Ketosis-prone type 2 diabetes in patients of sub-Saharan African origin -: Clinical pathophysiology and natural history of β-cell dysfunction and insulin resistance
Ketosis-prone type 2 diabetes in patients of sub-Saharan African origin -: Clinical pathophysiology and natural history of β-cell dysfunction and insulin resistance
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DOI：
10.2337/diabetes.53.3.645
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发表时间：
2004-03-01
期刊：
影响因子：
7.7
通讯作者：
Gautier, JF
中科院分区：
文献类型：
--
作者：
Mauvais-Jarvis, F;Sobngwi, E;Gautier, JF
非自身免疫性酮症倾向的糖尿病综合征在非白人人群中越来越常见。我们描述了一组撒哈拉以南非洲患者的特征，这些患者患有酮症倾向的2型糖尿病（n = 111），I型糖尿病（n = 21）和2型糖尿病（n = 88），并因未控制的糖尿病入院治疗。我们比较了糖尿病发病时的流行病学、临床和代谢特征，并在10年随访期间测量了胰岛素分泌（胰高血糖素刺激的C肽）和胰岛素作用（短静脉胰岛素耐量试验）。与1型糖尿病相比，酮症倾向的2型糖尿病显示出强烈的男性优势，更强的家族史，更高的年龄和BMI，以及更严重的代谢失代偿。在有酮症倾向的2型糖尿病患者中，76%的患者（非胰岛素依赖型）停止胰岛素治疗并出现胰岛素依赖缓解，而只有24%的患者保持胰岛素依赖。在进化过程中，2型糖尿病表现出特定的β细胞功能障碍特征，将其与1型和2型糖尿病区分开来。非胰岛素依赖性酮症倾向2型糖尿病的临床过程的特征是酮症复发，随后或没有新的缓解。进行性高血糖先于酮症复发，是酮症复发的一个强风险因素（风险比38）。非胰岛素依赖性酮症倾向的2型糖尿病在10年内复发的概率为90%，其中约50%的患者将最终成为胰岛素依赖型。胰岛素敏感性在酮症倾向的2型糖尿病和2型糖尿病中以相同比例降低，但在非胰岛素依赖性酮症倾向的2型糖尿病中显著改善，仅在纠正高血糖后。总之，通过临床病理生理学的特定特征以及反映葡萄糖毒性倾向的P细胞功能障碍和胰岛素抵抗的自然史，可将酮症倾向2型糖尿病与I型糖尿病和经典2型糖尿病区分开来。
Nonautoimmune ketosis-prone diabetic syndromes are increasingly frequent in nonwhite populations. We have characterized a cohort of patients of sub-Saharan African origin who had ketosis-prone type 2 diabetes (n = 111), type I diabetes (n = 21), and type 2 diabetes (n = 88) and were admitted to a hospital for management of uncontrolled diabetes. We compared epidemiological, clinical, and metabolic features at diabetes onset and measured insulin secretion (glucagon-stimulated C-peptide) and insulin action (short intravenous insulin tolerance test) during a 10-year follow-up. Ketosis-prone type 2 diabetes shows a strong male predominance, stronger family history, higher age and BMI, and more severe metabolic decompensation than type 1 diabetes. In ketosis-prone type 2 diabetes, discontinuation of insulin therapy with development of remission of insulin dependence is achieved in 76% of patients (noninsulin dependent), whereas only 24% of patients remain insulin dependent. During evolution, ketosisprone type 2 diabetes exhibit specific beta-cell dysfunction features that distinguish it from type 1 and type 2 diabetes. The clinical course of non-insulin-dependent ketosis-prone type 2 diabetes is characterized by ketotic relapses followed or not by a new remission. Progressive hyperglycemia precedes and is a strong risk factor for ketotic relapses (hazard ratio 38). The probability for non-insulin-dependent ketosis-prone type 2 diabetes to relapse is 90% within 10 years, of whom similar to50% will become definitively insulin dependent. Insulin sensitivity is decreased in equal proportion in both ketosis-prone type 2 diabetes and type 2 diabetes, but improves significantly in non-insulin-dependent ketosis-prone type 2 diabetes, only after correction of hyperglycemia. In conclusion, ketosis-prone type 2 diabetes can be distinguished from type I diabetes and classical type 2 diabetes by specific features of clinical pathophysiology and also by the natural history of P-cell dysfunction and insulin resistance reflecting a propensity to glucose toxicity.