University of Texas Health Science Center, San Antonio, Texas 78229-3900, USA.
J Clin Endocrinol Metab. 2011 Aug;96(8):2354-66. doi: 10.1210/jc.2011-0246. Epub 2011 Jun 22.
The Centers for Disease Control and Prevention estimates that there are approximately 79,000,000 individuals in the United States with prediabetes [impaired glucose tolerance (IGT) and/or impaired fasting glucose] and that approximately 40-50% will progress to type 2 diabetes mellitus (T2DM) during their lifetime. Therefore, treatment of high-risk IGT individuals to prevent T2DM has important medical, economic, social, and human implications. Individuals in the upper tertile of IGT are maximally/near-maximally insulin resistant, have lost 70-80% of their β-cell function, and have approximately a 10% incidence of diabetic retinopathy. Therefore, preservation of the remaining 20-30% of β-cell function is critical to prevent future development of T2DM.
We searched MEDLINE from 2000 to the present to identify placebo-controlled trials in which individuals with IGT received pharmacological therapy to prevent progression to diabetes.
Lifestyle modification reduces IGT conversion to T2DM, but it is difficult to implement and maintain. Moreover, 40-50% of IGT subjects progress to T2DM despite weight loss. In contrast, pharmacological intervention with medications that reverse known pathophysiological abnormalities (β-cell dysfunction and insulin resistance) uniformly prevents IGT progression to T2DM. Thiazolidinediones reduce IGT conversion to diabetes by approximately 50-70%. Metformin in the U.S. Diabetes Prevention Program reduced the development of T2DM by 31% and has been recommended by the American Diabetes Association. Because glucagon-like peptide-1 analogs augment insulin secretion, preserve β-cell function, and promote weight loss, they may be efficacious in preventing IGT progression to T2DM.
Pharmacological intervention with a variety of agents (thiazolidinediones, metformin, acarbose, glucagon-like peptide-1 analogs) consistently reduces the rate of conversion of IGT to T2DM.
疾病控制与预防中心估计，美国约有 7900 万人患有糖尿病前期[葡萄糖耐量受损（IGT）和/或空腹血糖受损]，其中约 40-50%在其一生中会进展为 2 型糖尿病（T2DM）。因此，治疗高危 IGT 个体以预防 T2DM 具有重要的医学、经济、社会和人文意义。IGT 中上三分位的个体胰岛素抵抗最大/接近最大，β细胞功能丧失 70-80%，并且约有 10%的糖尿病视网膜病变发生率。因此，保留剩余的 20-30%的β细胞功能对于预防未来 T2DM 的发生至关重要。
我们从 2000 年到现在在 MEDLINE 上进行了搜索，以确定在 IGT 个体中使用药物治疗预防糖尿病进展的安慰剂对照试验。
生活方式改变可以降低 IGT 向 T2DM 的转化率，但难以实施和维持。此外，尽管体重减轻，仍有 40-50%的 IGT 患者进展为 T2DM。相比之下，用药物逆转已知的病理生理异常（β细胞功能障碍和胰岛素抵抗）的药物干预可统一预防 IGT 向 T2DM 的进展。噻唑烷二酮类药物可使 IGT 向糖尿病的转化率降低约 50-70%。美国糖尿病预防计划中的二甲双胍可使 T2DM 的发生减少 31%，并已被美国糖尿病协会推荐。由于胰高血糖素样肽-1 类似物可增强胰岛素分泌、保护β细胞功能并促进体重减轻，因此它们可能在预防 IGT 向 T2DM 的进展方面有效。
各种药物（噻唑烷二酮类药物、二甲双胍、阿卡波糖、胰高血糖素样肽-1 类似物）的药物干预可一致降低 IGT 向 T2DM 的转化率。
