The Lancet Diabetes & Endocrinology最新文献

{"title":"The glucagon renaissance in obesity therapeutics.","authors":"Marcel H A Muskiet, Beatrice Bottini, Sander Kooijman, Patrick C N Rensen","doi":"10.1016/S2213-8587(26)00187-7","DOIUrl":"10.1016/S2213-8587(26)00187-7","url":null,"abstract":"","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":"868-870"},"PeriodicalIF":36.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148800185","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":"Hypoparathyroidism: translating science from the laboratory to the clinic.","authors":"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","doi":"10.1016/S2213-8587(26)00188-9","DOIUrl":"10.1016/S2213-8587(26)00188-9","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":"927-951"},"PeriodicalIF":36.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148907300","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":"Petrelintide and the evolving role of amylin agonism in obesity.","authors":"Sten Madsbad, Jens J Holst","doi":"10.1016/S2213-8587(26)00216-0","DOIUrl":"10.1016/S2213-8587(26)00216-0","url":null,"abstract":"","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":"872-873"},"PeriodicalIF":36.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082459","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":"Disease modification outcomes in type 2 diabetes: a modified Delphi.","authors":"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","doi":"10.1016/S2213-8587(26)00243-3","DOIUrl":"10.1016/S2213-8587(26)00243-3","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":"970-978"},"PeriodicalIF":36.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082472","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":"Ketoacidosis with SGLT2 inhibitors in routine clinical practice of type 2 diabetes: Scandinavian cohort and nested case-control study.","authors":"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","doi":"10.1016/S2213-8587(26)00162-2","DOIUrl":"10.1016/S2213-8587(26)00162-2","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Findings: </strong>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_1c (≥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/m²vs 20 to <25 kg/m²: 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.</p><p><strong>Interpretation: </strong>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.</p><p><strong>Funding: </strong>Region Stockholm, Swedish Society of Medicine, Karolinska Institutet.</p>","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":"903-913"},"PeriodicalIF":36.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148876028","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":"From adiposity to multisystem morbidity: the case for weight loss as disease modification.","authors":"Naveed Sattar, Lyn D Ferguson, Matthew M Y Lee","doi":"10.1016/S2213-8587(26)00186-5","DOIUrl":"10.1016/S2213-8587(26)00186-5","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":"952-969"},"PeriodicalIF":36.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148841701","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":"Efficacy and safety of mazdutide in adults with obesity or overweight: a US-based, multicentre, phase 2, randomised, placebo-controlled clinical trial.","authors":"Stanley H Hsia, Harold E Bays, Liana K Billings, Ann Marie K Weideman, Kieren J Mather, Tamer Coskun, Axel Haupt, Melissa K Thomas, Lai San Tham, Boris Calderon, Wei Ni, Olimpia Ferreira Galvao De Araujo","doi":"10.1016/S2213-8587(26)00160-9","DOIUrl":"10.1016/S2213-8587(26)00160-9","url":null,"abstract":"<p><strong>Background: </strong>Therapies targeting GLP-1 or glucose-dependent insulinotropic polypeptide (GIP) receptors have provided efficacious weight reduction in adults with obesity. Mazdutide, a glucagon and GLP-1 receptor dual agonist, presents a novel opportunity for differentiated weight reduction. We aimed to evaluate the efficacy, safety, and tolerability of once-weekly mazdutide across a dose range up to 16 mg in adults with obesity or overweight without type 2 diabetes in the USA.</p><p><strong>Methods: </strong>In this randomised, double-blind, placebo-controlled phase 2 trial at 24 centres in the USA, adults aged 18-75 years without type 2 diabetes and with a BMI of 30 kg/m² and higher-or of 27 kg/m² to less than 30 kg/m² with at least one weight-related comorbidity-were randomly allocated (3:2:3:3) to receive once-weekly subcutaneous injections of placebo or mazdutide (3-6 mg, 10 mg, or 16 mg) for 48 weeks. Participants assigned to 3-6 mg mazdutide maintained 3 mg from week 4 to week 32 before escalating to 6 mg at 32 weeks to assess 3 mg and 6 mg as potential maintenance doses. The primary endpoint was percentage change in bodyweight from baseline to 32 weeks, evaluated using the efficacy (hypothetical) estimand. Efficacy analyses included all randomly allocated participants, and safety analyses included all randomly allocated participants who received at least one treatment dose. This study is registered at ClinicalTrials.gov, NCT06124807, and is completed.</p><p><strong>Findings: </strong>Between Nov 17, 2023, and July 9, 2025, 179 participants were randomly allocated to receive mazdutide (32 participants to 3-6 mg, 48 to 10 mg, and 51 to 16 mg) or placebo (48 participants). The mean age was 47·7 years (SD 12·3), and 118 (66%) participants were female and 61 (34%) were male. At 32 weeks, the least-squares mean percentage change from baseline in bodyweight was -7·3% (SE 0·9) with mazdutide 3-6 mg, -15·6% (0·7) with 10 mg, and -18·1% (1·0) with 16 mg, versus -0·9% (0·8) with placebo. Estimated treatment differences versus placebo ranged from -6·5% to -17·2% (p<0·0001, all comparisons). Additional bodyweight reductions were observed at 48 weeks. The most common adverse events with mazdutide were gastrointestinal-related and mostly mild to moderate in severity; discontinuation of study treatment due to adverse events occurred most frequently with 16 mg (20%), associated primarily with gastrointestinal disorders.</p><p><strong>Interpretation: </strong>Once-weekly, subcutaneous mazdutide showed clinically meaningful bodyweight reduction in adults with obesity or overweight across all studied doses, with higher doses (10 mg and 16 mg) showing additional weight reduction.</p><p><strong>Funding: </strong>Eli Lilly and Company.</p>","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":"879-893"},"PeriodicalIF":36.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148800192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to Lancet Diabetes Endocrinol 2026; 14: 149-56.","authors":"","doi":"10.1016/S2213-8587(26)00238-X","DOIUrl":"10.1016/S2213-8587(26)00238-X","url":null,"abstract":"","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":"e12"},"PeriodicalIF":36.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148921294","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":"Petrelintide, a human amylin analogue for the treatment of obesity (ZUPREME 1): a randomised, double-blind, placebo-controlled, phase 2 trial.","authors":"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","doi":"10.1016/S2213-8587(26)00213-5","DOIUrl":"10.1016/S2213-8587(26)00213-5","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;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.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;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&lt;sup&gt;2&lt;/sup&gt; or with a BMI of at least 27 kg/m&lt;sup&gt;2&lt;/sup&gt; 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.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Findings: &lt;/strong&gt;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&lt;sup&gt;2&lt;/sup&gt; (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","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":"914-926"},"PeriodicalIF":36.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082462","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":"The development of obesity pharmacotherapy: from early challenges and setbacks to recognition by WHO.","authors":"Bruno Halpern, Louise A Baur, Matthias Blüher, Angela Jackson-Morris, Johanna Ralston, Donna Ryan","doi":"10.1016/S2213-8587(26)00234-2","DOIUrl":"https://doi.org/10.1016/S2213-8587(26)00234-2","url":null,"abstract":"<p><p>Obesity is a chronic, progressive disease associated with disability, increased morbidity, and reduced life expectancy. Global prevalence has risen sharply in recent decades, yet obesity and its treatment-particularly pharmacotherapy -have been highly stigmatised. A legacy of early medications withdrawn over safety concerns, together with poor efficacy, and widespread lack of recognition of obesity as a chronic disease contributed to persistent underuse of obesity pharmacotherapy. This underuse changed in the 2020s with GLP-1 receptor agonists and, later, multiagonist therapies, with their substantially greater efficacy, safety, and disease-modifying benefits compared with older agents. Reflecting this paradigm shift, WHO issued global guidelines and included GLP-1 receptor agonists in the Essential Medicines List, albeit for a narrowly defined population. We take a critical historical perspective, charting the highs and lows of obesity medication development and examining the scientific, regulatory, and societal factors that have slowed or impeded the translation of pharmacological advances into safe, effective, and widely accepted treatments for obesity.</p>","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":" ","pages":""},"PeriodicalIF":36.3,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225145","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}