Diabetologia最新文献

{"title":"MAP4K4 aggravates microvascular anomalies in diabetic retinopathy in a YTHDF2-dependent manner","authors":"Qian Yang, Pei-wen Zhu, Yan-jun Wen, Ran Zhang, Wen-wen Chen, Xin Huang, Qing Chang","doi":"10.1007/s00125-025-06398-3","DOIUrl":"https://doi.org/10.1007/s00125-025-06398-3","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Aims/hypothesis</h3><p>Signalling pathways that regulate endothelial cell (EC) dysfunction, ischaemia and inflammation play a crucial role in retinal microangiopathy such as diabetic retinopathy. MAP4K4 is highly expressed in ECs. However, the involvement of MAP4K4 in retinal vasculopathy of diabetic retinopathy remains unclear.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>We analysed publicly available single-cell RNA sequencing (scRNA-seq) data from fibrovascular membranes (FVMs) from eight individuals with proliferative diabetic retinopathy (PDR) and normal retinas from 11 individuals without diabetes. Using <i>db</i>/<i>db</i> mice and human primary retinal endothelial cells (HRMECs), we further investigated the effects of MAP4K4 on retinal microangiopathy and endothelial dysfunction to explore the underlying regulatory mechanisms.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>The scRNA-seq analysis revealed that <i>MAP4K4</i> was predominantly expressed in retinal ECs, with elevated expression in FVMs from individuals with PDR compared with normal retinas from individuals without diabetes. This finding was confirmed at the protein level, with MAP4K4 expression and activity being upregulated in both the FVMs of individuals with PDR and the retinas of <i>db</i>/<i>db</i> mice. Inhibition of MAP4K4 using DMX-5804 alleviated retinal microvascular leakage by enhancing the expression and integrity of junctional proteins in both ECs from <i>db</i>/<i>db</i> mice and HRMECs. Additionally, DMX-5804 reduced retinal angiogenesis by inhibiting EC migration and vascular sprouting. Mechanistically, MAP4K4 regulated EC characteristics through NF-κB signalling pathway activity. The exacerbating effect of recombinant MAP4K4 on diabetic retinopathy in <i>db</i>/<i>db</i> mice was mitigated by a p65 inhibitor, confirming the involvement of NF-κB. Moreover, MAP4K4 expression was regulated by YTH <i>N</i>⁶-methyladenosine RNA-binding protein 2 (YTHDF2), which modulates the stability of <i>MAP4K4</i> mRNA.</p><h3 data-test=\"abstract-sub-heading\">Conclusions/interpretation</h3><p>Our study highlights the critical role of MAP4K4 in EC dysfunction and diabetic retinal microangiopathy, providing new insights into its molecular pathogenesis. Targeting MAP4K4, particularly through modulation of the YTHDF2/MAP4K4/NF-κB axis, may provide a novel therapeutic strategy for diabetic retinopathy.</p><h3 data-test=\"abstract-sub-heading\">Graphical Abstract</h3>\u0000","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"20 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143599101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research and data sovereignty in genetically admixed populations.","authors":"Linda Zollner, Rajiv Kumar, Justo Lorenzo Bermejo","doi":"10.1007/s00125-025-06383-w","DOIUrl":"https://doi.org/10.1007/s00125-025-06383-w","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Islet autoantibodies in Thai individuals diagnosed with type 1 diabetes before 30 years of age: a large multicentre nationwide study.","authors":"Nattachet Plengvidhya, Sarocha Suthon, Tassanee Nakdontri, Nipaporn Teerawattanapong, Saranya Ingnang, Watip Tangjittipokin","doi":"10.1007/s00125-025-06404-8","DOIUrl":"https://doi.org/10.1007/s00125-025-06404-8","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rare MTNR1B variants causing diminished MT2 signalling associate with elevated HbA1c levels but not with type 2 diabetes","authors":"Kimmie V. Sørensen, Johanne M. Justesen, Lars Ängquist, Jette Bork-Jensen, Bolette Hartmann, Niklas R. Jørgensen, Jørgen Rungby, Henrik T. Sørensen, Allan Vaag, Jens S. Nielsen, Jens J. Holst, Oluf Pedersen, Allan Linneberg, Torben Hansen, Niels Grarup","doi":"10.1007/s00125-025-06381-y","DOIUrl":"https://doi.org/10.1007/s00125-025-06381-y","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Aims/hypothesis</h3><p>An intronic variant (rs10830963) in <i>MTNR1B</i> (encoding the melatonin receptor type 2 [MT2]) has been shown to strongly associate with impaired glucose regulation and elevated type 2 diabetes prevalence. However, <i>MTNR1B</i> missense variants have shown conflicting results on type 2 diabetes. Thus, we aimed to gain further insights into the impact of <i>MTNR1B</i> coding variants on type 2 diabetes prevalence and related phenotypes.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>We conducted a cross-sectional study, performing <i>MTNR1B</i> variant burden testing of glycaemic phenotypes (<i>N</i>=248,454, without diabetes), other cardiometabolic phenotypes (<i>N</i>=330,453) and type 2 diabetes prevalence (case–control study; <i>N</i>=263,739) in the UK Biobank. Similar burden testing with glycaemic phenotypes was performed in Danish Inter99 participants without diabetes (<i>N</i>=5711), and type 2 diabetes prevalence (DD2 cohort serving as cases [<i>N</i>=2930] and Inter99 serving as controls [<i>N</i>=4243]). Finally, we evaluated the effects of <i>MTNR1B</i> variants on the melatonin-induced glucose regulation response in a recall-by-genotype study of individuals without diabetes.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>In the UK Biobank, <i>MTNR1B</i> variants were not associated with cardiometabolic phenotypes, including type 2 diabetes prevalence, except that carriers of missense <i>MTNR1B</i> variants causing impaired MT2 signalling exhibited higher HbA_1c levels compared with non-carriers (effect size, β, 0.087 SD [95% CI 0.039, 0.135]). Similarly, no significant associations were observed with phenotypes associated with glycaemic phenotypes in the Inter99 population. However, carriers of variants impairing MT2 signalling demonstrated a nominally significant lower glucose-stimulated insulin response (β −0.47 SD [95% CI −0.82, −0.11]). A reduced insulin response was also observed in carriers of variants impairing MT2 signalling (β −476.0 [95% CI −928.6, −24.4]) or the rs10830963 variant (β −390.8 [95% CI −740.1, −41.6]) compared with non-carriers after melatonin treatment.</p><h3 data-test=\"abstract-sub-heading\">Conclusions/interpretation</h3><p>The higher type 2 diabetes prevalence previously observed in carriers of missense <i>MTNR1B</i> variants causing impairment in MT2 signalling was not replicated in the UK Biobank, yet carriers had elevated HbA_1c levels.</p><h3 data-test=\"abstract-sub-heading\">Data availability</h3><p>Data (Inter99 cohort and recall-by-genotype study) are available on reasonable request from the corresponding author. Requests for DD2 data are through the application form at https://dd2.dk/forskning/ansoeg-om-data. Access to UK Biobank data can be requested through the UK Biobank website (https://www.ukbiobank.ac.uk/enable-your-research).</p><h3 data-test=\"abstract-sub-heading\">Graphical Abstract</h3>\u0000","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"4 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143589632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clonal haematopoiesis of indeterminate potential: an emerging risk factor for type 2 diabetes and related complications","authors":"María A. Zuriaga, José J. Fuster","doi":"10.1007/s00125-025-06393-8","DOIUrl":"https://doi.org/10.1007/s00125-025-06393-8","url":null,"abstract":"<p>The accumulation of acquired somatic mutations is a natural consequence of ageing, but the pathophysiological implications of these mutations beyond cancer are only beginning to be understood. Most somatic mutations are functionally neutral, but a few may confer a competitive advantage to a stem cell, driving its clonal expansion. When such a mutation arises in haematopoietic stem cells, it leads to clonal haematopoiesis, in which a significant proportion of blood cells originate from the mutant stem cell and share the same mutation. Clonal haematopoiesis of indeterminate potential (CHIP), a specific subset of clonal haematopoiesis driven by myeloid leukaemia-related somatic mutations, has been linked to a higher risk of various age-related conditions, particularly CVD, by exacerbating inflammatory responses. Emerging evidence suggests that CHIP may also contribute to the pathogenesis of type 2 diabetes and some of its complications. This review synthesises current knowledge on CHIP and its potential as a novel risk factor for type 2 diabetes, highlighting the need for further research to clarify this relationship and to explore its potential value in developing personalised preventive care strategies for type 2 diabetes and related conditions.</p><h3 data-test=\"abstract-sub-heading\">Graphical Abstract</h3>\u0000","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"37 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143590278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TBC1D30 regulates proinsulin and insulin secretion and is the target of a genomic association signal for proinsulin","authors":"Victoria A. Parsons, Swarooparani Vadlamudi, Kayleigh M. Voos, Abigail E. Rohy, Anne H. Moxley, Maren E. Cannon, Jonathan D. Rosen, Christine A. Mills, Laura E. Herring, K. Alaine Broadaway, Damaris N. Lorenzo, Karen L. Mohlke","doi":"10.1007/s00125-025-06391-w","DOIUrl":"https://doi.org/10.1007/s00125-025-06391-w","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Aims/hypothesis</h3><p>Components of the insulin processing and secretion pathways remain incompletely understood. Here, we examined a genome-wide association study (GWAS) signal for plasma proinsulin levels. Lead GWAS variant rs150781447-T encodes an Arg279Cys substitution in TBC1 domain family member 30 (TBC1D30), but no role for this protein in insulin processing or secretion has been established previously. This study aimed to evaluate whether TBC1D30 drives the GWAS association signal by determining whether TBC1D30 is involved in proinsulin secretion and, if so, to examine the effects of variant alleles and potential mechanisms.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>Using CRISPR/Cas9 genome editing to create double-strand breaks and prime editing to install substitutions in INS1 832/13 insulinoma cells, we generated clonal cell lines with altered TBC1D30, as well as homozygous and heterozygous lines carrying the lead GWAS variant. We characterised lines by Sanger sequencing, quantitative PCR and ELISAs to measure glucose-stimulated proinsulin and insulin secretion. We also tested the effects of <i>TBC1D30</i> knockdown on proinsulin and insulin secretion in human islets. We further assessed TBC1D30’s contribution to secretory pathways by examining the effects of altered gene function on intracellular proinsulin and insulin content and insulin localisation, and by identifying potential proteins that interact with TBC1D30 using affinity purification mass spectrometry.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Compared with mock-edited cells, cell lines with reduced <i>TBC1D30</i> expression or altered Rab GTPase-activating protein (RabGAP) domain had significantly more secreted proinsulin, 1.8- and 2.6-fold more than controls, respectively. Similarly, cells expressing the variant substitution demonstrated increased proinsulin secretion. Cell lines with a partial deletion of a critical functional domain showed 1.8-fold higher expression of <i>Tbc1d30</i> and at least 2.0-fold less secreted proinsulin. Cells with altered RabGAP domain sequence also demonstrated, to a lesser extent, changes in secreted insulin levels. <i>TBC1D30</i> knockdown in human islets resulted in increased insulin secretion with no significant effect on proinsulin secretion. The effects of altered TBC1D30 on mislocalisation of insulin, intracellular proinsulin and insulin content and the identities of interacting proteins are consistent with a role for TBC1D30 in proinsulin and insulin secretion.</p><h3 data-test=\"abstract-sub-heading\">Conclusions/interpretation</h3><p>These findings suggest that effects on <i>TBC1D30</i> are responsible for the GWAS signal and that TBC1D30 plays a critical role in the secretion of mature insulin.</p><h3 data-test=\"abstract-sub-heading\">Graphical Abstract</h3>\u0000","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"40 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143589850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Up Front","authors":"","doi":"10.1007/s00125-025-06390-x","DOIUrl":"https://doi.org/10.1007/s00125-025-06390-x","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"27 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143570351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin therapy modifies corneal neuroimmune abnormalities in people with type 2 diabetes","authors":"Amy T. Tsoi, Janice Sng, Shyam S. Tummanapalli, Tushar Issar, Ann M. Poynten, Kerry-Lee Milner, Maria Markoulli, Roshan Dhanapalaratnam, Arun V. Krishnan","doi":"10.1007/s00125-025-06399-2","DOIUrl":"https://doi.org/10.1007/s00125-025-06399-2","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Aims/hypothesis</h3><p>Diabetic peripheral neuropathy is a debilitating microvascular complication of diabetes mellitus, with limited disease-modifying therapies to date. This study aimed to assess the effect of metformin on the corneal sub-basal nerve plexus as a peripheral neuropathy outcome measure in people with type 2 diabetes.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>A cohort of 36 participants with type 2 diabetes receiving metformin therapy were recruited and underwent clinical assessment, corneal confocal microscopy and nerve conduction studies. Concurrently, 36 participants with type 2 diabetes not receiving metformin therapy were selected as disease controls and matched to participants on metformin therapy for age, sex, diabetes duration, BMI, eGFR, HbA_1c, use of other oral glucose-lowering agents and therapies used for the treatment of the metabolic syndrome. Additionally, 25 healthy control participants were assessed and matched for age and sex. Medical record data over the previous 20 years were analysed for prior and current metformin use in all participants with type 2 diabetes.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Participants receiving metformin therapy had higher corneal nerve fibre density (<i>p</i>=0.020), corneal nerve fibre length (<i>p</i>=0.020) and corneal fractal dimension (<i>p</i>=0.003) compared with those not receiving metformin therapy. The inferior whorl dendritic cell density was significantly lower in the metformin group compared with the non-metformin group (<i>p</i>=0.043).</p><h3 data-test=\"abstract-sub-heading\">Conclusions/interpretation</h3><p>Metformin treatment is associated with superior corneal nerve parameters and neuroimmune tone in the corneal sub-basal nerve plexus. This study provides further evidence that metformin may be neuroprotective in diabetic peripheral neuropathy.</p><h3 data-test=\"abstract-sub-heading\">Graphical Abstract</h3>\u0000","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"7 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143570345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide association study identifying novel risk variants associated with glycaemic traits in the continental African AWI-Gen cohort","authors":"Vivien J. Chebii, Alisha N. Wade, Nigel J. Crowther, Engelbert A. Nonterah, Godfred Agongo, Z. Simayi, Palwende R. Boua, Isaac Kisiangani, Michèle Ramsay, Ananyo Choudhury, Dhriti Sengupta","doi":"10.1007/s00125-025-06395-6","DOIUrl":"https://doi.org/10.1007/s00125-025-06395-6","url":null,"abstract":"&lt;h3 data-test=\"abstract-sub-heading\"&gt;Aims/hypothesis&lt;/h3&gt;&lt;p&gt;Glycaemic traits such as high fasting glucose levels and insulin resistance are positively associated with the risk of type 2 diabetes and other cardiometabolic diseases. Genetic association studies have identified hundreds of associations for each glycaemic trait, yet very few studies have involved continental African populations. We report the results of genome-wide association studies (GWASs) in a pan-African cohort for four glycaemic traits, namely fasting glucose, fasting insulin, insulin resistance (HOMA-IR) and beta cell function (HOMA-B), which are quantitative variables that affect the risk of developing type 2 diabetes.&lt;/p&gt;&lt;h3 data-test=\"abstract-sub-heading\"&gt;Methods&lt;/h3&gt;&lt;p&gt;GWASs for the four traits were conducted in approximately 10,000 individuals from the Africa Wits-INDEPTH Partnership for Genomics Studies (AWI-Gen) cohort, with participants from Burkina Faso, Ghana, Kenya and South Africa. Association testing was performed using linear mixed models implemented in BOLT-LMM, with age, sex, BMI and principal components as covariates. Replication, fine mapping and functional annotation were performed using standard approaches.&lt;/p&gt;&lt;h3 data-test=\"abstract-sub-heading\"&gt;Results&lt;/h3&gt;&lt;p&gt;We identified a novel signal (rs574173815) in the intron of the ankyrin repeat domain 33B (&lt;i&gt;ANKRD33B&lt;/i&gt;) gene associated with fasting glucose, and a novel signal (rs114029796) in the intronic region of the WD repeat domain 7 (&lt;i&gt;WDR7&lt;/i&gt;) gene associated with fasting insulin. SNPs in &lt;i&gt;WDR7&lt;/i&gt; have been shown to be associated with type 2 diabetes. A variant (rs74806991) in the intron of ADAM metallopeptidase with thrombospondin type 1 motif 16 (&lt;i&gt;ADAMTS16&lt;/i&gt;) and another variant (rs6506934) in the β-1,4-galactosyltransferase 6 gene (&lt;i&gt;B4GALT6&lt;/i&gt;) are associated with HOMA-IR. Both &lt;i&gt;ADAMTS16&lt;/i&gt; and &lt;i&gt;B4GALT6&lt;/i&gt; are implicated in the development of type 2 diabetes. In addition, our study replicated several well-established fasting glucose signals in the &lt;i&gt;GCK-YTK6&lt;/i&gt;, &lt;i&gt;SLC2A2&lt;/i&gt; and &lt;i&gt;THORLNC&lt;/i&gt; gene regions.&lt;/p&gt;&lt;h3 data-test=\"abstract-sub-heading\"&gt;Conclusions/interpretation&lt;/h3&gt;&lt;p&gt;Our findings highlight the importance of performing GWASs for glycaemic traits in under-represented populations, especially continental African populations, to discover novel associated variants and broaden our knowledge of the genetic aetiology of glycaemic traits. The limited replication of well-known signals in this study hints at the possibility of a unique genetic architecture of these traits in African populations.&lt;/p&gt;&lt;h3 data-test=\"abstract-sub-heading\"&gt;Data availability&lt;/h3&gt;&lt;p&gt;The dataset used in this study is available in the European Genome–Phenome Archive (EGA) database (https://ega-archive.org/) under study accession code EGAS00001002482. The phenotype dataset accession code is EGAD00001006425 and the genotype dataset accession code is EGAD00010001996. The availability of these datasets is sub","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"25 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143526180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research and data sovereignty in genetically admixed populations. Reply to Zoller L, Kumar R and Lorenzo Bermejo J [letter].","authors":"Joseph Yracheta, Taylor Morriseau, Kali Dale, Ashlynn Gerth, Jonathan McGavock","doi":"10.1007/s00125-025-06400-y","DOIUrl":"https://doi.org/10.1007/s00125-025-06400-y","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}