DiabetologiaPub Date : 2025-07-22DOI: 10.1007/s00125-025-06494-4
Ananta Addala,Mcking I Amedari,Lauren E Figg,Osagie Ebekozien
{"title":"Disparities in access to and use of diabetes technologies and therapeutics: a narrative review.","authors":"Ananta Addala,Mcking I Amedari,Lauren E Figg,Osagie Ebekozien","doi":"10.1007/s00125-025-06494-4","DOIUrl":"https://doi.org/10.1007/s00125-025-06494-4","url":null,"abstract":"This narrative review applies neo-materialist theory to examine disparities in diabetes care across four domains: clinical trials, diabetes technology, immunotherapies and adjuvant digital technologies. Although systemic marginalisation can occur in many forms (e.g. based on ability, language, sex, gender or age), this review focuses on marginalisation based on race, ethnicity and socioeconomic status, as these are the key areas supported by the current evidence base. Under-representation of minoritised groups in clinical trials of diabetes interventions may limit the generalisability of the data generated. Contributing factors to under-representation include historical mistrust, exclusionary criteria and lack of cultural competence in research. Potential solutions to these disparities include revising trial protocols, engaging community partners and improving recruitment strategies; however, studies examining these solutions are limited. Disparities in access to diabetes technologies, such as continuous glucose monitoring and artificial pancreas systems, appear to be influenced by intersectional factors including race, ethnicity, socioeconomic status and insurance coverage. Despite awareness of these disparities, gaps in technology use persist because the causal pathways that determine these disparities are complex. Solutions are likely to involve education, improved access and policy reforms to address social and structural determinants of health. Disparities in access to immunotherapies, particularly in type 1 diabetes, may stem in part from under-representation of minoritised groups in research. Strategies to address these disparities include ensuring equitable access and performing inclusive data collection on social determinants of health. The digital divide in diabetes care is a key barrier to adjuvant digital technology use, with unequal access to smartphones, broadband and telemedicine. Bridging this gap will require improved infrastructure, increased access to digital tools and targeted telemedicine interventions to enhance care in underserved populations. Addressing these disparities requires comprehensive multifaceted strategies that recognise the complexity of structural inequities, including policy changes, improved technology access and inclusive research practices.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"673 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144684114","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}
DiabetologiaPub Date : 2025-07-22DOI: 10.1007/s00125-025-06482-8
Andrea O Y Luk,Yingnan Fan,Baoqi Fan,Edith W K Chow,Tony C K O
{"title":"Heterogeneity in the development of diabetes-related complications: narrative review of the roles of ancestry and geographical determinants.","authors":"Andrea O Y Luk,Yingnan Fan,Baoqi Fan,Edith W K Chow,Tony C K O","doi":"10.1007/s00125-025-06482-8","DOIUrl":"https://doi.org/10.1007/s00125-025-06482-8","url":null,"abstract":"The risk of developing diabetes-related complications is influenced by a combination of biological factors, clinical factors and social determinants of health that vary across countries and ethnic groups. Available evidence indicates that the incidence of diabetes-related complications is lower in high-income countries in Europe and North America, while other world regions have higher or variable incidence rates. By ethnicity, White individuals tend to have lower risks of most diabetes-related complications with the exception of coronary artery disease. In contrast, Black, East Asian and South Asian individuals have a greater propensity for most complications, notably chronic kidney disease and stroke. In general, ethnic groups that report a higher incidence of diabetes-related complications also exhibit a higher incidence of type 2 diabetes, particularly among younger age groups. Unique clinical phenotypes characterised by more severe insulin resistance and related comorbidities that drive both an earlier age of diabetes onset and manifestation of end-organ damage have been documented in several high-risk ethnic populations, but the genetic and epigenetic contributors have not been fully elucidated. Non-biological determinants, such as disparities in access to preventive care and the adoption of health-promoting behaviour, shaped by a combination of socioeconomic position, education and culture, are equally as significant as biological factors in influencing disease outcomes, if not more so. In this review we summarise the recent literature on the incidence of diabetes-related complications across countries and ethnic groups, highlighting current gaps in research. We provide perspectives on biological, clinical and social attributes as they relate to geographical and ethnic heterogeneity in the development of these complications. Finally, we discuss the effects of international migration on changing disease trajectories to emphasise the impact of environmental changes on the health of individuals with diabetes.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"18 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144684116","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":"Early induction of insulin sensitisation treated by tirzepatide: a prospective, single-arm, open-label study in Japanese individuals with obesity and type 2 diabetes.","authors":"Yuko Yamaguchi,Hitoshi Kuwata,Masahiro Imura,Shota Moyama,Ryota Usui,Mari Matsushiro,Yoshiyuki Hamamoto,Yuichiro Yamada,Yutaka Seino,Yuji Yamazaki","doi":"10.1007/s00125-025-06493-5","DOIUrl":"https://doi.org/10.1007/s00125-025-06493-5","url":null,"abstract":"AIMS/HYPOTHESISThis study investigated insulin sensitivity using the hyperinsulinaemic-euglycaemic clamp technique in individuals with obesity and type 2 diabetes treated with tirzepatide at the low dose of 5 mg over a 12-week treatment period.METHODSThis prospective, single-arm, open-label, single-centre study was conducted in obese individuals with type 2 diabetes. Participants received tirzepatide 2.5 mg once weekly for 4 weeks; the dose was then increased to 5 mg for the remaining 8 weeks. The primary outcome was change in the glucose infusion rate. Secondary outcomes were changes in HbA1c, body weight, body composition, lipid profile, glucagon level, the HOMA2-IR and HOMA2-%β indices, and the association of these variables with the glucose infusion rate (GIR).RESULTSSixteen participants completed the study. The GIR increased from 3.21 to 5.16 mg min-1 kg-1 (p<0.001). HbA1c decreased from 63.4 to 43.6 mmol/mol (7.95% to 6.14%, p<0.001) and body weight decreased by 4.9 kg (5.0%, p<0.001). Muscle mass, fat mass and fat percentage significantly decreased by 1.8%, 9.1% and 4.5%, respectively. Glucagon decreased significantly from 28.8 pg/ml to 20.8 pg/ml. However, simple linear regression analysis revealed no significant relationship between changes in GIR and other clinical variables.CONCLUSIONS/INTERPRETATIONTirzepatide significantly improves insulin sensitivity within 12 weeks, indicating an early metabolic effect that is not solely attributable to weight loss.TRIAL REGISTRATIONUMIN registration number: UMIN000056862.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"25 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144684115","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}
DiabetologiaPub Date : 2025-07-16DOI: 10.1007/s00125-025-06495-3
James Russ-Silsby,Milena Teles,Samar S Hassan,Nancy S Elbarbary,Cấn Thị Bích Ngọc,Elisa De Franco
{"title":"Global perspectives on monogenic forms of diabetes.","authors":"James Russ-Silsby,Milena Teles,Samar S Hassan,Nancy S Elbarbary,Cấn Thị Bích Ngọc,Elisa De Franco","doi":"10.1007/s00125-025-06495-3","DOIUrl":"https://doi.org/10.1007/s00125-025-06495-3","url":null,"abstract":"Monogenic forms of diabetes represent an uncommon but very heterogeneous subset of the disease, with variable associated clinical features and key differences in treatment options. In this review, we discuss how advances in precision medicine and genomic sequencing have enhanced our understanding of the aetiology and clinical variability of monogenic diabetes. We highlight current global challenges, including the over-representation of individuals of European genetic ancestry in research studies, which complicates diagnosis in non-European populations, and national disparities in genetic testing strategies, which influence diagnostic accuracy. Additionally, we address issues in variant interpretation stemming from the increased understanding of variable penetrance in monogenic diabetes and the need to expand current reference datasets to exclude common genetic variation. Finally, we explore future directions, including the potential benefits of ongoing genetic studies for under-represented populations, the benefits and potential pitfalls of newborn screening programmes, and the potential of stem cell-derived islet transplantation and glucagon-like peptide- 1 receptor agonists as treatments for some forms of monogenic diabetes.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"52 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639733","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}
DiabetologiaPub Date : 2025-07-15DOI: 10.1007/s00125-025-06487-3
Helene Nielsen,Fannie Lajeunesse-Trempe,Ai-Ling Lin,Maja H Nielsen,Bodil Hoffmeyer,Trine L J Larsen,Pierre Ayotte,Meera L Narayanan,Anne C B Thuesen,Torben Hansen,Michael L Pedersen,Marit E Jørgensen,Stine Byberg
{"title":"Societal and biological approaches to diabetes prevention and care for Inuit populations: a narrative review.","authors":"Helene Nielsen,Fannie Lajeunesse-Trempe,Ai-Ling Lin,Maja H Nielsen,Bodil Hoffmeyer,Trine L J Larsen,Pierre Ayotte,Meera L Narayanan,Anne C B Thuesen,Torben Hansen,Michael L Pedersen,Marit E Jørgensen,Stine Byberg","doi":"10.1007/s00125-025-06487-3","DOIUrl":"https://doi.org/10.1007/s00125-025-06487-3","url":null,"abstract":"The Inuit populations that inhabit the Arctic regions have adapted to survive in extreme conditions. However, recent societal changes and colonisation have led to rapid shifts in diet and physical activity, increasing the burden of chronic diseases, especially diabetes, in these regions. In addition, modern-day Inuit face significant challenges in accessing diabetes care and prevention and awareness programmes because of geographical isolation and fragmented healthcare services. This narrative review describes diabetes epidemiology in Inuit populations living in Canada, Alaska and Greenland and their genetic architecture, as well as the organisation of healthcare related to diabetes and interventions aimed at creating awareness and preventing the onset and complications of diabetes in these regions. Despite their shared genetic architecture, differences are observed across Inuit populations in Canada, Alaska and Greenland in diabetes prevalence and healthcare interventions, and especially in the organisation of diabetes healthcare. This narrative review highlights the importance of culturally sensitive healthcare interventions and comprehensive research and data collection that address the specific health needs of the Inuit. Integrating traditional knowledge with modern medical practices is essential for the development of effective, sustainable strategies for diabetes prevention and care for the Inuit living in the circumpolar Arctic regions.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"4 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639734","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":"Verapamil and low-dose anti-mouse thymocyte globulin combination therapy stably reverses recent-onset type 1 diabetes in NOD mice by acting on the beta cell and immune axes.","authors":"Laure Degroote,Pieter-Jan Martens,Marijke Viaene,Yves Heremans,Gunter Leuckx,Nick Geukens,Nico De Leu,Willem Staels,Chantal Mathieu,Conny Gysemans","doi":"10.1007/s00125-025-06490-8","DOIUrl":"https://doi.org/10.1007/s00125-025-06490-8","url":null,"abstract":"AIMS/HYPOTHESISVerapamil, a calcium channel blocker, and low doses of anti-thymocyte globulin (ATG) have individually shown efficacy in preserving beta cell function in people with recent-onset symptomatic type 1 diabetes (stage 3). We hypothesised that combining interventions with complementary modes of action and different targets would increase their efficacy in arresting beta cell demise and promoting disease recovery.METHODSContinuous administration of verapamil via drinking water, combined with a short course of low-dose rabbit-anti-mouse ATG (mATG), was studied in female recent-onset diabetic NOD mice for its potential to induce disease remission and mechanism of action.RESULTSVerapamil stably reversed diabetes in 3 out of 15 mice (20%) by day 56 after therapy start. Low-dose mATG reversed diabetes in 7 out of 18 mice (39%) by day 7 after therapy start, yet the effect waned to 3 out of 18 mice (17%) by day 56. The combination of verapamil with mATG induced durable diabetes reversal in 9 out of 20 mice (45%) by day 56, which was associated with preserved beta cell function, higher pancreatic insulin content and increased total beta cell volume with decreased severe insulitis. mATG, both alone and in combination, induced a temporary depletion of lymphocytes in peripheral blood on day 3 after therapy start, which largely recovered by day 14, when naive cells had shifted to a memory phenotype in both CD4+ and CD8+ T cells. Only in combination-treated mice was a higher CD4+ regulatory T cell to CD8+ effector memory T cell ratio observed in the pancreatic draining lymph nodes. The expression of the glucose-induced gene encoding thioredoxin-interacting protein (Txnip), a key regulator of beta cell apoptosis and dysfunction, was reduced in pancreatic beta cells in reversed mice, irrespective of whether they received verapamil or not.CONCLUSIONS/INTERPRETATIONThe combination of verapamil and low-dose mATG outperformed monotherapy in reversing recent-onset type 1 diabetes in NOD mice. This approach targets both the beta cell and immune axes, suggesting a promising strategy for disease reversal in human type 1 diabetes.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"23 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144612823","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}
DiabetologiaPub Date : 2025-07-10DOI: 10.1007/s00125-025-06466-8
Adam J Buckley,Garry D Tan,Marta Gruszka-Goh,Peter H Scanlon,Imran Ansari,Sara G I Suliman
{"title":"Early worsening of diabetic retinopathy in individuals with type 2 diabetes treated with tirzepatide: a real-world cohort study.","authors":"Adam J Buckley,Garry D Tan,Marta Gruszka-Goh,Peter H Scanlon,Imran Ansari,Sara G I Suliman","doi":"10.1007/s00125-025-06466-8","DOIUrl":"https://doi.org/10.1007/s00125-025-06466-8","url":null,"abstract":"AIMS/HYPOTHESISEarly worsening of diabetic retinopathy (EWDR) has been described during treatment with glucagon-like peptide-1 receptor agonists including subcutaneous semaglutide. Whether EWDR occurs after initiating treatment with the potent glucagon-like peptide 1 / gastric inhibitory polypeptide receptor agonist tirzepatide is unknown.METHODSIn this retrospective cohort study using real-world clinical data, we matched 3435 tirzepatide-exposed (≥180 days treatment) individuals with type 2 diabetes 1:1 with 3434 tirzepatide-unexposed individuals for sex, diabetes duration, retinopathy status, HbA1c, number of retinal screening episodes and use of glucose-lowering medications. New-onset diabetic retinopathy and retinopathy progression were explored using conditional logistic regression.RESULTSIndividuals included in the study had tight baseline glycaemic control (mean HbA1c 56.1 ± 15.8 mmol/mol [7.28 ± 1.43%]). New-onset proliferative diabetic retinopathy (PDR) (grade R3M0, R3M1) occurred in 1.1% of tirzepatide-exposed (n=33) and 0.5% of tirzepatide-unexposed (n=17) individuals. Tirzepatide was significantly associated with new-onset PDR in multivariate analysis after adjustment for established risk factors (OR 2.15 [95% CI 1.24, 3.74], p<0.01). However, tirzepatide was also associated with reduced odds of new onset of retinopathy (OR 0.73 [95% CI 0.62, 0.86], p<0.001) in individuals without diabetic retinopathy (R0M0) at initiation in multivariate analysis, and was not significantly associated with retinopathy progression in individuals with mild non-proliferative diabetic retinopathy (NPDR, grade R1M0 or R1M1).CONCLUSIONS/INTERPRETATIONTirzepatide therapy resulted in significantly increased odds of incident PDR, particularly in individuals with mild NPDR with maculopathy (grade R1M1), or moderate-to-severe NPDR with or without maculopathy (grade R2M0, R2M1). The increase in odds of progression would justify specialist ophthalmologist referral by Early Treatment Diabetic Retinopathy Study (ETDRS) criteria.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"28 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594099","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}
DiabetologiaPub Date : 2025-07-09DOI: 10.1007/s00125-025-06489-1
Michael Roden
{"title":"In Memoriam Werner Waldhäusl, 27 September 1937-22 May 2025.","authors":"Michael Roden","doi":"10.1007/s00125-025-06489-1","DOIUrl":"https://doi.org/10.1007/s00125-025-06489-1","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"694 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586668","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}
DiabetologiaPub Date : 2025-07-09DOI: 10.1007/s00125-025-06481-9
Andreas Gübeli,Nicole Steiner,Andreas Limacher,Déborah Mathis,Andreas Melmer,Markus Laimer
{"title":"Dapagliflozin's impact on hormonal regulation and ketogenesis in type 1 diabetes: a randomised controlled crossover trial.","authors":"Andreas Gübeli,Nicole Steiner,Andreas Limacher,Déborah Mathis,Andreas Melmer,Markus Laimer","doi":"10.1007/s00125-025-06481-9","DOIUrl":"https://doi.org/10.1007/s00125-025-06481-9","url":null,"abstract":"AIMS/HYPOTHESISThis study aimed to assess the impact of adding dapagliflozin to insulin therapy on key hormonal determinants of glucose regulation and ketogenesis. We hypothesise that dapagliflozin increases glucagon-like peptide 1 (GLP-1), glucagon and ketone body concentrations, based on the results of a pilot study.METHODSThe study was designed as a randomised, placebo-controlled, open-label, crossover intervention study with two periods (dapagliflozin and placebo intake), including patients of the Department of Diabetes, Endocrinology, Clinical Nutrition & Metabolism, Inselspital, Bern University Hospital, University of Bern. Individuals with type 1 diabetes (C-peptide concentrations <0.1 nmol/l) with a duration >5 years and a BMI of 20-29 kg/m2 were included. They received 10 mg of dapagliflozin or placebo daily for 7 days throughout two independent treatment periods, separated by a 14 day washout period. Allocation was done by a computed randomisation tool (REDCap), without blinding of the participants or the investigators. On day 7 of each treatment period, hyperinsulinaemic-euglycaemic clamps (HECs) and OGTT clamps (OGTTCs) were performed to assess changes in the secretion of GLP-1, glucagon, somatostatin and total ketone bodies. The objective was to evaluate the effects of adding the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin to insulin therapy on GLP-1 during OGTTC (primary endpoint), GLP-1 secretion during HEC, and glucagon, somatostatin and ketogenesis during OGTTC and HEC (secondary endpoints). The primary endpoint was concentrations of GLP-1 during OGTTC. Secondary endpoints included GLP-1 during HEC and glucagon, somatostatin and ketone body concentrations during OGTTC and HEC.RESULTSA total of 13 individuals with type 1 diabetes were included and randomised. All of them received dapagliflozin and placebo, finished the sequences per protocol and were analysed per protocol. GLP-1 concentrations did not differ significantly between treatments in the OGTTC (median [IQR] dapagliflozin 192.8 [129.8-257.2] pmol/l vs placebo 176.3 [138.4-227.4] pmol/l; p=0.7) or HEC (median [IQR] dapagliflozin 208.6 [133.6-294.0] pmol/l vs placebo 203.1 [150.2-291.8] pmol/l; p=0.7). Glucagon concentrations did not significantly differ between treatments in the OGTTC (median [IQR] dapagliflozin 1.54 [0.84-3.68] ng/l vs placebo 1.54 [0.82-4.64] ng/l; p=0.8) or HEC (median [IQR] dapagliflozin 1.59 [0.87-3.54] ng/l vs placebo 1.63 [0.91-3.96] ng/l; p=0.3). Somatostatin concentrations remained comparable between treatments during the HEC (median [IQR] dapagliflozin 41.1 [26.8-73.8] pmol/l vs placebo 47.0 [23.0-77.6] pmol/l; p=0.2) and OGTTC (median [IQR] dapagliflozin 51.1 [31.1-77.0] pmol/l vs placebo 45.3 [30.0-70.5] pmol/l; p=0.2). Plasma ketone bodies were higher with dapagliflozin during the HEC (median [IQR] dapagliflozin 0.15 [0.04-0.47] mmol/l vs placebo 0.03 [0.01-0.12] mmol/l; p<0.001) and OGTTC (median [IQR] dapagliflozin 0.10 [0","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"17 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586671","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}
DiabetologiaPub Date : 2025-07-08DOI: 10.1007/s00125-025-06472-w
Christian Herder,Anna Zhu,Andreas Schmitt,Maria C Spagnuolo,Bernhard Kulzer,Michael Roden,Dominic Ehrmann,Norbert Hermanns
{"title":"Biomarkers of inflammation and improvement in depressive symptoms in type 1 and type 2 diabetes: differential associations with depressive symptom clusters.","authors":"Christian Herder,Anna Zhu,Andreas Schmitt,Maria C Spagnuolo,Bernhard Kulzer,Michael Roden,Dominic Ehrmann,Norbert Hermanns","doi":"10.1007/s00125-025-06472-w","DOIUrl":"https://doi.org/10.1007/s00125-025-06472-w","url":null,"abstract":"AIMS/HYPOTHESISPeople with diabetes and depression show large heterogeneity in their response to depression treatment. This study aimed to identify biomarkers of subclinical inflammation that were associated with improvement of depressive symptoms in people with type 1 diabetes and type 2 diabetes.METHODSThe prospective analysis combined data from three studies (DIAMOS, ECCE HOMO and DDCT). A total of 332 people with type 1 diabetes and 189 people with type 2 diabetes completed both the baseline and 1 year follow-up examinations. Depressive symptoms were assessed using the Center for Epidemiological Studies depression scale (CES-D). Associations between baseline serum levels of 76 biomarkers of inflammation and 1 year changes in depressive symptoms were estimated using multiple linear regression.RESULTSIn people with type 2 diabetes, higher levels of 26 biomarkers were associated with greater reductions in depressive symptoms (β=0.128 to 0.255; p<0.05), whereas in people with type 1 diabetes, higher levels of 13 biomarkers were linked with lower reductions in depressive symptoms (β=-0.189 to -0.094; p<0.05). A significant effect modification was observed for 33 biomarkers (pinteraction<0.05). The positive associations in type 2 diabetes were strongest for improvements in cognitive-affective and anhedonia symptoms, while the inverse associations in type 1 diabetes were strongest for improvements in somatic symptoms.CONCLUSIONS/INTERPRETATIONHigher baseline levels of multiple biomarkers of inflammation were associated with greater depression reduction in type 2 diabetes but lower depression reduction in type 1 diabetes. There were also diabetes type-specific differences in the associations with symptom clusters of depression. This suggests that different inflammation-related pathways may be relevant for the response to depression treatment in people with type 1 diabetes or type 2 diabetes.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"3 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144578721","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}