issues might help reduce or even reverse the brain changes linked to AD. This review aims to explore the rela-tionship between DM and AD, with a focus on the role of IR. It also explores the molecular mechanisms by which IR might lead to brain changes and assesses current treatments that target IR. Understanding IR's role in the connection between DM and AD offers new possibilities for treatments and highlights the importance of continued research in this interdisciplinary field.","PeriodicalId":509005,"journal":{"name":"World Journal of Diabetes","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141647960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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