723-P：在生活方式干预中实现糖尿病前期缓解比减肥更有效预防2型糖尿病

IF 7.5 1区医学 Q1 ENDOCRINOLOGY & METABOLISM

Diabetes Pub Date : 2025-06-13 DOI:10.2337/db25-723-p

ARVID SANDFORTH, LEONTINE SANDFORTH, SARAH KATZENSTEIN, JOCHEN SEISSLER, NIKOLAOS PERAKAKIS, ROBERT WAGNER, ANDREAS PETER, RAINER LEHMANN, HUBERT PREISSL, IRYNA YURCHENKO, JULIA SZENDROEDI, MATTHIAS BLÜHER, ANNETTE SCHÜRMANN, STEFAN KABISCH, KNUT MAI, PETER E. SCHWARZ, MARTIN HENI, MICHAEL RODEN, NORBERT STEFAN, ANDREAS FRITSCHE, REINER JUMPERTZ VON SCHWARTZENBERG, ANDREAS L. BIRKENFELD

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Methods: We studied 903 individuals with prediabetes from the German Prediabetes Lifestyle Intervention Study for whom data for weight loss and glycemic category classification was available. Glucose regulation was assessed by a 75 g oral glucose tolerance test. Prediabetes remission was defined as return to normal glucose regulation and normalized HbA1c according to ADA criteria. T2D risk was compared between responders and non-responders (R and NR) who lost weight (WL, n=298; &lt; -5% of initial body weight), remained weight stable (WS, n=371; -5-0%) and gained weight (WG, n=234; &gt;0%). Cox regression models were fit with age, sex and intervention intensity as covariates. Results: At baseline, age (p=0.11), fasting glucose (p=0.09), 2-hour glucose (p=0.98) and beta cell function were comparable between all three responder groups. WL-, WS- and WG-response was similarly protective from developing future T2D (HR for WL R vs. WL NR 0.11 [95 CI: 0.03-0.36], p = 0.00026, HR for WS R vs. WS NR 0.40 [95 CI: 0.17-0.93], p = 0.033, HR for WG R vs. WG NR 0.25 [95 CI: 0.09 -0.69], p = 0.0072,). T2D risk did not differ between weight loss strata (HR 0.82 [95 CI: 0.54-1.25], p = 0.36 for WS-R vs WG-R; and HR 0.91 [0.64-1.30], p = 0.61 for WL-R vs WG-R). Conclusion: Prediabetes remission, i.e. glycemic targets rather than weight loss targets, should be the primary treatment goal for T2D prevention. Disclosure A. Sandforth: None. L. Sandforth: None. S. Katzenstein: None. J. Seissler: None. N. Perakakis: Other Relationship; Novo Nordisk, Lilly Diabetes. Advisory Panel; Bayer Pharmaceuticals, Inc. Other Relationship; APOGEPHA, Transmedac Innovations AG, GWT-TUD, Elbe-Gesundsheintszentrum GmbH, Open Exploration. R. Wagner: Speaker's Bureau; Boehringer-Ingelheim, Novo Nordisk. Advisory Panel; Sanofi. Speaker's Bureau; Sanofi. Advisory Panel; Lilly Diabetes. A. Peter: None. R. Lehmann: None. H. Preissl: None. I. Yurchenko: None. J. Szendroedi: Advisory Panel; Novo Nordisk, Lilly Diabetes, Novartis AG, Boehringer-Ingelheim. M. Blüher: Advisory Panel; AstraZeneca. Speaker's Bureau; Amgen Inc. Advisory Panel; Bayer Pharmaceuticals, Inc, Boehringer-Ingelheim. Speaker's Bureau; Daiichi Sankyo. Advisory Panel; Eli Lilly and Company, Novo Nordisk, Nestlé Health Science, Sanofi-Aventis Deutschland GmbH. A. Schürmann: None. S. Kabisch: Research Support; Almond Board California, California Walnut Commission. Other Relationship; JuZo-Akademie, Boehringer-Ingelheim. Research Support; J. Rettenmaier & Söhne. Other Relationship; Lilly Diabetes. Research Support; Wilhelm-Doerenkamp-Foundation. K. Mai: None. P.E. Schwarz: None. M. Heni: Advisory Panel; Amryt Pharma. Speaker's Bureau; Amryt Pharma, AstraZeneca, Boehringer-Ingelheim. Advisory Panel; Boehringer-Ingelheim. 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引用次数: 0

摘要

简介和目的：目前的指南推荐了2型糖尿病（T2D）高危人群的减肥目标。糖尿病前期是T2D的高危状态，减肥期间糖尿病前期的缓解对预防T2D有额外的好处。因此，我们假设达到血糖目标是比减肥目标更有效的预防T2D的策略。方法：我们研究了903名来自德国糖尿病前期生活方式干预研究的糖尿病前期患者，他们的体重减轻和血糖分类数据是可用的。通过75 g口服葡萄糖耐量试验评估葡萄糖调节。根据ADA标准，糖尿病前期缓解被定义为恢复正常的血糖调节和正常的HbA1c。比较体重减轻的应答者和无应答者（R和NR）之间的T2D风险(WL, n=298；, lt;-初始体重的5%)，保持体重稳定(WS, n=371；-5-0%)和体重增加(WG, n=234；和gt; 0%)。Cox回归模型以年龄、性别、干预强度为协变量进行拟合。结果：在基线时，年龄（p=0.11）、空腹血糖（p=0.09）、2小时血糖（p=0.98）和β细胞功能在所有三个应答组之间具有可比性。WL-、WS-和WG-反应对未来发生的T2D具有相似的保护作用（WL R对WL NR的HR为0.11 [95 CI: 0.03-0.36], p = 0.00026， WS R对WS NR的HR为0.40 [95 CI: 0.17-0.93], p = 0.033， WG R对WG NR的HR为0.25 [95 CI: 0.09 -0.69], p = 0.0072,）。不同体重减轻组的T2D风险无差异(HR 0.82 [95 CI: 0.54-1.25]， WS-R组vs WG-R组p = 0.36；WL-R vs WG-R的HR为0.91 [0.64-1.30],p = 0.61)。结论：糖尿病前期缓解，即血糖目标，而不是体重减轻目标，应该是预防T2D的主要治疗目标。A.桑德福斯：没有。L.桑德福斯：没有。卡岑斯坦：没有。J.赛斯勒：没有。N. Perakakis：其他关系；诺和诺德，礼来糖尿病公司。顾问小组;拜耳制药公司其他关系;APOGEPHA, Transmedac Innovations AG, GWT-TUD, Elbe-Gesundsheintszentrum GmbH, Open Exploration。R. Wagner：发言人局；勃林格殷格翰，诺和诺德。顾问小组;赛诺菲。演讲者的局;赛诺菲。顾问小组;莉莉糖尿病。A.彼得：没有。莱曼：没有。H. Preissl：没有。尤尔琴科：没有。J. Szendroedi：咨询小组；诺和诺德，礼来糖尿病，诺华公司，勃林格殷格翰。M. bl her：咨询小组；阿斯利康。演讲者的局;安进公司。顾问小组;拜耳制药公司，勃林格殷格翰公司。演讲者的局;第一三共制药。顾问小组;礼来公司，诺和诺德，雀巢健康科学，赛诺菲-安万特德国有限公司。A. sch rmann：没有。S. Kabisch：研究支持；加州杏仁委员会，加州核桃委员会。其他关系;JuZo-Akademie,勃林格殷格翰的发言。研究支持;J. Rettenmaier &；Sohne。其他关系;莉莉糖尿病。研究支持;Wilhelm-Doerenkamp-Foundation。麦：没有。P.E. Schwarz：没有。Heni先生：咨询小组；Amryt制药。演讲者的局;Amryt Pharma, AstraZeneca, Boehringer-Ingelheim。顾问小组;勃林格殷格翰集团。演讲者的局;礼来糖尿病，诺华，诺和诺德，赛诺菲。M. Roden：研究支持；勃林格殷格翰集团。顾问小组;Echosens。演讲者的局;马德里加尔制药公司顾问小组;生命科学基金会。董事会成员;诺和诺德公司。顾问小组;塔吉特制药解决方案公司N. Stefan：发言人局；阿斯利康,勃林格殷格翰的发言。顾问;莉莉糖尿病。演讲者的局;莉莉糖尿病。顾问;辉瑞公司演讲者的局;赛诺菲。研究支持;赛诺菲。演讲者的局;诺和诺德，葛兰素史克公司。顾问;葛兰素史克。A. Fritsche：顾问小组；阿伯特。演讲者的局;阿斯利康。R. Jumpertz von schwartzberg：没有。A.L. Birkenfeld：没有。

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723-P: Achieving Prediabetes Remission during Lifestyle Intervention Is More Effective Than Weight Loss for Type 2 Diabetes Prevention

Introduction and Objective: Current guidelines recommend weight loss targets for individuals at risk for type 2 diabetes (T2D). Prediabetes is a high-risk state for T2D, and remission of prediabetes during weight loss has additional benefits for T2D prevention. Thus, we hypothesized that reaching glycemic targets is a more effective strategy for T2D prevention than weight loss targets. Methods: We studied 903 individuals with prediabetes from the German Prediabetes Lifestyle Intervention Study for whom data for weight loss and glycemic category classification was available. Glucose regulation was assessed by a 75 g oral glucose tolerance test. Prediabetes remission was defined as return to normal glucose regulation and normalized HbA1c according to ADA criteria. T2D risk was compared between responders and non-responders (R and NR) who lost weight (WL, n=298; < -5% of initial body weight), remained weight stable (WS, n=371; -5-0%) and gained weight (WG, n=234; >0%). Cox regression models were fit with age, sex and intervention intensity as covariates. Results: At baseline, age (p=0.11), fasting glucose (p=0.09), 2-hour glucose (p=0.98) and beta cell function were comparable between all three responder groups. WL-, WS- and WG-response was similarly protective from developing future T2D (HR for WL R vs. WL NR 0.11 [95 CI: 0.03-0.36], p = 0.00026, HR for WS R vs. WS NR 0.40 [95 CI: 0.17-0.93], p = 0.033, HR for WG R vs. WG NR 0.25 [95 CI: 0.09 -0.69], p = 0.0072,). T2D risk did not differ between weight loss strata (HR 0.82 [95 CI: 0.54-1.25], p = 0.36 for WS-R vs WG-R; and HR 0.91 [0.64-1.30], p = 0.61 for WL-R vs WG-R). Conclusion: Prediabetes remission, i.e. glycemic targets rather than weight loss targets, should be the primary treatment goal for T2D prevention. Disclosure A. Sandforth: None. L. Sandforth: None. S. Katzenstein: None. J. Seissler: None. N. Perakakis: Other Relationship; Novo Nordisk, Lilly Diabetes. Advisory Panel; Bayer Pharmaceuticals, Inc. Other Relationship; APOGEPHA, Transmedac Innovations AG, GWT-TUD, Elbe-Gesundsheintszentrum GmbH, Open Exploration. R. Wagner: Speaker's Bureau; Boehringer-Ingelheim, Novo Nordisk. Advisory Panel; Sanofi. Speaker's Bureau; Sanofi. Advisory Panel; Lilly Diabetes. A. Peter: None. R. Lehmann: None. H. Preissl: None. I. Yurchenko: None. J. Szendroedi: Advisory Panel; Novo Nordisk, Lilly Diabetes, Novartis AG, Boehringer-Ingelheim. M. Blüher: Advisory Panel; AstraZeneca. Speaker's Bureau; Amgen Inc. Advisory Panel; Bayer Pharmaceuticals, Inc, Boehringer-Ingelheim. Speaker's Bureau; Daiichi Sankyo. Advisory Panel; Eli Lilly and Company, Novo Nordisk, Nestlé Health Science, Sanofi-Aventis Deutschland GmbH. A. Schürmann: None. S. Kabisch: Research Support; Almond Board California, California Walnut Commission. Other Relationship; JuZo-Akademie, Boehringer-Ingelheim. Research Support; J. Rettenmaier & Söhne. Other Relationship; Lilly Diabetes. Research Support; Wilhelm-Doerenkamp-Foundation. K. Mai: None. P.E. Schwarz: None. M. Heni: Advisory Panel; Amryt Pharma. Speaker's Bureau; Amryt Pharma, AstraZeneca, Boehringer-Ingelheim. Advisory Panel; Boehringer-Ingelheim. Speaker's Bureau; Lilly Diabetes, Novartis AG, Novo Nordisk, Sanofi. M. Roden: Research Support; Boehringer-Ingelheim. Advisory Panel; Echosens. Speaker's Bureau; Madrigal Pharmaceuticals, Inc. Advisory Panel; MSD Life Science Foundation. Board Member; Novo Nordisk. Advisory Panel; TARGET PharmaSolutions, Inc. N. Stefan: Speaker's Bureau; AstraZeneca, Boehringer-Ingelheim. Consultant; Lilly Diabetes. Speaker's Bureau; Lilly Diabetes. Consultant; Pfizer Inc. Speaker's Bureau; Sanofi. Research Support; Sanofi. Speaker's Bureau; Novo Nordisk, GlaxoSmithKline plc. Consultant; GlaxoSmithKline plc. A. Fritsche: Advisory Panel; Abbott. Speaker's Bureau; AstraZeneca. R. Jumpertz von Schwartzenberg: None. A.L. Birkenfeld: None.

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来源期刊

Diabetes 医学-内分泌学与代谢

CiteScore

12.50

自引率

2.60%

发文量

1968

审稿时长

1 months

期刊介绍： Diabetes is a scientific journal that publishes original research exploring the physiological and pathophysiological aspects of diabetes mellitus. We encourage submissions of manuscripts pertaining to laboratory, animal, or human research, covering a wide range of topics. Our primary focus is on investigative reports investigating various aspects such as the development and progression of diabetes, along with its associated complications. We also welcome studies delving into normal and pathological pancreatic islet function and intermediary metabolism, as well as exploring the mechanisms of drug and hormone action from a pharmacological perspective. Additionally, we encourage submissions that delve into the biochemical and molecular aspects of both normal and abnormal biological processes. However, it is important to note that we do not publish studies relating to diabetes education or the application of accepted therapeutic and diagnostic approaches to patients with diabetes mellitus. Our aim is to provide a platform for research that contributes to advancing our understanding of the underlying mechanisms and processes of diabetes.