Davidson Mayer B
Charles R. Drew University, 1731 East 120th Street, Los Angeles, CA, 90059, USA.
Diabetes Ther. 2023 Oct;14(10):1585-1593. doi: 10.1007/s13300-023-01449-7. Epub 2023 Jul 25.
In this commentary I will evaluate whether prediabetes should be treated pharmacologically. To consider this question, certain information concerning prediabetes is relevant.
(1) Prediabetes is not independently associated with cardiovascular disease; the other factors in the metabolic syndrome increase that risk; (2) various tests and criteria for diagnosing prediabetes are recommended, yielding prevalences varying from 6% to 38% depending on which are used; (3) one-third of patients with prediabetes revert to normal over time; (4) up to two-thirds of patients with prediabetes do not develop diabetes; (5) people with prediabetes have insulin resistance and impaired insulin secretion; (6) although pharmacological treatment of the dysglycemia temporarily lowers it, when the drugs are discontinued, incident diabetes develops similarly as that in those who received placebos; (7) when the drugs are discontinued, there are no changes in insulin resistance or impaired insulin secretion; (8) incident diabetes was similar at 10 years in people remaining on metformin in the Diabetes Prevention Program Outcome Study compared with those who did not receive the drug; (9) no current drugs will directly increase insulin secretion (except sulfonylureas and glinides which have not been used to treat prediabetes because of hypoglycemia concerns); (10) sufficient weight loss to lower insulin resistance by nutritional means is challenging and especially difficult to maintain.
Pharmacological treatment of the dysglycemia of prediabetes is not warranted. On the other hand, the ability of high doses of glucagon-like peptide (GLP)-1 receptor agonists and the combination of a GLP-1 receptor agonist and the glucose-dependent insulinotropic polypeptide (GIP) to lower weight by 15% and 20%, respectively, deserves consideration for the treatment of prediabetes. This amount of weight loss should decrease insulin resistance, allowing endogenous insulin secretion to be more effective and lower the risk for developing diabetes.
在本评论中，我将评估糖尿病前期是否应进行药物治疗。为了思考这个问题，一些关于糖尿病前期的信息是相关的。
（1）糖尿病前期并非独立与心血管疾病相关；代谢综合征中的其他因素会增加该风险；（2）推荐了多种用于诊断糖尿病前期的检测方法和标准，根据所使用的方法不同，患病率在6%至38%之间变化；（3）三分之一的糖尿病前期患者随时间推移会恢复正常；（4）高达三分之二的糖尿病前期患者不会发展为糖尿病；（5）糖尿病前期患者存在胰岛素抵抗和胰岛素分泌受损；（6）尽管对血糖异常进行药物治疗可暂时降低血糖，但停药后，糖尿病的发生情况与接受安慰剂治疗的患者相似；（7）停药后，胰岛素抵抗或胰岛素分泌受损并无变化；（8）在糖尿病预防计划结局研究中，继续使用二甲双胍的患者与未接受该药物治疗的患者相比，10年后糖尿病的发生率相似；（9）目前没有药物会直接增加胰岛素分泌（除了磺脲类和格列奈类药物，由于担心低血糖，尚未用于治疗糖尿病前期）；（10）通过营养手段充分减重以降低胰岛素抵抗具有挑战性，且尤其难以维持。
糖尿病前期血糖异常的药物治疗并不必要。另一方面，高剂量胰高血糖素样肽（GLP）-1受体激动剂以及GLP-1受体激动剂与葡萄糖依赖性促胰岛素多肽（GIP）联合使用分别使体重降低15%和20%的能力，值得考虑用于糖尿病前期的治疗。这种程度的体重减轻应可降低胰岛素抵抗，使内源性胰岛素分泌更有效，并降低患糖尿病的风险。
