Lancet Diabetes & Endocrinology柳叶刀糖尿病与内分泌学

Lancet Diabetes & Endocrinology(英文缩写 LANCET DIABETES ENDO),ISSN 2213-8587,eISSN 2213-8595,中文译名:柳叶刀糖尿病与内分泌学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。

2026 年数据 · 影响因子
36.300
JCR 分区
Q1
CAS 分区
B1
近一年发文量
198
本站 PubMed 收录统计

发文量统计区间:2025-11-01 至 2026-10-31,按本站收录文献的发表日期统计。

ISSN: 2213-8587 · eISSN: 2213-8595 · 缩写: LANCET DIABETES ENDO ·中文: 柳叶刀糖尿病与内分泌学

期刊介绍

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期刊简介

《Lancet Diabetes & Endocrinology》是内分泌与代谢病领域的高影响力期刊,聚焦糖尿病、肥胖、甲状腺疾病、骨代谢及内分泌肿瘤等方向。内容涵盖原创临床研究、大型试验、综述与专家评论,强调证据等级与临床转化。读者群主要为内分泌科医师、糖尿病研究者、代谢病相关专科医生及公共卫生决策者。

研究方向

主要发表糖尿病、内分泌疾病与代谢紊乱的临床和转化研究,包括随机对照试验、队列研究、系统综述、荟萃分析及指南解读。主题涉及血糖管理、胰岛素抵抗、肥胖干预、内分泌肿瘤、骨与钙磷代谢、生殖内分泌等,兼载评论与热点争鸣。

期刊特色

研究取向偏重高质量临床证据与改变实践的结果,论文多具多中心、大样本特点,方法学要求严格。综述与评论由领域权威撰写,观点鲜明。适合内分泌专科医生、临床研究者及希望跟踪前沿证据的医学读者阅读与参考。

投稿难度

投稿难度较高,对创新性、样本量、统计方法和临床意义均有严格要求。建议在投稿前完善试验设计、遵循相应报告规范,并充分比较已有证据以突出增量价值。适合已有较成熟数据和多中心协作基础的研究团队尝试。

历年影响因子趋势

JCR 数据年份影响因子JCR 分区
202144.867Q1
202244.500Q1
202344.000Q1
202441.800Q1
202536.300Q1

Lancet Diabetes & Endocrinology 最新收录文献

  1. JCR分区: Q1 CAS分区: B1 影响因子: 36.3
  2. JCR分区: Q1 CAS分区: B1 影响因子: 36.3

    2. Diabetes and the role of primary care: a global perspective.

    2. 糖尿病与初级保健的作用:全球视角
    作者:
    Partha Kar, Harini Sathanapally, Pablo Aschner, Leonard Baatiema, Alice Cheng, Yashdeep Gupta, Clare Hambling, Ronald Ma, Samuel Seidu, Kamlesh Khunti
    日期:
    2026-10-01

    The global prevalence of diabetes is rising rapidly, with the steepest increases and greatest unmet need occurring in low-income and middle-income countries. Despite strong evidence that early detection and continuous management reduce morbidity and mortality, many health systems face persistent gaps in diagnosis, treatment, and follow-up of people with diabetes. Primary care is the most accessible platform for screening and care coordination, and is central to addressing these challenges. Primary care-led models, including nurse-led and pharmacist-led interventions, integrated multidisciplinary teams, and digitally enabled care pathways, have shown improvements in glycaemic control, cardiometabolic outcomes, and health-care use in people with type 2 diabetes across primary care and community settings. Global initiatives, such as the WHO Global Diabetes Compact and UN non-communicable disease targets, emphasise strengthening primary care to deliver equitable, cost-effective diabetes care at scale. Future priorities include workforce development, addressing health inequalities, scalable implementation strategies, and robust evaluation of long-term outcomes to enable person-centred type 2 diabetes care across diverse health-system contexts.

  3. JCR分区: Q1 CAS分区: B1 影响因子: 36.3

    3. Efficacy and safety of low-dose IL-2 in people with newly diagnosed type 1 diabetes (DIABIL-2): a double-blind, multicentre, randomised, placebo-controlled, phase 2b trial.

    作者:
    Michelle Rosenzwajg, Agnès Hartemann, Marine Halbron, Chloé Amouyal, Charles Thivolet, Vincent Rigalleau, Pierre Fontaine, Brigitte Mignot, Rachel Reynaud, Jean-Claude Carel, Elise Bismuth, Caroline Storey, Karine Bourdet, Emmanuel Sonnet, Sabine Baron, Marc Nicolino, Kevin Perge, Lucy Chaillous, Laurence Kessler, Marie Mansilla, Peter Achenbach, Anette-Gabriele Ziegler, Henk-Jan Aanstoot, Thierry Mouraux, Kristina Casteels, Marc Y Donath, Bart O Roep, Roberta Lorenzon, Claire Ribet, Joe-Elie Salem, Fabien Pitoiset, Alexandra Roux, Eric Vicaut, David Klatzmann
    日期:
    2026-10-01

    Type 1 diabetes results from immune-mediated destruction of pancreatic β cells, driven partly by regulatory T-cell (Treg) insufficiency. We previously showed that low-dose interleukin-2 (IL-2) selectively activates Tregs in people with type 1 diabetes. We aimed to evaluate the efficacy of low-dose IL-2 in preserving residual pancreatic β-cell function and select an optimal regimen of administration in this patient population. This double-blind, multicentre, randomised, placebo-controlled, phase 2b trial was done in 19 academic hospital centres across Belgium, France, Germany, Switzerland, and the Netherlands. Eligible participants were aged 6-35 years; had a diagnosis of type 1 diabetes; received insulin for less than 3 months; and had a peak C-peptide concentration of at least 0·2 pmol/mL. Participants were randomly assigned (1:1:1) to a maintenance course of regimen A, regimen B, or placebo (with a 2:1 allocation ratio of IL-2 to placebo within each regimen) and were stratified by pubertal stage (children and adolescents with a Tanner score ≤4 [stratum 1] and adults with a Tanner score of ≥5 [stratum 2]). Both regimens started with an induction course of once per day subcutaneous injections for 5 consecutive days (days 1-5), then a maintenance course of injections (once per 2 weeks [regimen A] or once per week [regimen B]) from day 15 to 351. Adults received 1 million IU per injection, whereas children and adolescents received 0·5 million IU/m per injection. The primary endpoint was the change from baseline to month 12 in serum C-peptide area under the curve (AUC) from 0 to 120 min during a mixed meal tolerance test, analysed in the intention-to-treat population. This trial is registered with ClinicalTrials.gov, NCT02411253 (completed). Between June 18, 2015, and Nov 19, 2020, 159 people were assessed for eligibility, of whom 18 were ineligible and 141 were enrolled (48 randomly assigned to regimen A, 46 to regimen B, and 47 to placebo). 66 participants were in stratum 1 and 75 in stratum 2. 125 (89%) of 141 participants completed the study and 16 (11%) ended participation early. 54 (38%) participants were female and 87 (62%) were male. For log-transformed C-peptide AUC at month 12, there was no statistically significant difference in the overall population between placebo and IL-2 groups (geometric mean ratio 1·06 [95% CI 0·56 to 2·01]; p=0·85), with similar results when considering each regimen separately and by pubertal status. A marked Treg expansion was observed shortly after treatment initiation, peaking at day 5, with adjusted means of 1·31 (1·24 to 1·37) in the IL-2 group versus 1·04 (0·95 to 1·14) in the placebo group (difference -0·27 [-0·38 to -0·15]). Low-dose IL-2 was well tolerated across all age groups and treatment regimens. Nine (20%) of 46 participants in the placebo group and nine (10%) of 94 in the IL-2 group reported serious adverse events; one in each group was considered probably related to treatment. Despite robust Treg expansion confirming target engagement, low-dose IL-2 did not preserve β-cell function in people with newly diagnosed type 1 diabetes. The inflammatory environment at diagnosis might be too intense for this monotherapy, but the observed safety profile and confirmed biological activity support further investigation of low-dose IL-2 in earlier disease stages or combination strategies. Assistance Publique-Hôpitaux de Paris (European Research Network), ILTOO Pharma, and the Investissements d'Avenir programme. For the French translation of the abstract see Supplementary Materials section.

  4. JCR分区: Q1 CAS分区: B1 影响因子: 36.3

    4. Petrelintide, a human amylin analogue for the treatment of obesity (ZUPREME 1): a randomised, double-blind, placebo-controlled, phase 2 trial.

    4. Petrelintide,一种用于治疗肥胖症的人胰淀素类似物(ZUPREME 1):一项随机、双盲、安慰剂对照的2期试验
    作者:
    W Timothy Garvey, Jamy Ard, Lisa Connery, Juan Pablo Frias, Carel W le Roux, Kirsi H Pietiläinen, Maj Dinesen, Berith F Hagen, Louise Larsen, Dan Hesse, David M Kendall
    日期:
    2026-09-29

    Petrelintide is a novel, long-acting amylin analogue being developed for long-term treatment of obesity, leveraging a mechanism of action distinct from incretin-based treatments. This phase 2 trial aimed to evaluate the efficacy and safety of once-weekly petrelintide versus placebo in people with obesity. This multicentre, randomised, double-blind, placebo-controlled trial involved 32 sites (public hospitals and private clinics) in Poland, Romania, and the USA. Adults aged at least 18 years without type 2 diabetes, with a BMI of at least 30 kg/m or with a BMI of at least 27 kg/m with hypertension or dyslipidaemia, or both, were randomly assigned (5:1) to self-administered subcutaneous injections of once-weekly maintenance doses of petrelintide (1·0-9·0 mg) or placebo for 42 weeks including dose escalation. Randomisation was done via a central interactive response technology system and was stratified by MRI participation. Participants, trial staff, and the study funder were masked to treatment assignment but not to different maintenance doses; masking was maintained by use of identical vials for petrelintide and placebo. The primary endpoint was percentage change in bodyweight from baseline after 28 weeks. Analyses included all randomly assigned participants who received at least one dose. Missing data were assumed to be missing at random. The trial is registered with ClinicalTrials.gov (NCT06662539) and the Clinical Trials Information System (2024-512549-18) and was completed on Mar 7, 2026. From Dec 9, 2024, to Feb 25, 2025, we screened 714 participants, of whom 493 were randomly assigned and 485 received at least one dose of petrelintide or placebo. 79 participants received at least one dose of treatment with petrelintide 1·0 mg, 81 with petrelintide 2·5 mg, 83 with petrelintide 5·0 mg, 79 with petrelintide 7·0 mg, 82 with petrelintide 9·0 mg, and 81 with placebo. 255 (53%) participants were female, 230 (47%) were male, mean age was 47 (SD 12) years, mean bodyweight 107·1 kg (20·3), mean BMI 36·7 kg/m (5·5), and 419 (86%) were White. Mean percentage change in bodyweight from baseline after 28 weeks (efficacy estimand) was -7·9% (95% CI -9·0 to -6·7) with petrelintide 1·0 mg, -7·9% (-9·0 to -6·7) with petrelintide 2·5 mg, -9·8% (-10·9 to -8·6) with petrelintide 5·0 mg, -9·3% (-10·5 to -8·2) with petrelintide 7·0 mg, and -9·4% (-10·5 to -8·3) with petrelintide 9·0 mg versus -1·7% (-2·8 to -0·5) with placebo. Estimated treatment differences versus placebo were -6·2% (-7·9 to -4·5) with petrelintide 1·0 mg, -6·2% (-7·8 to -4·5) with petrelintide 2·5 mg, -8·1% (-9·7 to -6·5) with petrelintide 5·0 mg, -7·7% (-9·3 to -6·0) with petrelintide 7·0 mg, and -7·7% (-9·4 to -6·1) with petrelintide 9·0 mg. Bodyweight continued to decline to week 42, with reductions of up to -10·7% with petrelintide. The most common adverse event with petrelintide was nausea (79 [20%] of 404 participants vs five [6%] participants with placebo). Vomiting was infrequent with petrelintide (12 [3%] participants vs five [6%] with placebo); active treatment and placebo had similarly low rates for diarrhoea (30 [7%] participants vs six [7%] with placebo) and constipation (28 [7%] vs three [4%] with placebo). No deaths were reported. Petrelintide achieved clinically meaningful weight reduction and had similar gastrointestinal tolerability to that of placebo apart from predominantly mild nausea during dose escalation, supporting further evaluation as a long-term obesity therapy. Zealand Pharma.

  5. JCR分区: Q1 CAS分区: B1 影响因子: 36.3

    5. Disease modification outcomes in type 2 diabetes: a modified Delphi.

    5. 2型糖尿病的疾病修饰结局:一项改良德尔菲研究
    作者:
    Kamlesh Khunti, Mark P Funnell, Patrick J Highton, Ashkon Ardavani, Javed Butler, Jon Campbell, Melanie J Davies, Rachel Evley, Jose C Florez, Jason Gaglia, Rohit N Kulkarni, Nicolas Musi, Leigh Perreault, Bryce B Reeve, Sylvia E Rosas, Ash Routen, Zobair Younossi, Nuha El Sayed
    日期:
    2026-09-29

    Type 2 diabetes is a heterogeneous, progressive chronic condition for which management has traditionally focused on glycaemic control and cardiovascular risk factors, rather than focusing on altering long-term disease trajectory. Increasing evidence indicates that progression and complications might be modifiable, but the absence of a core outcome set for disease modification limits trial design and intervention comparison. To address this gap, we developed a core outcome set for disease modification in type 2 diabetes through a modified Delphi process conducted according to COMET guidance. Candidate outcomes were identified from the literature and refined by an international multidisciplinary steering group comprising clinicians, researchers, and people living with type 2 diabetes. Across two Delphi rounds involving health-care professionals, researchers, and patients (round one n=233; round two n=79), agreement was reached for 35 outcomes spanning 11 domains. This framework aims to support outcome selection, consistency across trials, comparison of interventions, and evaluation of disease-modifying strategies in type 2 diabetes.

  6. JCR分区: Q1 CAS分区: B1 影响因子: 36.3
  7. JCR分区: Q1 CAS分区: B1 影响因子: 36.3
  8. JCR分区: Q1 CAS分区: B1 影响因子: 36.3

    8. Hypoparathyroidism: translating science from the laboratory to the clinic.

    8. 甲状旁腺功能减退症:将科学从实验室转化到临床
    作者:
    Maria Luisa Brandi, Hajar AbuAlrob, Wenhan Chang, Bart L Clarke, Michael T Collins, Richard DiMarchi, Thomas J Gardella, Caroline Gorvin, Diane Krause, Michael A Levine, Michael Mannstadt, Francesca Marini, Kelly Roszko, Heide Siggelkow, Karen K Winer, Hao Zuo, Aliya A Khan
    日期:
    2026-09-07

    Chronic hypoparathyroidism is a rare endocrine disorder characterised by hypocalcaemia due to insufficient parathyroid hormone (PTH) that is associated with a multidimensional reduced quality of life, impairing physical and cognitive functioning, and compromising emotional, psychological, and social wellbeing. This Review integrates recent findings on hypoparathyroidism diagnosis, PTH analogues, calcilytics, preclinical therapeutic agents, parathyroid tissue transplantation, and pluripotent stem cell-based therapies. Emerging diagnostic technologies, including targeted genetic testing, parathyroid autoimmunity assays, and point-of-care calcium monitoring, could enable individualised and real-time management. PTH analogues with extended action (eg, palopegteriparatide, eneboparatide, and canvuparatide) show sustained activation of PTH receptors with reduced requirements for active forms of vitamin D and calcium supplements. Calcilytics (eg, encaleret) normalise calcium-sensing receptor (CaSR) hyperactivation in patients with autosomal dominant hypocalcaemia type 1 and have the potential for broader application in other forms of hypoparathyroidism. Advances in parathyroid regenerative biology with pluripotent stem cells provide platforms for future curative therapies. Progress in parathyroid autotransplantation, allotransplantation, and graft-preservation strategies further expands the therapeutic landscape. Translational research is redefining the future of hypoparathyroidism management. Developments in receptor-targeted therapies, long-acting PTH analogues, negative allosteric modulators of CaSR, and regenerative approaches reflects a shift towards restoring mineral homoeostasis to a more physiological state.

  9. JCR分区: Q1 CAS分区: B1 影响因子: 36.3

    9. Ketoacidosis with SGLT2 inhibitors in routine clinical practice of type 2 diabetes: Scandinavian cohort and nested case-control study.

    9. 2型糖尿病常规临床实践中SGLT2抑制剂相关的酮症酸中毒:斯堪的纳维亚队列及巢式病例对照研究
    作者:
    Erik Kadesjö, Jonas Söderling, Anders Hviid, Viktor Wintzell, Henrik Svanström, Björn Eliasson, Soffia Gudbjörnsdóttir, Mads Melbye, Kristian Hveem, Christian Jonasson, Daniel P Andersson, Björn Pasternak, Peter Ueda
    日期:
    2026-09-01

    SGLT2 inhibitors increase the risk of ketoacidosis, but data from routine clinical practice are scarce. We used nationwide registers with the aim of assessing the incidence, risk factors, and prognosis of ketoacidosis during SGLT2 inhibitor treatment in patients with type 2 diabetes. In this cohort and nested case-control study we used data from three Scandinavian countries. In a cohort of SGLT2 inhibitor-treatment episodes among patients with type 2 diabetes aged at least 18 years in Sweden, Denmark, and Norway, we estimated ketoacidosis incidence. Using a nested case-control design (matched on age, sex, region of birth, calendar time, and time since treatment initiation), we assessed risk factors and precipitating or co-occurring events. Changes in diabetes medications were evaluated. The study period was Jan 1, 2013, to Dec 31, 2021, in Denmark and Sweden, and Jan 1, 2013, to Dec 31, 2022, in Norway. We included 322 597 treatment episodes among 282 282 patients with type 2 diabetes (mean age 63 years, 116 521 [36·1%] of 322 597 women). During a median (IQR) follow-up of 1·3 (0·7-2·8) years, 1452 ketoacidosis events occurred (incidence 2·43 per 1000 person-years). Although highest shortly after initiation, risk persisted throughout follow-up. Strong risk factors included high HbA (≥83 vs ≤52 mmol/mol: odds ratio [OR] 15·37 [95% CI 11·50-20·53]), malnutrition (OR 10·54 [7·32-15·18]), previous ketoacidosis (OR 10·40 [7·09-15·24]), low BMI (<20 kg/mvs 20 to <25 kg/m: OR 9·98 [5·68-17·53]), and recent hypoglycaemia (OR 5·22 [2·60-10·49]). Infection was the most common precipitating or co-occurring event (454 [31·8%] of 1428 vs 862 [6·1%] of 14 233 for ketoacidosis cases vs controls; OR 7·60 [6·62-8·71]). The strongest associations were observed for alcohol intoxication, acute renal events, acute abdomen, stroke, and major surgery, although associations for some transient exposures, particularly milder conditions, might have been overestimated because of under-registration among controls. Exploratory analyses suggested that the observed associations were largely general to patients with type 2 diabetes rather than specific to SGLT2 inhibitor use. At 1 year after ketoacidosis, 211 (25·1%) of 842 remained on SGLT2 inhibitors and insulin use increased from 269 (31·9%) of 842 to 615 (73·0%) of 842. Ketoacidosis risk with SGLT2 inhibitors varies greatly by patient characteristics and is not confined to early in treatment. Risk should be assessed throughout treatment, and patients should be instructed to pause treatment during acute illness and stress. Region Stockholm, Swedish Society of Medicine, Karolinska Institutet.

  10. JCR分区: Q1 CAS分区: B1 影响因子: 36.3

    10. From adiposity to multisystem morbidity: the case for weight loss as disease modification.

    作者:
    Naveed Sattar, Lyn D Ferguson, Matthew M Y Lee
    日期:
    2026-08-27

    Obesity (ie, excess adiposity) is a major driver of multisystem morbidity, spanning musculoskeletal (eg, osteoarthritis), metabolic (eg, type 2 diabetes), cardiovascular (eg, heart failure), mental health (eg, depression), respiratory (eg, obstructive sleep apnoea), and gastrointestinal and hepatic (eg, metabolic dysfunction-associated steatotic liver disease) disorders. However, the extent to which weight-loss interventions can prevent or modify these conditions varies considerably. In this Review, we synthesise evidence from epidemiological studies, genetic analyses (including Mendelian randomisation), observational weight-change studies, and randomised trials, using a triangulation framework to assess causal links between adiposity and common diseases. Although robust trial evidence supports weight loss as a disease-modifying strategy in some conditions, including but not limited to type 2 diabetes and heart failure with preserved ejection fraction, many other conditions, including musculoskeletal, respiratory, cardiovascular, and mental health disorders, remain under-investigated. Incretin-based therapies, in particular the glucagon-like peptide 1 receptor agonist semaglutide and the dual glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide receptor agonist tirzepatide, now achieve average weight losses of approximately 14-20% in people without diabetes and have generated the first large-scale randomised evidence of disease modification across several of these conditions. We highlight key gaps and propose priorities for future trials, including the need for studies across different disease stages, incorporation of mechanistic and mediation analyses, and evaluation of the impact on disease outcomes of varying magnitudes of weight loss with differing agents. Future research should also consider multimorbidity, individualised treatment targets, and long-term outcomes-including potential legacy effects. Addressing global access gaps and conducting trials in diverse populations will be essential to inform scalable and equitable obesity care.

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