Pub Date : 2025-11-08DOI: 10.1007/s00125-025-06573-6
Salla Kuusela, Jaakko J. Koskenniemi, Toni Valtanen, Tytti Pokka, Taina Härkönen, Jorma Ilonen, Johanna Lempainen, Anni Kyrönniemi, Jorma Toppari, Mikael Knip, Päivi Keskinen, Riitta Veijola
Aims/hypothesis Islet autoimmunity during presymptomatic type 1 diabetes is heterogeneous. We hypothesised that a positive family history of type 1 diabetes is associated with specific characteristics of the autoimmune process resulting in clinical diabetes. In a prospective birth cohort study, we compared the initiation and evolution of islet autoimmunity and the rate of progression from islet autoimmunity to diabetes between children with and without a first-degree relative (FDR) with type 1 diabetes. Methods In the Finnish Type 1 Diabetes Prediction and Prevention (DIPP) study, we prospectively followed children with HLA-conferred susceptibility from birth for the appearance of islet autoantibodies (IAA, GADA, IA-2A, ZnT8A), further development of islet autoimmunity, and progression to clinical diabetes. The presence of type 1 diabetes among their FDRs was recorded at the time of birth, and the family history data was updated during the follow-up period. Results Among a total of 1334 children with confirmed positivity for at least one islet autoantibody, 145 (10.9%) had one or more FDRs with type 1 diabetes at the time of birth (FDR+). During a median follow-up period of 8.6 years, FDRs of an additional 87 children developed type 1 diabetes (FDR− FDR+). At seroconversion, both FDR+ and FDR− FDR+ children were significantly more often positive for GADA and multiple autoantibodies than children without affected FDRs (FDR−). The seroconversion age was similar between the three groups (median 2.7 vs 2.1 vs 3.0 years in FDR+, FDR− FDR+ and FDR− children, respectively). During the follow-up period, FDR+ and FDR− FDR+ children more often had IAA, GADA, IA-2A and multiple autoantibodies than FDR− children, and progressed more frequently to diabetes (55.9 vs 57.5 vs 38.9%, respectively). Time from seroconversion to clinical diabetes was significantly shorter in FDR+ children compared with FDR− children (2.7 vs 3.6 years). Children with paternal type 1 diabetes at birth ( n =71; i.e., the father had type 1 diabetes) were twice as often positive for multiple autoantibodies at seroconversion as those with maternal type 1 diabetes ( n =50; i.e. the mother had type 1 diabetes) (39.4% vs 20.0%). Conclusions/interpretation At seroconversion, genetically susceptible children who had one or more FDRs with type 1 diabetes, especially an affected father, were more often positive for GADA and multiple islet autoantibodies. During the follow-up period, children with an affected FDR were more often positive for IAA, GADA and IA-2A, and progressed to clinical type 1 diabetes more often and faster than children without an affected FDR. These data should be considered when designing intervention and screening studies. Graphical
目的/假设症状前1型糖尿病患者的胰岛自身免疫是异质性的。我们假设阳性的1型糖尿病家族史与导致临床糖尿病的自身免疫过程的特定特征相关。在一项前瞻性出生队列研究中，我们比较了患有和没有一级亲属（FDR）患有1型糖尿病的儿童的胰岛自身免疫的发生和进化，以及从胰岛自身免疫到糖尿病的进展速度。方法在芬兰1型糖尿病预测和预防（DIPP）研究中，我们前瞻性地跟踪了从出生开始就具有hla敏感性的儿童胰岛自身抗体（IAA， GADA, IA-2A, ZnT8A）的出现，胰岛自身免疫的进一步发展以及临床糖尿病的进展。他们的fdr在出生时被记录1型糖尿病的存在，并在随访期间更新家族史数据。结果在1334例至少一种胰岛自身抗体阳性的患儿中，145例（10.9%）出生时伴有1型糖尿病的FDR （FDR+）。在8.6年的中位随访期间，另外87名FDR儿童发展为1型糖尿病（FDR−FDR+）。在血清转换中，FDR+和FDR - FDR+儿童的GADA和多种自身抗体阳性明显高于未受FDR影响的儿童（FDR -）。三组之间的血清转换年龄相似（FDR+、FDR - FDR+和FDR -儿童的中位年龄分别为2.7年、2.1年和3.0年）。在随访期间，FDR+和FDR - FDR+儿童比FDR -儿童更容易出现IAA、GADA、IA-2A和多种自身抗体，并且更容易发展为糖尿病（分别为55.9%、57.5%和38.9%）。与FDR -儿童相比，FDR+儿童从血清转换到临床糖尿病的时间明显更短（2.7年vs 3.6年）。出生时父亲患有1型糖尿病的儿童（n =71，即父亲患有1型糖尿病）在血清转换中多种自身抗体阳性的几率是母亲患有1型糖尿病的儿童（n =50，即母亲患有1型糖尿病）的两倍（39.4% vs 20.0%）。结论/解释在血清转换时，患有1型糖尿病的一个或多个fdr的遗传易感儿童，特别是受影响的父亲，GADA和多种胰岛自身抗体更常呈阳性。在随访期间，受影响的FDR患儿的IAA、GADA和IA-2A阳性发生率高于未受影响的FDR患儿，且进展为临床1型糖尿病的发生率和速度高于未受影响的FDR患儿。在设计干预和筛查研究时应考虑这些数据。图形化的
{"title":"Islet autoimmunity and progression to type 1 diabetes in the Finnish DIPP study: comparison between genetically susceptible children with and without an affected first-degree relative","authors":"Salla Kuusela, Jaakko J. Koskenniemi, Toni Valtanen, Tytti Pokka, Taina Härkönen, Jorma Ilonen, Johanna Lempainen, Anni Kyrönniemi, Jorma Toppari, Mikael Knip, Päivi Keskinen, Riitta Veijola","doi":"10.1007/s00125-025-06573-6","DOIUrl":"https://doi.org/10.1007/s00125-025-06573-6","url":null,"abstract":"Aims/hypothesis Islet autoimmunity during presymptomatic type 1 diabetes is heterogeneous. We hypothesised that a positive family history of type 1 diabetes is associated with specific characteristics of the autoimmune process resulting in clinical diabetes. In a prospective birth cohort study, we compared the initiation and evolution of islet autoimmunity and the rate of progression from islet autoimmunity to diabetes between children with and without a first-degree relative (FDR) with type 1 diabetes. Methods In the Finnish Type 1 Diabetes Prediction and Prevention (DIPP) study, we prospectively followed children with HLA-conferred susceptibility from birth for the appearance of islet autoantibodies (IAA, GADA, IA-2A, ZnT8A), further development of islet autoimmunity, and progression to clinical diabetes. The presence of type 1 diabetes among their FDRs was recorded at the time of birth, and the family history data was updated during the follow-up period. Results Among a total of 1334 children with confirmed positivity for at least one islet autoantibody, 145 (10.9%) had one or more FDRs with type 1 diabetes at the time of birth (FDR+). During a median follow-up period of 8.6 years, FDRs of an additional 87 children developed type 1 diabetes (FDR− FDR+). At seroconversion, both FDR+ and FDR− FDR+ children were significantly more often positive for GADA and multiple autoantibodies than children without affected FDRs (FDR−). The seroconversion age was similar between the three groups (median 2.7 vs 2.1 vs 3.0 years in FDR+, FDR− FDR+ and FDR− children, respectively). During the follow-up period, FDR+ and FDR− FDR+ children more often had IAA, GADA, IA-2A and multiple autoantibodies than FDR− children, and progressed more frequently to diabetes (55.9 vs 57.5 vs 38.9%, respectively). Time from seroconversion to clinical diabetes was significantly shorter in FDR+ children compared with FDR− children (2.7 vs 3.6 years). Children with paternal type 1 diabetes at birth ( <jats:italic>n</jats:italic> =71; i.e., the father had type 1 diabetes) were twice as often positive for multiple autoantibodies at seroconversion as those with maternal type 1 diabetes ( <jats:italic>n</jats:italic> =50; i.e. the mother had type 1 diabetes) (39.4% vs 20.0%). Conclusions/interpretation At seroconversion, genetically susceptible children who had one or more FDRs with type 1 diabetes, especially an affected father, were more often positive for GADA and multiple islet autoantibodies. During the follow-up period, children with an affected FDR were more often positive for IAA, GADA and IA-2A, and progressed to clinical type 1 diabetes more often and faster than children without an affected FDR. These data should be considered when designing intervention and screening studies. Graphical","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"5 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145461273","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}
Pub Date : 2025-11-07DOI: 10.1007/s00125-025-06585-2
Anders N. Ø. Schultz, Robin Christensen, Georg Bollig, Kristian Kidholm, Frans Brandt
Aims/hypothesis The aim of this work was to assess the effect of video consultations over 1 year compared with usual care for patients with type 1 diabetes treated with insulin pumps, with time in range (TiR) as the primary outcome measure. Methods We carried out a 52 week, open label, randomised, controlled superiority trial including adult type 1 diabetes patients treated with insulin pumps. Participants were recruited from the Hospital of Southern Jutland and were adult patients, diagnosed with type 1 diabetes mellitus who had used an insulin pump for at least 6 months. Participants were randomised to video consultations (intervention) or physical consultations (control) using a computer-generated block randomisation sequence in a 1:1 allocation, stratified for sensor type (continuous glucose monitor and flash glucose monitor, respectively).Since this was an ‘open-label’ trial, neither the healthcare professionals providing the treatment nor the participants were blinded to allocation after randomisation. The primary outcome measure was the percentage of TiR (glucose levels 3.9–10.0 mmol/l) from week 51 to 52, measured by continuous glucose monitoring. Continuous endpoints were analysed using ANCOVA, with randomised treatment and stratification groups as fixed effects and the baseline value as a covariate. Missing data in the intention-to-treat (ITT) population were addressed using multiple imputation. Results Of the 76 randomised participants (ITT population, 38 per group, median age 49 years, 51% women), 32 participants in the intervention group and 31 in the control group completed the study. Least square means TiR at 1 year was 64.3% in the video group and 63.5% in the control group, with a clinically insignificant difference of 0.8 percentage points (95% CI −5.3, 6.9; p =0.25). For secondary outcomes, the video group was superior in terms of treatment satisfaction and reduction in HbA 1c . However, the video group experienced an inferior impact on quality of life. Conclusions/interpretation Video consultations did not significantly improve the primary endpoint. However, compared with control, the intervention was associated with superior treatment satisfaction and a favourable effect on HbA 1c , albeit with an inferior impact on quality of life. Trial registration ClinicalTrials.gov NCT04612933 Funding The study received funding from Knud and Edith Eriksens Mindefond. The Section for Biostatistics and Evidence-Based Research, the Parker Institute, Bispebjerg and Frederiksberg Hospital is supported by a core grant from the Oak Foundation. Graphical
目的/假设本研究的目的是以时间范围（TiR）为主要结局指标，评估1年以上视频会诊与常规治疗对1型糖尿病患者胰岛素泵治疗的效果。方法我们开展了一项为期52周、开放标签、随机、对照的优势试验，纳入了接受胰岛素泵治疗的成人1型糖尿病患者。参与者从南日德兰医院招募，均为诊断为1型糖尿病且使用胰岛素泵至少6个月的成年患者。参与者被随机分配到视频咨询（干预）或物理咨询（对照组），使用计算机生成的块随机化序列，按1:1分配，按传感器类型分层（分别为连续血糖监测仪和闪烁血糖监测仪）。由于这是一项“开放标签”试验，提供治疗的医疗保健专业人员和参与者在随机化后都没有对分配进行盲法。主要结局指标为第51周至第52周的TiR百分比（葡萄糖水平3.9-10.0 mmol/l），通过连续血糖监测测量。使用ANCOVA分析连续终点，随机化治疗和分层组作为固定效应，基线值作为协变量。在意向治疗（ITT）人群中缺失的数据使用多重输入处理。结果76名随机参与者（ITT人群，每组38人，中位年龄49岁，51%为女性），干预组32名参与者和对照组31名参与者完成研究。视频组1年的最小二乘平均TiR为64.3%，对照组为63.5%，临床差异无统计学意义（95% CI−5.3,6.9;p =0.25）。对于次要结果，视频组在治疗满意度和降低HbA 1c方面优于对照组。然而，录像组对生活质量的影响较低。视频咨询并没有显著改善主要终点。然而，与对照组相比，干预与更高的治疗满意度和对HbA 1c的有利影响相关，尽管对生活质量的影响较低。本研究由Knud and Edith Eriksens Mindefond资助。帕克研究所、比斯堡和腓特烈斯堡医院的生物统计和循证研究科得到橡树基金会核心赠款的支持。图形化的
{"title":"Effectiveness of video consultations in type 1 diabetes patients treated with insulin pumps in the outpatient clinic: a randomised controlled trial","authors":"Anders N. Ø. Schultz, Robin Christensen, Georg Bollig, Kristian Kidholm, Frans Brandt","doi":"10.1007/s00125-025-06585-2","DOIUrl":"https://doi.org/10.1007/s00125-025-06585-2","url":null,"abstract":"Aims/hypothesis The aim of this work was to assess the effect of video consultations over 1 year compared with usual care for patients with type 1 diabetes treated with insulin pumps, with time in range (TiR) as the primary outcome measure. Methods We carried out a 52 week, open label, randomised, controlled superiority trial including adult type 1 diabetes patients treated with insulin pumps. Participants were recruited from the Hospital of Southern Jutland and were adult patients, diagnosed with type 1 diabetes mellitus who had used an insulin pump for at least 6 months. Participants were randomised to video consultations (intervention) or physical consultations (control) using a computer-generated block randomisation sequence in a 1:1 allocation, stratified for sensor type (continuous glucose monitor and flash glucose monitor, respectively).Since this was an ‘open-label’ trial, neither the healthcare professionals providing the treatment nor the participants were blinded to allocation after randomisation. The primary outcome measure was the percentage of TiR (glucose levels 3.9–10.0 mmol/l) from week 51 to 52, measured by continuous glucose monitoring. Continuous endpoints were analysed using ANCOVA, with randomised treatment and stratification groups as fixed effects and the baseline value as a covariate. Missing data in the intention-to-treat (ITT) population were addressed using multiple imputation. Results Of the 76 randomised participants (ITT population, 38 per group, median age 49 years, 51% women), 32 participants in the intervention group and 31 in the control group completed the study. Least square means TiR at 1 year was 64.3% in the video group and 63.5% in the control group, with a clinically insignificant difference of 0.8 percentage points (95% CI −5.3, 6.9; <jats:italic>p</jats:italic> =0.25). For secondary outcomes, the video group was superior in terms of treatment satisfaction and reduction in HbA <jats:sub>1c</jats:sub> . However, the video group experienced an inferior impact on quality of life. Conclusions/interpretation Video consultations did not significantly improve the primary endpoint. However, compared with control, the intervention was associated with superior treatment satisfaction and a favourable effect on HbA <jats:sub>1c</jats:sub> , albeit with an inferior impact on quality of life. Trial registration ClinicalTrials.gov NCT04612933 Funding The study received funding from Knud and Edith Eriksens Mindefond. The Section for Biostatistics and Evidence-Based Research, the Parker Institute, Bispebjerg and Frederiksberg Hospital is supported by a core grant from the Oak Foundation. Graphical","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"1 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145455460","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}
Pub Date : 2025-11-07DOI: 10.1007/s00125-025-06587-0
Stine Smedegaard, Nikolaj Rittig, Per G. Ovesen, Louise B. Suder, Janni H. Knudsen, Lise H. Brunsgaard, Ulla Kampmann
Aims/hypothesis This study aimed to investigate how pre-meal whey protein (WP) supplementation throughout the third trimester of pregnancy affects glycaemic and metabolic outcomes in women with gestational diabetes mellitus (GDM). The hypothesis was that WP, when administered as a pre-meal 30 min before breakfast daily, lowers glycaemic variability (primary outcome: CV%). Methods In a double-blinded, randomised, placebo-controlled, parallel trial, 62 women with GDM were randomised to receive 20 g WP isolate/day or placebo 30 min before breakfast throughout the third trimester. Participants were randomly assigned ( <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://www.randomiser.org" ext-link-type="uri">www.randomiser.org</jats:ext-link> ) to WP or placebo using a computer-generated list. Allocation was concealed with sealed strips. Participants, caregivers, investigators and outcome assessors were masked, except the dietitian providing dietary guidance. Eligibility criteria included GDM, normotension and age ≥18 years. Exclusion criteria included special dietary regimens ≥1 month, daily protein supplements, food allergies, glucose-metabolism-affecting drugs, twin pregnancies, polycystic ovary syndrome, severe comorbidity, hyperemesis or non-breakfast eaters. The study included laboratory visits, home-based measurements under controlled-living and free-living conditions during the early and late third trimester, and follow-up at delivery. Glucose levels were assessed using continuous glucose monitoring. Results A total of 29 women were randomised to placebo and 33 were randomised to WP, with 25 in the placebo group and 30 women in the WP group completing the study. In the WP group, the 1 h postprandial glucose following breakfast was −20% (95% CI −28%, −11%) lower in the early and −15% (95% CI −24%, −5%) lower in the late third trimester compared with the placebo group under controlled conditions. Similarly, the 1 h postprandial glucose was −14% (95% CI −23%, −4%) lower in the early and −8% (95% CI −18%, 3%) lower in the late third trimester under free-living conditions. Glycaemic variability was lower in the WP group under controlled-living conditions. The mean amplitude of glycaemic excursions (MAGE) was lower during both the early and late third trimester, and the SD and CV% were lower during the early third trimester (all <jats:italic>p</jats:italic> <0.05). Time in range (proportion of time spent with glucose levels 3.5–7.8 mmol/l) was lower during free-living in the late third trimester ( <jats:italic>p</jats:italic> =0.05). Conclusions/interpretation Pre-meal WP improves glycaemic management and reduces glucose variability in women with GDM under controlled-living and free-living conditions. Future research should evaluate whether WP can delay or prevent pharmacological treatments such as insulin initiation. Trial registration ClinicalTrials.gov NCT04767880 Funding Department of Clinical Medicine, Aarhus Univer
目的/假设本研究旨在探讨妊娠晚期补充餐前乳清蛋白（WP）如何影响妊娠期糖尿病（GDM）妇女的血糖和代谢结局。假设是，每日早餐前30分钟服用白蛋白可降低血糖变异性（主要结局：CV%）。方法在一项双盲、随机、安慰剂对照、平行试验中，62名GDM妇女在妊娠晚期随机分为每天20 g分离WP或早餐前30分钟安慰剂两组。参与者使用计算机生成的列表随机分配（www.randomiser.org）到WP或安慰剂组。分配用密封条隐藏。除了提供饮食指导的营养师外，参与者、护理人员、调查人员和结果评估人员均被掩盖。入选标准包括GDM、血压正常、年龄≥18岁。排除标准包括特殊饮食方案≥1个月、每日补充蛋白质、食物过敏、影响葡萄糖代谢的药物、双胎妊娠、多囊卵巢综合征、严重合并症、呕吐或不吃早餐。该研究包括实验室访问，在妊娠早期和晚期的控制生活和自由生活条件下的家庭测量，以及分娩时的随访。采用连续血糖监测评估血糖水平。结果共有29名妇女被随机分配到安慰剂组，33名妇女被随机分配到WP组，其中25名妇女在安慰剂组，30名妇女在WP组完成研究。在对照条件下，与安慰剂组相比，WP组早餐后1小时的餐后血糖在妊娠早期降低了- 20% (95% CI - 28%, - 11%)，在妊娠晚期降低了- 15% （95% CI - 24%, - 5%）。同样，在自由生活条件下，早期1小时餐后血糖降低- 14% (95% CI - 23%, - 4%)，晚期低- 8% （95% CI - 18%, 3%）。在控制生活条件下，WP组的血糖变异性较低。妊娠早期和晚期血糖漂移（MAGE）平均振幅较低，妊娠早期SD和CV%较低（均p <；0.05）。在妊娠晚期自由生活期间，在范围内的时间（葡萄糖水平为3.5-7.8 mmol/l的时间所占比例）较低（p =0.05）。餐前WP改善了控制生活和自由生活条件下GDM女性的血糖管理并降低了血糖变异性。未来的研究应评估白粉病是否可以延迟或阻止胰岛素启动等药物治疗。试验注册ClinicalTrials.gov NCT04767880奥胡斯大学临床医学部和Arla食品配料集团P/S （Agr-2020-731-12107）。图形化的
{"title":"Once-daily supplementation with pre-meal whey protein lowers breakfast postprandial glucose levels in women with GDM throughout the third trimester: a randomised, controlled, clinical trial","authors":"Stine Smedegaard, Nikolaj Rittig, Per G. Ovesen, Louise B. Suder, Janni H. Knudsen, Lise H. Brunsgaard, Ulla Kampmann","doi":"10.1007/s00125-025-06587-0","DOIUrl":"https://doi.org/10.1007/s00125-025-06587-0","url":null,"abstract":"Aims/hypothesis This study aimed to investigate how pre-meal whey protein (WP) supplementation throughout the third trimester of pregnancy affects glycaemic and metabolic outcomes in women with gestational diabetes mellitus (GDM). The hypothesis was that WP, when administered as a pre-meal 30 min before breakfast daily, lowers glycaemic variability (primary outcome: CV%). Methods In a double-blinded, randomised, placebo-controlled, parallel trial, 62 women with GDM were randomised to receive 20 g WP isolate/day or placebo 30 min before breakfast throughout the third trimester. Participants were randomly assigned ( <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://www.randomiser.org\" ext-link-type=\"uri\">www.randomiser.org</jats:ext-link> ) to WP or placebo using a computer-generated list. Allocation was concealed with sealed strips. Participants, caregivers, investigators and outcome assessors were masked, except the dietitian providing dietary guidance. Eligibility criteria included GDM, normotension and age ≥18 years. Exclusion criteria included special dietary regimens ≥1 month, daily protein supplements, food allergies, glucose-metabolism-affecting drugs, twin pregnancies, polycystic ovary syndrome, severe comorbidity, hyperemesis or non-breakfast eaters. The study included laboratory visits, home-based measurements under controlled-living and free-living conditions during the early and late third trimester, and follow-up at delivery. Glucose levels were assessed using continuous glucose monitoring. Results A total of 29 women were randomised to placebo and 33 were randomised to WP, with 25 in the placebo group and 30 women in the WP group completing the study. In the WP group, the 1 h postprandial glucose following breakfast was −20% (95% CI −28%, −11%) lower in the early and −15% (95% CI −24%, −5%) lower in the late third trimester compared with the placebo group under controlled conditions. Similarly, the 1 h postprandial glucose was −14% (95% CI −23%, −4%) lower in the early and −8% (95% CI −18%, 3%) lower in the late third trimester under free-living conditions. Glycaemic variability was lower in the WP group under controlled-living conditions. The mean amplitude of glycaemic excursions (MAGE) was lower during both the early and late third trimester, and the SD and CV% were lower during the early third trimester (all <jats:italic>p</jats:italic> <0.05). Time in range (proportion of time spent with glucose levels 3.5–7.8 mmol/l) was lower during free-living in the late third trimester ( <jats:italic>p</jats:italic> =0.05). Conclusions/interpretation Pre-meal WP improves glycaemic management and reduces glucose variability in women with GDM under controlled-living and free-living conditions. Future research should evaluate whether WP can delay or prevent pharmacological treatments such as insulin initiation. Trial registration ClinicalTrials.gov NCT04767880 Funding Department of Clinical Medicine, Aarhus Univer","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"92 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145461272","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}
Pub Date : 2025-11-07DOI: 10.1007/s00125-025-06597-y
Nefeli M. Dimitropoulou, Magdalena Beran, Simone J. P. M. Eussen, Cassy F. Dingena, Pieter C. Dagnelie, Carla J. H. van der Kallen, Annemarie Koster, Marleen M. J. van Greevenbroek, Martijn C. G. J. Brouwers, Miranda T. Schram, Bastiaan E. de Galan
{"title":"Liver fat content is not elevated in people with type 1 diabetes: the Maastricht Study","authors":"Nefeli M. Dimitropoulou, Magdalena Beran, Simone J. P. M. Eussen, Cassy F. Dingena, Pieter C. Dagnelie, Carla J. H. van der Kallen, Annemarie Koster, Marleen M. J. van Greevenbroek, Martijn C. G. J. Brouwers, Miranda T. Schram, Bastiaan E. de Galan","doi":"10.1007/s00125-025-06597-y","DOIUrl":"https://doi.org/10.1007/s00125-025-06597-y","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"20 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145455426","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}
Pub Date : 2025-11-06DOI: 10.1007/s00125-025-06586-1
Stephen E. Gitelman, Kimber Simmons, Jennifer L. Sherr, Steven B. Leichter, Teresa Quattrin, William E. Russell, Bhuvana Sunil, Steven M. Willi, Laura A. Knecht, Elisabeth Niemoeller, Idlir Licaj, Wolfgang Schmider, Diana Miller, Linda A. DiMeglio
Aims/hypothesis Teplizumab is approved in the USA and seven other countries to delay stage 3 type 1 diabetes onset in individuals ≥8 years of age with stage 2 type 1 diabetes. As part of a US Food and Drug Administration post-marketing requirement, this study evaluated the safety, tolerability and pharmacokinetics of teplizumab in children aged <8 years with stage 2 type 1 diabetes. Methods The PETITE-T1D trial is a 2 year single-arm, open-label, multicentre study of 23 children <8 years of age with stage 2 type 1 diabetes. Participants received a 14 day teplizumab course. A prespecified interim analysis was performed after 15 participants completed 1 year of follow-up and included all 23 participants. Primary endpoints included treatment-emergent adverse events (TEAEs), TEAEs causing treatment discontinuation, and serious adverse events (SAEs). Other endpoints assessed immunogenicity, pharmacokinetics, pharmacodynamics and time from study treatment to stage 3 type 1 diabetes. Results Mean participant age was 4.8 years (range 1.7–6.8). Median follow-up duration was 51.9 weeks (range 3.9–77.1). All participants experienced one or more TEAE, with most being mild to moderate. No grade 4 or 5 TEAEs were reported. Three participants (13%) had TEAEs leading to teplizumab discontinuation: anaemia, elevated liver enzymes and maculo-papular rash. Two participants (9%) each had two SAEs. Serum teplizumab concentrations peaked at day 14. Two participants progressed to stage 3 type 1 diabetes. The estimated probability of lack of progression to stage 3 was 89.6% (95% CI 64.3%, 97.3%) at the time of interim analysis. Conclusions/interpretation Teplizumab was safe and well tolerated in children <8 years of age with stage 2 type 1 diabetes. Adverse events were consistent with those seen in previous studies, with no new safety risks identified. Two participants progressed to stage 3 type 1 diabetes during the observation period; surveillance is ongoing. Trial registration ClinicalTrials.gov NCT05757713. Graphical
Teplizumab已在美国和其他7个国家获得批准，用于延缓年龄≥8岁的2期1型糖尿病患者的3期1型糖尿病发病。作为美国食品和药物管理局上市后要求的一部分，本研究评估了teplizumab在8岁2期1型糖尿病儿童中的安全性、耐受性和药代动力学。PETITE-T1D试验是一项为期2年的单臂、开放标签、多中心研究，纳入23名8岁2期1型糖尿病儿童。参与者接受了为期14天的teplizumab疗程。在15名参与者完成1年随访后进行预先指定的中期分析，包括所有23名参与者。主要终点包括治疗中出现的不良事件（teae）、导致治疗中断的teae和严重不良事件（SAEs）。其他终点评估了免疫原性、药代动力学、药效学和从研究治疗到3期1型糖尿病的时间。结果参与者平均年龄4.8岁（范围1.7-6.8岁）。中位随访时间为51.9周（范围3.9-77.1）。所有参与者都经历过一次或多次TEAE，大多数为轻度至中度。未见4级或5级teae报告。3名参与者（13%）有teae导致替普利单抗停药：贫血、肝酶升高和斑疹丘疹。两名参与者（9%）均有两次急性呼吸道感染。血清teplizumab浓度在第14天达到峰值。两名参与者进展为3期1型糖尿病。在中期分析时，估计没有进展到第3期的概率为89.6% （95% CI 64.3%, 97.3%）。结论/解释Teplizumab在8岁2期1型糖尿病儿童中是安全且耐受性良好的。不良事件与以前的研究一致，未发现新的安全风险。两名参与者在观察期间进展为3期1型糖尿病；监测正在进行中。试验注册ClinicalTrials.gov NCT05757713。图形化的
{"title":"Safety and pharmacokinetics of teplizumab in children less than 8 years of age with stage 2 type 1 diabetes","authors":"Stephen E. Gitelman, Kimber Simmons, Jennifer L. Sherr, Steven B. Leichter, Teresa Quattrin, William E. Russell, Bhuvana Sunil, Steven M. Willi, Laura A. Knecht, Elisabeth Niemoeller, Idlir Licaj, Wolfgang Schmider, Diana Miller, Linda A. DiMeglio","doi":"10.1007/s00125-025-06586-1","DOIUrl":"https://doi.org/10.1007/s00125-025-06586-1","url":null,"abstract":"Aims/hypothesis Teplizumab is approved in the USA and seven other countries to delay stage 3 type 1 diabetes onset in individuals ≥8 years of age with stage 2 type 1 diabetes. As part of a US Food and Drug Administration post-marketing requirement, this study evaluated the safety, tolerability and pharmacokinetics of teplizumab in children aged <8 years with stage 2 type 1 diabetes. Methods The PETITE-T1D trial is a 2 year single-arm, open-label, multicentre study of 23 children <8 years of age with stage 2 type 1 diabetes. Participants received a 14 day teplizumab course. A prespecified interim analysis was performed after 15 participants completed 1 year of follow-up and included all 23 participants. Primary endpoints included treatment-emergent adverse events (TEAEs), TEAEs causing treatment discontinuation, and serious adverse events (SAEs). Other endpoints assessed immunogenicity, pharmacokinetics, pharmacodynamics and time from study treatment to stage 3 type 1 diabetes. Results Mean participant age was 4.8 years (range 1.7–6.8). Median follow-up duration was 51.9 weeks (range 3.9–77.1). All participants experienced one or more TEAE, with most being mild to moderate. No grade 4 or 5 TEAEs were reported. Three participants (13%) had TEAEs leading to teplizumab discontinuation: anaemia, elevated liver enzymes and maculo-papular rash. Two participants (9%) each had two SAEs. Serum teplizumab concentrations peaked at day 14. Two participants progressed to stage 3 type 1 diabetes. The estimated probability of lack of progression to stage 3 was 89.6% (95% CI 64.3%, 97.3%) at the time of interim analysis. Conclusions/interpretation Teplizumab was safe and well tolerated in children <8 years of age with stage 2 type 1 diabetes. Adverse events were consistent with those seen in previous studies, with no new safety risks identified. Two participants progressed to stage 3 type 1 diabetes during the observation period; surveillance is ongoing. Trial registration ClinicalTrials.gov NCT05757713. Graphical","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"52 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145448174","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}
Pub Date : 2025-11-01DOI: 10.1007/s00125-025-06576-3
Wilfred Aniagyei, Osei Sarfo-Kantanka, Sumaya Mohayideen, Monika M. Vivekanandan, Ernest Adankwah, Shadrack O. Asibey, Agnes O. Boateng, Elisabeth Owusu, Joseph F. Arthur, Augustine Yeboah, Hubert S. Ahor, Dorcas O. Owusu, Maximilian Huttasch, Yanislava Karusheva, Volker Burkart, Robert Wagner, Michael Roden, Vera Balz, Jürgen Enczmann, Maike Sterzenbach, Sebastian Kummer, Thomas Meissner, Diran Herebian, Ertan Mayatepek, Marc Jacobsen, Richard O. Phillips, Julia Seyfarth
Aims/hypothesis In sub-Saharan Africa, type 1 diabetes is typically diagnosed clinically, which can be challenging due to atypical diabetes presentations such as ketosis-prone type 2 diabetes or type 2 diabetes in the absence of overweight and obesity. C-peptide, a marker of residual insulin secretion capacity, is crucial for understanding these variations but understudied in the region. Here, we investigated whether C-peptide measurement and concomitant genetic, autoimmune and metabolic characterisation of individuals with clinically diagnosed type 1 diabetes confirm diabetes classification and highlight population-specific features. Methods In this case–control study from Ghana, we recruited 266 individuals with clinically diagnosed and insulin-treated long-term type 1 diabetes and 266 healthy control individuals. We compared clinical features, HLA class II haplotypes, autoantibodies, and inflammatory and metabolic serum profiles across control and patient groups classified by random C-peptide levels: low (<0.2 nmol/l), mid (0.2–0.6 nmol/l) and high (>0.6 nmol/l). Results Only 28.9% of individuals with clinically diagnosed type 1 diabetes had low C-peptide concentrations. They were the youngest and leanest group, with higher frequencies of HLA class II risk haplotypes and GAD and ZnT8 autoantibodies compared with all other groups. By contrast, 34.6% and 36.5% had mid-range or high C-peptide levels, respectively. These subgroups resembled the control group in terms of low autoantibody titres and one protective HLA class II haplotype. Ketosis at onset was most prevalent in individuals with high C-peptide. Serum proinflammatory biomarkers differed between individuals with diabetes and control participants, but not between C-peptide subgroups. Aromatic and branched-chain amino acids varied between diabetes subgroups and positively correlated with C-peptide levels. Conclusions/interpretation Maintained C-peptide levels in two-thirds of individuals with long-term type 1 diabetes in Ghana, combined with the absence of autoantibodies and HLA risk association, highlight the necessity for better differentiation from atypical diabetes presentations to optimise patient care and improve health outcomes in resource-limited settings. Graphical
{"title":"Heterogeneity in clinically diagnosed type 1 diabetes: characterising a unique cohort with maintained C-peptide secretion in Ghana","authors":"Wilfred Aniagyei, Osei Sarfo-Kantanka, Sumaya Mohayideen, Monika M. Vivekanandan, Ernest Adankwah, Shadrack O. Asibey, Agnes O. Boateng, Elisabeth Owusu, Joseph F. Arthur, Augustine Yeboah, Hubert S. Ahor, Dorcas O. Owusu, Maximilian Huttasch, Yanislava Karusheva, Volker Burkart, Robert Wagner, Michael Roden, Vera Balz, Jürgen Enczmann, Maike Sterzenbach, Sebastian Kummer, Thomas Meissner, Diran Herebian, Ertan Mayatepek, Marc Jacobsen, Richard O. Phillips, Julia Seyfarth","doi":"10.1007/s00125-025-06576-3","DOIUrl":"https://doi.org/10.1007/s00125-025-06576-3","url":null,"abstract":"Aims/hypothesis In sub-Saharan Africa, type 1 diabetes is typically diagnosed clinically, which can be challenging due to atypical diabetes presentations such as ketosis-prone type 2 diabetes or type 2 diabetes in the absence of overweight and obesity. C-peptide, a marker of residual insulin secretion capacity, is crucial for understanding these variations but understudied in the region. Here, we investigated whether C-peptide measurement and concomitant genetic, autoimmune and metabolic characterisation of individuals with clinically diagnosed type 1 diabetes confirm diabetes classification and highlight population-specific features. Methods In this case–control study from Ghana, we recruited 266 individuals with clinically diagnosed and insulin-treated long-term type 1 diabetes and 266 healthy control individuals. We compared clinical features, HLA class II haplotypes, autoantibodies, and inflammatory and metabolic serum profiles across control and patient groups classified by random C-peptide levels: low (<0.2 nmol/l), mid (0.2–0.6 nmol/l) and high (>0.6 nmol/l). Results Only 28.9% of individuals with clinically diagnosed type 1 diabetes had low C-peptide concentrations. They were the youngest and leanest group, with higher frequencies of HLA class II risk haplotypes and GAD and ZnT8 autoantibodies compared with all other groups. By contrast, 34.6% and 36.5% had mid-range or high C-peptide levels, respectively. These subgroups resembled the control group in terms of low autoantibody titres and one protective HLA class II haplotype. Ketosis at onset was most prevalent in individuals with high C-peptide. Serum proinflammatory biomarkers differed between individuals with diabetes and control participants, but not between C-peptide subgroups. Aromatic and branched-chain amino acids varied between diabetes subgroups and positively correlated with C-peptide levels. Conclusions/interpretation Maintained C-peptide levels in two-thirds of individuals with long-term type 1 diabetes in Ghana, combined with the absence of autoantibodies and HLA risk association, highlight the necessity for better differentiation from atypical diabetes presentations to optimise patient care and improve health outcomes in resource-limited settings. Graphical","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"83 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145411714","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}
Pub Date : 2025-11-01Epub Date: 2025-08-28DOI: 10.1007/s00125-025-06535-y
Dario Giugliano, Miriam Longo, Paola Caruso, Lorenzo Scappaticcio, Alessandro Pontillo, Nicole Di Martino, Chiara Porcellini, Silvia Angelino, Mariangela Caputo, Giuseppe Bellastella, Maria Ida Maiorino, Katherine Esposito
{"title":"BEYOND 4 years: simplification of complex insulin regimens with a fixed-ratio combination of basal insulin plus a GLP-1 receptor agonist or basal insulin plus an SGLT-2 inhibitor.","authors":"Dario Giugliano, Miriam Longo, Paola Caruso, Lorenzo Scappaticcio, Alessandro Pontillo, Nicole Di Martino, Chiara Porcellini, Silvia Angelino, Mariangela Caputo, Giuseppe Bellastella, Maria Ida Maiorino, Katherine Esposito","doi":"10.1007/s00125-025-06535-y","DOIUrl":"10.1007/s00125-025-06535-y","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"2630-2633"},"PeriodicalIF":10.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946201","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}
<p><strong>Aims/hypothesis: </strong>Glucose 6-phosphate dehydrogenase (G6PD) deficiency, the most common inherited enzymopathy, can affect HbA<sub>1c</sub> levels and the diagnosis of type 2 diabetes. This cross-sectional study aimed to investigate the association between G6PD deficiency, its common mutations (G6PD Viangchan<sup>G871A</sup>, G6PD Mahidol<sup>G487A</sup>) and HbA<sub>1c</sub> levels in a Thai cohort.</p><p><strong>Methods: </strong>Blood samples from 1007 healthy hospital staff were collected during annual health checkups. Individuals with diabetes, diabetes medication use and conditions affecting erythrocyte turnover were excluded. HbA<sub>1c</sub> levels were measured by enzymatic assay and HPLC, while fasting plasma glucose (FPG) and haematological variables were obtained from checkup records. Fructosamine levels and G6PD activity (classified as deficiency, intermediate, normal) were measured by spectrophotometric assay. Genotyping was performed using TaqMan SNP, PCR-Restriction Fragment Length Polymorphism (RFLP) and Sanger sequencing. Prediabetes and diabetes were diagnosed based on two abnormal results from FPG and HbA<sub>1c</sub> at the same time, following the modified ADA criteria. Optimal HbA<sub>1c</sub> cutoffs were determined using receiver operating characteristic curve analysis with bootstrapping in RStudio, optimising Youden's index and the harmonic mean of sensitivity and specificity.</p><p><strong>Results: </strong>HbA<sub>1c</sub> levels were significantly lower in individuals with G6PD deficiency (25.68 mmol/mol [4.50%] by enzymatic assay; 27.33 mmol/mol [4.65%] by HPLC; n=28; p<0.001) compared with those with normal G6PD levels (34.05 mmol/mol [5.27%] by enzymatic assay; 36.61 mmol/mol [5.50%] by HPLC; n=492). Similarly, individuals with G6PD Viangchan<sup>G871A</sup> (29.46 mmol/mol [4.85%] by enzymatic assay; 31.15 mmol/mol [5.00%] by HPLC; n=52; p<0.001) and G6PD Mahidol<sup>G487A</sup> (28.63 mmol/mol [4.77%] by enzymatic assay; 31.15 mmol/mol [5.00%] by HPLC; n=15; p<0.001) had significantly lower HbA<sub>1c</sub> levels. HbA<sub>1c</sub> levels positively correlated with G6PD activity (r=0.208, p<0.001 by enzymatic assay; r=0.211, p<0.001 by HPLC). The optimal HbA<sub>1c</sub> cutoffs for predicting prediabetes in participants with G6PD mutation were 33 to <42 mmol/mol (5.2% to <6.0%) by enzymatic assay (sensitivity 70%; specificity 88.64%; accuracy 86.74%) and 34 to <43 mmol/mol (5.3% to <6.1%) measured by HPLC (sensitivity 72.73%; specificity 86.21%; accuracy 84.70%). For diabetes, the optimal cutoffs were ≥42 mmol/mol (≥6.0%) by enzymatic assay (sensitivity 100%; specificity 97.92%; accuracy 97.96%) and ≥43 mmol/mol (≥6.1%) by HPLC (sensitivity 100%; specificity 96.88%; accuracy 96.94%). Using the mutation-specific HbA<sub>1c</sub> cutoffs resulted in the proportion of individuals being diagnosed with diabetes remaining the same but the proportion diagnosed with prediabetes rose from 8.2% (ADA crite
{"title":"Glucose 6-phosphate dehydrogenase deficiency and Southeast Asian-specific mutations lower HbA<sub>1c</sub> levels in a Thai population: implications for diabetes diagnosis.","authors":"Punchalee Mungkalasut, Makamas Chanda, Watcharapong Jugnam-Ang, Poonlarp Cheepsunthorn, Poranee Ganokroj, Chalisa L Cheepsunthorn","doi":"10.1007/s00125-025-06523-2","DOIUrl":"10.1007/s00125-025-06523-2","url":null,"abstract":"<p><strong>Aims/hypothesis: </strong>Glucose 6-phosphate dehydrogenase (G6PD) deficiency, the most common inherited enzymopathy, can affect HbA<sub>1c</sub> levels and the diagnosis of type 2 diabetes. This cross-sectional study aimed to investigate the association between G6PD deficiency, its common mutations (G6PD Viangchan<sup>G871A</sup>, G6PD Mahidol<sup>G487A</sup>) and HbA<sub>1c</sub> levels in a Thai cohort.</p><p><strong>Methods: </strong>Blood samples from 1007 healthy hospital staff were collected during annual health checkups. Individuals with diabetes, diabetes medication use and conditions affecting erythrocyte turnover were excluded. HbA<sub>1c</sub> levels were measured by enzymatic assay and HPLC, while fasting plasma glucose (FPG) and haematological variables were obtained from checkup records. Fructosamine levels and G6PD activity (classified as deficiency, intermediate, normal) were measured by spectrophotometric assay. Genotyping was performed using TaqMan SNP, PCR-Restriction Fragment Length Polymorphism (RFLP) and Sanger sequencing. Prediabetes and diabetes were diagnosed based on two abnormal results from FPG and HbA<sub>1c</sub> at the same time, following the modified ADA criteria. Optimal HbA<sub>1c</sub> cutoffs were determined using receiver operating characteristic curve analysis with bootstrapping in RStudio, optimising Youden's index and the harmonic mean of sensitivity and specificity.</p><p><strong>Results: </strong>HbA<sub>1c</sub> levels were significantly lower in individuals with G6PD deficiency (25.68 mmol/mol [4.50%] by enzymatic assay; 27.33 mmol/mol [4.65%] by HPLC; n=28; p<0.001) compared with those with normal G6PD levels (34.05 mmol/mol [5.27%] by enzymatic assay; 36.61 mmol/mol [5.50%] by HPLC; n=492). Similarly, individuals with G6PD Viangchan<sup>G871A</sup> (29.46 mmol/mol [4.85%] by enzymatic assay; 31.15 mmol/mol [5.00%] by HPLC; n=52; p<0.001) and G6PD Mahidol<sup>G487A</sup> (28.63 mmol/mol [4.77%] by enzymatic assay; 31.15 mmol/mol [5.00%] by HPLC; n=15; p<0.001) had significantly lower HbA<sub>1c</sub> levels. HbA<sub>1c</sub> levels positively correlated with G6PD activity (r=0.208, p<0.001 by enzymatic assay; r=0.211, p<0.001 by HPLC). The optimal HbA<sub>1c</sub> cutoffs for predicting prediabetes in participants with G6PD mutation were 33 to <42 mmol/mol (5.2% to <6.0%) by enzymatic assay (sensitivity 70%; specificity 88.64%; accuracy 86.74%) and 34 to <43 mmol/mol (5.3% to <6.1%) measured by HPLC (sensitivity 72.73%; specificity 86.21%; accuracy 84.70%). For diabetes, the optimal cutoffs were ≥42 mmol/mol (≥6.0%) by enzymatic assay (sensitivity 100%; specificity 97.92%; accuracy 97.96%) and ≥43 mmol/mol (≥6.1%) by HPLC (sensitivity 100%; specificity 96.88%; accuracy 96.94%). Using the mutation-specific HbA<sub>1c</sub> cutoffs resulted in the proportion of individuals being diagnosed with diabetes remaining the same but the proportion diagnosed with prediabetes rose from 8.2% (ADA crite","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"2535-2551"},"PeriodicalIF":10.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946227","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}
Pub Date : 2025-11-01Epub Date: 2025-06-17DOI: 10.1007/s00125-025-06450-2
Sirisha Kusuma Boddu, Cosimo Giannini, M Loredana Marcovecchio
Youth-onset metabolic diseases, including obesity and type 1 and type 2 diabetes, and their associated cardiometabolic complications represent a major global health challenge. The incidence and prevalence of these conditions vary across regions, with rising trends and a heavier burden observed in middle- and low-income countries. Diet, physical activity and lifestyle choices are key factors in the development and progression of metabolic diseases during childhood and adolescence, along with additional risk factors such as genetic predisposition, ancestry, ethnicity, lifetime events (i.e. puberty) and other environmental factors. Disparities in access to healthcare, diagnostic and management capabilities and treatment options across the world affect outcomes, contributing to high morbidity and mortality rates, particularly in low-resource settings. Compared with onset during adulthood, an early diagnosis of metabolic diseases is associated with a higher risk and severity of complications, including adverse vascular outcomes and premature mortality. Although clinical signs of cardiovascular complications typically appear in adulthood, they are the result of a long, subclinical disease process that can begin in childhood and adolescence. This underscores the need for early prevention strategies and effective treatments to reduce the short- and long-term health impacts of these conditions. Addressing the rising prevalence of metabolic diseases, especially among vulnerable populations, requires comprehensive, culturally tailored actions that consider the available resources in diverse settings.
{"title":"Metabolic disorders in young people around the world.","authors":"Sirisha Kusuma Boddu, Cosimo Giannini, M Loredana Marcovecchio","doi":"10.1007/s00125-025-06450-2","DOIUrl":"10.1007/s00125-025-06450-2","url":null,"abstract":"<p><p>Youth-onset metabolic diseases, including obesity and type 1 and type 2 diabetes, and their associated cardiometabolic complications represent a major global health challenge. The incidence and prevalence of these conditions vary across regions, with rising trends and a heavier burden observed in middle- and low-income countries. Diet, physical activity and lifestyle choices are key factors in the development and progression of metabolic diseases during childhood and adolescence, along with additional risk factors such as genetic predisposition, ancestry, ethnicity, lifetime events (i.e. puberty) and other environmental factors. Disparities in access to healthcare, diagnostic and management capabilities and treatment options across the world affect outcomes, contributing to high morbidity and mortality rates, particularly in low-resource settings. Compared with onset during adulthood, an early diagnosis of metabolic diseases is associated with a higher risk and severity of complications, including adverse vascular outcomes and premature mortality. Although clinical signs of cardiovascular complications typically appear in adulthood, they are the result of a long, subclinical disease process that can begin in childhood and adolescence. This underscores the need for early prevention strategies and effective treatments to reduce the short- and long-term health impacts of these conditions. Addressing the rising prevalence of metabolic diseases, especially among vulnerable populations, requires comprehensive, culturally tailored actions that consider the available resources in diverse settings.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"2374-2385"},"PeriodicalIF":10.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12534309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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