研究动态
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用于体重管理的胰高血糖素样肽 1 (GLP-1) 受体激动剂:妇科肿瘤学家综述。

Glucagon-like peptide-1 (GLP-1) receptor agonists for weight management: A review for the gynecologic oncologist.

发表日期:2024 Aug 07
作者: Courtney J Riedinger, Julia Sakach, Jill M Maples, Jessica Fulton, Jessica Chippior, Benjamin O'Donnell, David M O'Malley, Laura M Chambers
来源: GYNECOLOGIC ONCOLOGY

摘要:

在美国肥胖流行期间,胰高血糖素样肽-1 受体激动剂 (GLP-1RA) 的使用迅速增长。虽然最初开发用于 2 型糖尿病的血糖控制,但这些药物的范围现在已扩展到包括减肥和降低心血管风险。 GLP-1RA 结合生活方式的改变,有可能使超重或肥胖的成年人显着减轻体重。此外,这些药物在改善高血糖、增强胰岛素敏感性、调节血压、改善心脏代谢参数、减轻肾功能障碍以及潜在降低几种与肥胖相关的癌症的风险方面具有功效。药物相关毒性主要是胃肠道毒性,积极管理可以防止停药。肥胖不仅与恶性肿瘤发病率增加有关,而且与生存率下降有关。需要更多的研究来评估 GLP-1RA 改变脂肪细胞内分泌功能、调节与肥胖相关的慢性炎症状态的潜在用途,以及在肿瘤学中的前瞻性应用。这些药物可以通过其直接作用机制以及潜在的药物毒性影响妇科恶性肿瘤患者。版权所有 © 2024。由 Elsevier Inc. 出版。
The use of glucagon-like peptide-1 receptor agonists (GLP-1RA) has experienced rapid growth amidst the obesity epidemic in the United States. While originally developed for glucose control in Type 2 Diabetes Mellitus, the scope of these agents now extends to encompass weight loss and cardiovascular risk reduction. GLP-1RAs have the potential to induce significant weight loss, in combination with lifestyle modifications, among adults who are overweight or obese. Furthermore, these agents demonstrate efficacy in ameliorating hyperglycemia, enhancing insulin sensitivity, regulating blood pressure, improving cardiometabolic parameters, mitigating kidney dysfunction, and potentially reducing the risk of several obesity-related cancers. Drug-related toxicity is primarily gastrointestinal and active management can prevent drug discontinuation. Obesity is associated both with an increased incidence of malignancy but also with decreased survival. More research is needed to evaluate the potential use of GLP-1RA to modify the endocrine function of adipocytes, regulate the chronic inflammatory state associated with obesity, and prospective applications in oncology. These agents can impact patients with gynecologic malignancies both through their direct mechanism of action as well as potential drug toxicity.Copyright © 2024. Published by Elsevier Inc.