Department of Pediatrics, Yale School of Medicine and Yale Center for Clinical Investigation, Yale University, New Haven, CT 06520, USA.
Diabetes Obes Metab. 2012 Oct;14 Suppl 3:40-5. doi: 10.1111/j.1463-1326.2012.01643.x.
Concurrent with the epidemic of childhood obesity, an unprecedented increase in the prevalence of several adiposity-related complications in this age group has emerged. In particular, type 2 diabetes (T2D), once considered an illness restricted to adulthood, is progressively affecting more and more adolescents, and represents now roughly 20-45% of new-onset cases in this age group. To unravel the pathogenesis of diabetes development during adolescence, many studies have focused on defining early defects in both insulin sensitivity and secretion that might be implicated in the natural history of the disease. Although a lot still need to be clarified, studies have shown that the progression from normal glucose tolerance to T2D involves intermediate stages of impaired fasting glucose and/or impaired glucose tolerance, also known as prediabetes. Insulin resistance and β-cell dysfunction represent the two major key pathogenetic defects underlying the progression to diabetes in obese youth. In this review, we have sought to mainly describe the role of β-cell function in relation to the ambient insulin resistance in the development of T2D in obese adolescents.
随着儿童肥胖症的流行，该年龄段几种与肥胖相关的并发症的患病率也以前所未有的速度上升。特别是 2 型糖尿病（T2D），曾经被认为是一种仅限于成年期的疾病，现在越来越多的青少年受到影响，约占该年龄段新发病例的 20-45%。为了解青少年时期糖尿病发病的发病机制，许多研究集中在定义胰岛素敏感性和分泌的早期缺陷，这些缺陷可能与疾病的自然史有关。尽管还有很多需要澄清，但研究表明，从正常糖耐量到 T2D 的进展涉及空腹血糖受损和/或糖耐量受损的中间阶段，也称为糖尿病前期。胰岛素抵抗和β细胞功能障碍是肥胖青少年向糖尿病进展的两个主要关键发病缺陷。在这篇综述中，我们主要描述了β细胞功能在肥胖青少年中与环境胰岛素抵抗相关的 T2D 发展中的作用。
