We aimed to compare the effects of cardiovascular disease risk in Japanese patients with type 2 diabetes on sodium–glucose cotransporter 2 inhibitors (SGLT2Is) or metformin. This retrospective, real-world cohort study was carried out using a claims database and propensity score matching; 58,402 eligible patients (29,201 per group) were included. The outcomes included nonfatal myocardial infarction, angina pectoris, nonfatal stroke, hospitalization for heart failure and composite end-points. The hazard ratio (HR) for the composite end-point was 0.79, which was lower for SGLT2Is than for metformin. For male patients (HR 0.76), patients aged <65 years (HR 0.94), patients aged ≥75 years (HR 0.78) and patients with body mass index ≥25 kg/m2 (HR 0.76), the HRs for the composite end-point were significantly lower in the SGLT2I group than in the metformin group. SGLT2Is might be superior to metformin in reducing the composite risk of cardiovascular disease in patients with type 2 diabetes.
{"title":"Real-world risk of cardiovascular diseases in patients with type 2 diabetes associated with sodium–glucose cotransporter 2 inhibitors in comparison with metformin: A propensity score-matched model analysis in Japan","authors":"Takeshi Horii, Yoichi Oikawa, Akira Shimada, Kiyoshi Mihara","doi":"10.1111/jdi.14062","DOIUrl":"10.1111/jdi.14062","url":null,"abstract":"<p>We aimed to compare the effects of cardiovascular disease risk in Japanese patients with type 2 diabetes on sodium–glucose cotransporter 2 inhibitors (SGLT2Is) or metformin. This retrospective, real-world cohort study was carried out using a claims database and propensity score matching; 58,402 eligible patients (29,201 per group) were included. The outcomes included nonfatal myocardial infarction, angina pectoris, nonfatal stroke, hospitalization for heart failure and composite end-points. The hazard ratio (HR) for the composite end-point was 0.79, which was lower for SGLT2Is than for metformin. For male patients (HR 0.76), patients aged <65 years (HR 0.94), patients aged ≥75 years (HR 0.78) and patients with body mass index ≥25 kg/m<sup>2</sup> (HR 0.76), the HRs for the composite end-point were significantly lower in the SGLT2I group than in the metformin group. SGLT2Is might be superior to metformin in reducing the composite risk of cardiovascular disease in patients with type 2 diabetes.</p>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 11","pages":"1262-1267"},"PeriodicalIF":3.2,"publicationDate":"2023-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14062","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9897325","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}
Kyuho Kim, Su-Nam Lee, Yu-Bae Ahn, Seung-Hyun Ko, Jae-Seung Yun
Aims/Introduction
We investigated the association of polyneuropathy (PN) with all-cause and cardiovascular (CV) mortality and with cardiovascular disease (CVD) events stratified by diabetes status.
Materials and Methods
This prospective cohort study used the UK Biobank. Polyneuropathy was defined based on nurse-led interviews or ICD codes for polyneuropathy. Cox proportional hazards models were used to investigate the association of polyneuropathy with clinical outcomes.
Results
A total of 459,127 participants were included in the analysis. Polyneuropathy was significantly associated with all-cause and cardiovascular mortality, and with CVD events even after adjusting for CVD risk factors across all diabetes statuses. Metabolic parameters HbA1c, waist circumference, BMI and the inflammatory parameter C-reactive protein showed significant mediation effects for the association between polyneuropathy and CVD. Adherence to a favorable lifestyle was associated with a lower risk of all-cause and cardiovascular mortality regardless of polyneuropathy status.
Conclusions
Polyneuropathy was associated with all-cause and cardiovascular mortality, and with CVD events in subjects with diabetes or prediabetes, even those having normal glucose tolerance. This study suggests the importance of polyneuropathy as a risk factor for death and highlights the necessity of early diagnosis and lifestyle intervention for those with type 2 diabetes and polyneuropathy.
{"title":"Associations of polyneuropathy with risk of all-cause and cardiovascular mortality, cardiovascular disease events stratified by diabetes status","authors":"Kyuho Kim, Su-Nam Lee, Yu-Bae Ahn, Seung-Hyun Ko, Jae-Seung Yun","doi":"10.1111/jdi.14063","DOIUrl":"10.1111/jdi.14063","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims/Introduction</h3>\u0000 \u0000 <p>We investigated the association of polyneuropathy (PN) with all-cause and cardiovascular (CV) mortality and with cardiovascular disease (CVD) events stratified by diabetes status.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>This prospective cohort study used the UK Biobank. Polyneuropathy was defined based on nurse-led interviews or ICD codes for polyneuropathy. Cox proportional hazards models were used to investigate the association of polyneuropathy with clinical outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 459,127 participants were included in the analysis. Polyneuropathy was significantly associated with all-cause and cardiovascular mortality, and with CVD events even after adjusting for CVD risk factors across all diabetes statuses. Metabolic parameters HbA<sub>1c</sub>, waist circumference, BMI and the inflammatory parameter C-reactive protein showed significant mediation effects for the association between polyneuropathy and CVD. Adherence to a favorable lifestyle was associated with a lower risk of all-cause and cardiovascular mortality regardless of polyneuropathy status.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Polyneuropathy was associated with all-cause and cardiovascular mortality, and with CVD events in subjects with diabetes or prediabetes, even those having normal glucose tolerance. This study suggests the importance of polyneuropathy as a risk factor for death and highlights the necessity of early diagnosis and lifestyle intervention for those with type 2 diabetes and polyneuropathy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 11","pages":"1279-1288"},"PeriodicalIF":3.2,"publicationDate":"2023-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14063","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9951314","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}
Needle phobia is a specific phobia classified as an anxiety disorder in the Diagnostic and Statistical Manual of Mental Disorders-5, and can be a serious problem for patients requiring insulin injections. However, there have been few reports to date on the management of adults with diabetes and needle phobia. We here report a case of a woman with pancreatic diabetes who developed needle phobia and could no longer perform self-injections. She started to use a sensor-augmented pump (SAP), and was able to perform a puncture for the insulin pump and the continuous glucose monitoring sensor by herself. The SAP treatment achieved self-management, better glycemic control, and high treatment satisfaction quantified using the Diabetes Treatment Satisfaction Questionnaire in this patient. Our case suggests the therapeutic potential of SAP in adults with needle phobia and diabetes requiring insulin therapy.
{"title":"Successful introduction of sensor-augmented pump therapy in a patient with diabetes and needle phobia: A case report","authors":"Keiji Sugai, Junpei Shikuma, Satoshi Hiroike, Hironori Abe, Ryo Suzuki","doi":"10.1111/jdi.14061","DOIUrl":"10.1111/jdi.14061","url":null,"abstract":"<p>Needle phobia is a specific phobia classified as an anxiety disorder in the Diagnostic and Statistical Manual of Mental Disorders-5, and can be a serious problem for patients requiring insulin injections. However, there have been few reports to date on the management of adults with diabetes and needle phobia. We here report a case of a woman with pancreatic diabetes who developed needle phobia and could no longer perform self-injections. She started to use a sensor-augmented pump (SAP), and was able to perform a puncture for the insulin pump and the continuous glucose monitoring sensor by herself. The SAP treatment achieved self-management, better glycemic control, and high treatment satisfaction quantified using the Diabetes Treatment Satisfaction Questionnaire in this patient. Our case suggests the therapeutic potential of SAP in adults with needle phobia and diabetes requiring insulin therapy.</p>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 11","pages":"1318-1320"},"PeriodicalIF":3.2,"publicationDate":"2023-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14061","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9866997","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}
Impaired insulin secretion from pancreatic islet β-cells is a major cause of metabolic dysregulation and type 2 diabetes mellitus. Complete transcriptomic characterization of islets in patients with type 2 diabetes mellitus has yet to be completed, and it remains challenging to link insulin secretion dysfunction with precise changes in gene expression. There are several ongoing initiatives aimed at enabling the discovery of regulatory molecules that might contribute to insulin secretion dysfunction and whole-body glucose homeostasis impairment. In one such line of research, Bacos et al.1 obtained evidence suggesting that the gene PAX5 might play an important role in impaired insulin secretion in human islets (Figure 1).
Given the established differences between mouse and human islets, type 2 diabetes mellitus candidate genes that were identified in mice might not have the same regulative effects on human islets. There is an unmet need for powerful transcriptomic analyses that can be applied to human islets isolated from individuals with type 2 diabetes mellitus and nondiabetic controls. Due to the difficulties associated with obtaining human islets, most human islet transcriptomic studies thus far have involved small cohorts and have lacked functional validation. Bacos et al.1 generated a ribonucleic acid sequencing (RNA-Seq) resource bank from the large Lund University Diabetes Center pancreatic islet cohort. It is one of the largest existing type 2 diabetes mellitus human islet cohorts in existence, providing an extensive gene expression resource based on 309 islet preparations in total from individuals with type 2 diabetes mellitus and nondiabetic controls. They then identified 395 differentially expressed genes (DEGs) from the Lund University Diabetes Center cohort, and further performed some functional validation of DEGs in vitro.
The utility of transcriptomic resources can be affirmed by robust replication of DEGs across studies and databases. To date, few DEG replication studies in type 2 diabetes mellitus human islets have been reported, and the various studies in the literature showing replication have been relatively small, including the work by Bacos et al.1 Unsurprisingly, the variance in demographic and pathophysiological profiles among sample donors affects DEG overlap across study cohorts. There remains a need to analyze human islets from a more diverse donor pool, and larger cohorts to clarify whether islet gene expression differs among individuals with type 2 diabetes mellitus in relation to demographic and pathophysiological variables. Another important factor affecting DEG overlap is the particular screen technology applied. RNA-Seq, microarray analysis and other screening technologies have been used to identify genes with altered expression in type 2 diabetes mellitus human islets, generating transcriptiona
{"title":"Delineating the transcriptional atlas for impaired insulin secretion: A window into type 2 diabetes pathophysiology","authors":"Jian Li, Jin Yang, Tianpei Hong","doi":"10.1111/jdi.14060","DOIUrl":"10.1111/jdi.14060","url":null,"abstract":"<p>Impaired insulin secretion from pancreatic islet β-cells is a major cause of metabolic dysregulation and type 2 diabetes mellitus. Complete transcriptomic characterization of islets in patients with type 2 diabetes mellitus has yet to be completed, and it remains challenging to link insulin secretion dysfunction with precise changes in gene expression. There are several ongoing initiatives aimed at enabling the discovery of regulatory molecules that might contribute to insulin secretion dysfunction and whole-body glucose homeostasis impairment. In one such line of research, Bacos <i>et al</i>.<span><sup>1</sup></span> obtained evidence suggesting that the gene <i>PAX5</i> might play an important role in impaired insulin secretion in human islets (Figure 1).</p><p>Given the established differences between mouse and human islets, type 2 diabetes mellitus candidate genes that were identified in mice might not have the same regulative effects on human islets. There is an unmet need for powerful transcriptomic analyses that can be applied to human islets isolated from individuals with type 2 diabetes mellitus and nondiabetic controls. Due to the difficulties associated with obtaining human islets, most human islet transcriptomic studies thus far have involved small cohorts and have lacked functional validation. Bacos <i>et al</i>.<span><sup>1</sup></span> generated a ribonucleic acid sequencing (RNA-Seq) resource bank from the large Lund University Diabetes Center pancreatic islet cohort. It is one of the largest existing type 2 diabetes mellitus human islet cohorts in existence, providing an extensive gene expression resource based on 309 islet preparations in total from individuals with type 2 diabetes mellitus and nondiabetic controls. They then identified 395 differentially expressed genes (DEGs) from the Lund University Diabetes Center cohort, and further performed some functional validation of DEGs <i>in vitro</i>.</p><p>The utility of transcriptomic resources can be affirmed by robust replication of DEGs across studies and databases. To date, few DEG replication studies in type 2 diabetes mellitus human islets have been reported, and the various studies in the literature showing replication have been relatively small, including the work by Bacos <i>et al</i>.<span><sup>1</sup></span> Unsurprisingly, the variance in demographic and pathophysiological profiles among sample donors affects DEG overlap across study cohorts. There remains a need to analyze human islets from a more diverse donor pool, and larger cohorts to clarify whether islet gene expression differs among individuals with type 2 diabetes mellitus in relation to demographic and pathophysiological variables. Another important factor affecting DEG overlap is the particular screen technology applied. RNA-Seq, microarray analysis and other screening technologies have been used to identify genes with altered expression in type 2 diabetes mellitus human islets, generating transcriptiona","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 11","pages":"1231-1233"},"PeriodicalIF":3.2,"publicationDate":"2023-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10175128","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}
The term laminopathies refers to a group of congenital diseases characterized by accelerated degeneration of human tissues. Mutations in LMNA, LMNB, ZMPSTE24, and other genes lead to structural and functional abnormalities associated with lamins. One subtype of laminopathy is the generalized lipodystrophy-associated progeroid syndrome (GLPS), which occurs in patients with heterozygous mutations of the LMNA gene c.29C>T(p.T10I). This paper reports the first case of GLPS in China and compares the clinical features of other GLPS patients with literature reports. A 16-year-old male patient was treated for diabetic ketoacidosis, presenting with premature aging appearance, systemic lipodystrophy, severe fatty liver, and decreased bone density. After peripheral blood DNA extraction and second-generation sequencing, a heterozygous mutation of exon 1 of the LMNA gene c.29C>T(p.T10I) was detected. This case of GLPS may provide a diagnostic and therapeutic basis for potential patients.
{"title":"A subtype of laminopathies: Generalized lipodystrophy-associated progeroid syndrome caused by LMNA gene c.29C>T mutation","authors":"Shipeng Huang, Yan Zhang, Zuan Zhan, Shuhao Gong","doi":"10.1111/jdi.14055","DOIUrl":"https://doi.org/10.1111/jdi.14055","url":null,"abstract":"<p>The term laminopathies refers to a group of congenital diseases characterized by accelerated degeneration of human tissues. Mutations in LMNA, LMNB, ZMPSTE24, and other genes lead to structural and functional abnormalities associated with lamins. One subtype of laminopathy is the generalized lipodystrophy-associated progeroid syndrome (GLPS), which occurs in patients with heterozygous mutations of the LMNA gene c.29C>T(p.T10I). This paper reports the first case of GLPS in China and compares the clinical features of other GLPS patients with literature reports. A 16-year-old male patient was treated for diabetic ketoacidosis, presenting with premature aging appearance, systemic lipodystrophy, severe fatty liver, and decreased bone density. After peripheral blood DNA extraction and second-generation sequencing, a heterozygous mutation of exon 1 of the LMNA gene c.29C>T(p.T10I) was detected. This case of GLPS may provide a diagnostic and therapeutic basis for potential patients.</p>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 10","pages":"1221-1225"},"PeriodicalIF":3.2,"publicationDate":"2023-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41081519","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}
Depression is prevalent in diabetes patients and associated with poor outcomes, but is currently underdiagnosed, with no firm consensus on screening methods. We evaluated the validity of the short-form five-item Problem Areas in Diabetes (PAID-5) questionnaire as a screening tool for depression, comparing it with the Beck Depression Inventory-II (BDI-II) and nine-item Patient Health Questionnaire (PHQ-9).
Materials and Methods
A total of 208 English-speaking adults with type 2 diabetes, recruited from outpatient clinics, completed the BDI-II, PHQ-9 and PAID-5 questionnaires in English. Cronbach's α was used for internal reliability. Convergent validity was examined with BDI-II and PHQ-9. Receiver operating characteristics analyses were used to identify optimal PAID-5 cut-offs for the diagnosis of depression.
Results
All three screening tools were highly reliable, with BDI-II, PHQ-9 and PAID-5 having a Cronbach's α of 0.910, 0.870 and 0.940, respectively. There was a good correlation between BDI-II and PHQ-9, with a correlation co-efficient (r) of 0.73; and a moderate correlation between PAID-5 and PHQ-9, and PAID-5 and BDI-II, with r of 0.55 and 0.55 respectively (P values <0.01). An optimal PAID-5 cut-off ≥9 corresponded to both a BDI-II cut-off >14 (sensitivity 72%, specificity 784%, area under the curve 0.809) and a PHQ-9 cut-off >10 (sensitivity 84%, specificity 74%, area under the curve 0.806). Using a PAID-5 cut-off ≥9, the prevalence of depressive symptoms was 36.1%.
Conclusions
Depressive symptoms are prevalent in people with type 2 diabetes, with the degree of distress significantly related to the severity of depressive symptoms. PAID-5 is a valid and reliable screening tool, and a score ≥9 could prompt further confirmation for depression.
抑郁症在糖尿病患者中普遍存在,且与不良预后相关,但目前尚未得到充分诊断,在筛查方法上尚无坚定的共识。我们评估了简短的五项糖尿病问题领域问卷(PAID-5)作为抑郁症筛查工具的有效性,并将其与贝克抑郁量表- ii (BDI-II)和九项患者健康问卷(PHQ-9)进行了比较。材料与方法从门诊招募208例英语为母语的成人2型糖尿病患者,用英语填写BDI-II、PHQ-9和PAID-5问卷。内部信度采用Cronbach’s α。采用BDI-II和PHQ-9检测收敛效度。受试者工作特征分析用于确定抑郁症诊断的最佳PAID-5截止值。结果3种筛选工具均具有较高的可靠性,其中BDI-II、PHQ-9和PAID-5的Cronbach′s α分别为0.910、0.870和0.940。BDI-II与PHQ-9相关性较好,相关系数(r)为0.73;pai -5与PHQ-9、pai -5与BDI-II呈正相关,r分别为0.55和0.55 (P值<0.01)。最佳PAID-5临界值≥9对应于BDI-II的临界值>14(灵敏度72%,特异性784%,曲线下面积0.809)和PHQ-9的临界值>10(灵敏度84%,特异性74%,曲线下面积0.806)。采用PAID-5临界值≥9,抑郁症状的患病率为36.1%。结论2型糖尿病患者普遍存在抑郁症状,且抑郁程度与抑郁症状严重程度显著相关。pay -5是有效可靠的筛查工具,得分≥9分可提示进一步确认抑郁。
{"title":"Validity of the short-form five-item Problem Area in Diabetes questionnaire as a depression screening tool in type 2 diabetes mellitus patients","authors":"Donovan Tay, Marvin Chua, Joan Khoo","doi":"10.1111/jdi.14051","DOIUrl":"https://doi.org/10.1111/jdi.14051","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims/Introduction</h3>\u0000 \u0000 <p>Depression is prevalent in diabetes patients and associated with poor outcomes, but is currently underdiagnosed, with no firm consensus on screening methods. We evaluated the validity of the short-form five-item Problem Areas in Diabetes (PAID-5) questionnaire as a screening tool for depression, comparing it with the Beck Depression Inventory-II (BDI-II) and nine-item Patient Health Questionnaire (PHQ-9).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>A total of 208 English-speaking adults with type 2 diabetes, recruited from outpatient clinics, completed the BDI-II, PHQ-9 and PAID-5 questionnaires in English. Cronbach's α was used for internal reliability. Convergent validity was examined with BDI-II and PHQ-9. Receiver operating characteristics analyses were used to identify optimal PAID-5 cut-offs for the diagnosis of depression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>All three screening tools were highly reliable, with BDI-II, PHQ-9 and PAID-5 having a Cronbach's α of 0.910, 0.870 and 0.940, respectively. There was a good correlation between BDI-II and PHQ-9, with a correlation co-efficient (<i>r</i>) of 0.73; and a moderate correlation between PAID-5 and PHQ-9, and PAID-5 and BDI-II, with <i>r</i> of 0.55 and 0.55 respectively (<i>P</i> values <0.01). An optimal PAID-5 cut-off ≥9 corresponded to both a BDI-II cut-off >14 (sensitivity 72%, specificity 784%, area under the curve 0.809) and a PHQ-9 cut-off >10 (sensitivity 84%, specificity 74%, area under the curve 0.806). Using a PAID-5 cut-off ≥9, the prevalence of depressive symptoms was 36.1%.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Depressive symptoms are prevalent in people with type 2 diabetes, with the degree of distress significantly related to the severity of depressive symptoms. PAID-5 is a valid and reliable screening tool, and a score ≥9 could prompt further confirmation for depression.</p>\u0000 </section>\u0000 </div>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 9","pages":"1128-1135"},"PeriodicalIF":3.2,"publicationDate":"2023-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5728989","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}
Diabetes mellitus is still expanding globally and is epidemic in developing countries. The combat of this plague has caused enormous economic and social burdens related to a lowered quality of life in people with diabetes. Despite recent significant improvements of life expectancy in patients with diabetes, there is still a need for efforts to elucidate the complexities and mechanisms of the disease processes to overcome this difficult disorder. To this end, the use of appropriate animal models in diabetes studies is invaluable for translation to humans and for the development of effective treatment. In this review, a variety of animal models of diabetes with spontaneous onset in particular will be introduced and discussed for their implication in diabetes research.
{"title":"Contribution of animal models to diabetes research: Its history, significance, and translation to humans","authors":"Soroku Yagihashi","doi":"10.1111/jdi.14034","DOIUrl":"https://doi.org/10.1111/jdi.14034","url":null,"abstract":"<p>Diabetes mellitus is still expanding globally and is epidemic in developing countries. The combat of this plague has caused enormous economic and social burdens related to a lowered quality of life in people with diabetes. Despite recent significant improvements of life expectancy in patients with diabetes, there is still a need for efforts to elucidate the complexities and mechanisms of the disease processes to overcome this difficult disorder. To this end, the use of appropriate animal models in diabetes studies is invaluable for translation to humans and for the development of effective treatment. In this review, a variety of animal models of diabetes with spontaneous onset in particular will be introduced and discussed for their implication in diabetes research.</p>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 9","pages":"1015-1037"},"PeriodicalIF":3.2,"publicationDate":"2023-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6102867","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}
microRNA may be a new therapeutic direction for diabetes. As a typical tumor marker, miR-31 is involved in a variety of metabolic diseases, but the specific role is still unclear. This study aimed to investigate the effect of miR-31 on type 2 diabetes mellitus and its accompanying vascular injury, as well as on the effects of hypoxia-inducible factor-1α inhibitor (HIF1AN), hypoxia-inducible factor (HIF)-1α, and vascular endothelial growth factor (VEGF)-A expression in vitro and in vivo.
Materials and Methods
In vitro, a model of high-fat and high-glucose-induced human aortic endothelial cell (HAEC) injury was established to simulate diabetes mellitus (DM). Cell functions were compared between the control group, the DM damage group, and the group transfected with miR-31 after DM damage. In vivo, overexpressing miR-31 FVB mice and FVB mice were divided into the control and induced type 2 diabetes mellitus groups. Type 2 diabetes mellitus models were induced by a high-fat diet combined with streptozotocin. The lipid metabolism levels, viscera, and vascular damage were compared between the control and type 2 diabetes mellitus groups.
Results
In vitro, miR-31 improved the proliferation ability of damaged cells by targeting HIF1AN and up-regulating the expression of HIF-1α and VEGF-A. In vivo, miR-31 ameliorated the development of type 2 diabetes mellitus, disturbance of glucose and lipid metabolism, and damage to some organs. Meanwhile, miR-31 had a protective effect on vascular damage complicated by type 2 diabetes mellitus by increasing the levels of HIF-1α and VEGF-A.
Conclusion
Our experiments show that miR-31 can delay the progression of type 2 diabetes mellitus and ameliorate diabetic vascular injury.
{"title":"miR-31 ameliorates type 2 diabetic vascular damage through up-regulation of hypoxia-inducible factor-1α/vascular endothelial growth factor-A","authors":"Yuan Fu, Ruochen Du, Yufei Wang, Yitong Yuan, Yujuan Zhang, Chunfang Wang, Xuanping Zhang","doi":"10.1111/jdi.14039","DOIUrl":"https://doi.org/10.1111/jdi.14039","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>microRNA may be a new therapeutic direction for diabetes. As a typical tumor marker, miR-31 is involved in a variety of metabolic diseases, but the specific role is still unclear. This study aimed to investigate the effect of miR-31 on type 2 diabetes mellitus and its accompanying vascular injury, as well as on the effects of hypoxia-inducible factor-1α inhibitor (HIF1AN), hypoxia-inducible factor (HIF)-1α, and vascular endothelial growth factor (VEGF)-A expression <i>in vitro</i> and <i>in vivo</i>.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p><i>In vitro</i>, a model of high-fat and high-glucose-induced human aortic endothelial cell (HAEC) injury was established to simulate diabetes mellitus (DM). Cell functions were compared between the control group, the DM damage group, and the group transfected with miR-31 after DM damage. <i>In vivo</i>, overexpressing miR-31 FVB mice and FVB mice were divided into the control and induced type 2 diabetes mellitus groups. Type 2 diabetes mellitus models were induced by a high-fat diet combined with streptozotocin. The lipid metabolism levels, viscera, and vascular damage were compared between the control and type 2 diabetes mellitus groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p><i>In vitro</i>, miR-31 improved the proliferation ability of damaged cells by targeting HIF1AN and up-regulating the expression of HIF-1α and VEGF-A. <i>In vivo</i>, miR-31 ameliorated the development of type 2 diabetes mellitus, disturbance of glucose and lipid metabolism, and damage to some organs. Meanwhile, miR-31 had a protective effect on vascular damage complicated by type 2 diabetes mellitus by increasing the levels of HIF-1α and VEGF-A.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our experiments show that miR-31 can delay the progression of type 2 diabetes mellitus and ameliorate diabetic vascular injury.</p>\u0000 </section>\u0000 </div>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 9","pages":"1070-1080"},"PeriodicalIF":3.2,"publicationDate":"2023-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6089076","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}
Reham Hammad, Maisa A Abdel Wahab, Nehal Farouk, Mohamed Yahia Zakaria, Mona A Eldosoky, Asmaa A Elmadbouly, Sara A Tahoun, Eman Mahmoud, Seham K Khirala, Amena Rezk Mohammed, Wafaa Abdelaziz Emam, Asmaa A Abo Elqasem, Fatma M Kotb, Rasha Abd Elaziz Abd Elghany
Aims/Introduction
Peripheral artery disease (PAD) serves as a risk factor for diabetic foot ulcers (DFUs). PAD pathology involves atherosclerosis and impaired immunity. Non-classical monocytes are believed to have an anti-inflammatory role. 1,25-Dihydroxy vitamin D (vitamin D3) is claimed to have immune-modulating and lipid-regulating roles. Vitamin D receptor is expressed on monocytes. We aimed to investigate if circulating non-classical monocytes and vitamin D3 were implicated in DFUs associated with PAD.
Materials and Methods
There were two groups of DFU patients: group 1 (n = 40) included patients with first-degree DFUs not associated with PAD, and group 2 (n = 50) included patients with DFU with PAD. The monocyte phenotypes were detected using flow cytometry. Vitamin D3 was assessed by enzyme-linked immunosorbent assay.
Results
DFU patients with PAD showed a significant reduction in the frequency of non-classical monocytes and vitamin D3 levels, when compared with DFU patients without PAD. The percentage of non-classical monocytes positively correlated with vitamin D3 level (r = 0.4, P < 0.01) and high-density lipoprotein (r = 0.5, P < 0.001), whereas it was negatively correlated with cholesterol (r = −0.5, P < 0.001). Vitamin D3 was negatively correlated with triglyceride/high-density lipoprotein (r = −0.4, P < 0.01). Regression analysis showed that a high vitamin D3 serum level was a protective factor against PAD occurrence.
Conclusions
Non-classical monocytes frequency and vitamin D3 levels were significantly reduced in DFU patients with PAD. Non-classical monocytes frequency was associated with vitamin D3 in DFUs patients, and both parameters were linked to lipid profile. Vitamin D3 upregulation was a risk-reducing factor for PAD occurrence.
{"title":"Non-classical monocytes frequency and serum vitamin D3 levels are linked to diabetic foot ulcer associated with peripheral artery disease","authors":"Reham Hammad, Maisa A Abdel Wahab, Nehal Farouk, Mohamed Yahia Zakaria, Mona A Eldosoky, Asmaa A Elmadbouly, Sara A Tahoun, Eman Mahmoud, Seham K Khirala, Amena Rezk Mohammed, Wafaa Abdelaziz Emam, Asmaa A Abo Elqasem, Fatma M Kotb, Rasha Abd Elaziz Abd Elghany","doi":"10.1111/jdi.14048","DOIUrl":"https://doi.org/10.1111/jdi.14048","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims/Introduction</h3>\u0000 \u0000 <p>Peripheral artery disease (PAD) serves as a risk factor for diabetic foot ulcers (DFUs). PAD pathology involves atherosclerosis and impaired immunity. Non-classical monocytes are believed to have an anti-inflammatory role. 1,25-Dihydroxy vitamin D (vitamin D<sub>3</sub>) is claimed to have immune-modulating and lipid-regulating roles. Vitamin D receptor is expressed on monocytes. We aimed to investigate if circulating non-classical monocytes and vitamin D<sub>3</sub> were implicated in DFUs associated with PAD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>There were two groups of DFU patients: group 1 (<i>n</i> = 40) included patients with first-degree DFUs not associated with PAD, and group 2 (<i>n</i> = 50) included patients with DFU with PAD. The monocyte phenotypes were detected using flow cytometry. Vitamin D<sub>3</sub> was assessed by enzyme-linked immunosorbent assay.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>DFU patients with PAD showed a significant reduction in the frequency of non-classical monocytes and vitamin D<sub>3</sub> levels, when compared with DFU patients without PAD. The percentage of non-classical monocytes positively correlated with vitamin D<sub>3</sub> level (<i>r</i> = 0.4, <i>P</i> < 0.01) and high-density lipoprotein (<i>r</i> = 0.5, <i>P</i> < 0.001), whereas it was negatively correlated with cholesterol (<i>r</i> = −0.5, <i>P</i> < 0.001). Vitamin D<sub>3</sub> was negatively correlated with triglyceride/high-density lipoprotein (<i>r</i> = −0.4, <i>P</i> < 0.01). Regression analysis showed that a high vitamin D<sub>3</sub> serum level was a protective factor against PAD occurrence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Non-classical monocytes frequency and vitamin D<sub>3</sub> levels were significantly reduced in DFU patients with PAD. Non-classical monocytes frequency was associated with vitamin D<sub>3</sub> in DFUs patients, and both parameters were linked to lipid profile. Vitamin D<sub>3</sub> upregulation was a risk-reducing factor for PAD occurrence.</p>\u0000 </section>\u0000 </div>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 10","pages":"1192-1201"},"PeriodicalIF":3.2,"publicationDate":"2023-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41081848","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}
It is crucial to develop practical and noninvasive methods to assess the functional beta-cell mass in a donor pancreas, in which monitoring and precise evaluation is challenging. A patient with type 1 diabetes underwent noninvasive imaging following simultaneous kidney–pancreas transplantation with positron emission tomography/computed tomography (PET/CT) using an exendin-based probe, [18F]FB(ePEG12)12-exendin-4. Following transplantation, PET imaging with [18F]FB(ePEG12)12-exendin-4 revealed simultaneous and distinct accumulations in the donor and native pancreases. The pancreases were outlined at a reasonable distance from the surrounding organs using [18F]FB(ePEG12)12-exendin-4 whole-body maximum intensity projection and axial PET images. At 1 and 2 h after [18F]FB(ePEG12)12-exendin-4 administration, the mean standardized uptake values were 2.96 and 3.08, respectively, in the donor pancreas and 1.97 and 2.25, respectively, in the native pancreas. [18F]FB(ePEG12)12-exendin-4 positron emission tomography imaging allowed repeatable and quantitative assessment of beta-cell mass following simultaneous kidney–pancreas transplantation.
{"title":"Noninvasive evaluation of donor and native pancreases following simultaneous pancreas–kidney transplantation using positron emission tomography/computed tomography","authors":"Takaaki Murakami, Toshihiro Nakamura, Hiroyuki Fujimoto, Junji Fujikura, Yoichi Shimizu, Kanae K. Miyake, Daisuke Otani, Kentaro Sakaki, Sakura Kiyobayashi, Takayuki Anazawa, Yuji Nakamoto, Nobuya Inagaki","doi":"10.1111/jdi.14045","DOIUrl":"https://doi.org/10.1111/jdi.14045","url":null,"abstract":"<p>It is crucial to develop practical and noninvasive methods to assess the functional beta-cell mass in a donor pancreas, in which monitoring and precise evaluation is challenging. A patient with type 1 diabetes underwent noninvasive imaging following simultaneous kidney–pancreas transplantation with positron emission tomography/computed tomography (PET/CT) using an exendin-based probe, [<sup>18</sup>F]FB(ePEG12)12-exendin-4. Following transplantation, PET imaging with [<sup>18</sup>F]FB(ePEG12)12-exendin-4 revealed simultaneous and distinct accumulations in the donor and native pancreases. The pancreases were outlined at a reasonable distance from the surrounding organs using [<sup>18</sup>F]FB(ePEG12)12-exendin-4 whole-body maximum intensity projection and axial PET images. At 1 and 2 h after [<sup>18</sup>F]FB(ePEG12)12-exendin-4 administration, the mean standardized uptake values were 2.96 and 3.08, respectively, in the donor pancreas and 1.97 and 2.25, respectively, in the native pancreas. [<sup>18</sup>F]FB(ePEG12)12-exendin-4 positron emission tomography imaging allowed repeatable and quantitative assessment of beta-cell mass following simultaneous kidney–pancreas transplantation.</p>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 10","pages":"1187-1191"},"PeriodicalIF":3.2,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14045","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41082024","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}