Ramos-Román María A, Piñero-Piloña Antonio, Adams-Huet Beverley, Raskin Philip
Department of Internal Medicine at the University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-8858, USA.
J Diabetes Complications. 2006 May-Jun;20(3):137-44. doi: 10.1016/j.jdiacomp.2006.01.005.
Atypical ketosis-prone diabetes (KPD) is frequently detected in obese individuals at diagnosis of diabetes, yet its precise pathophysiology is not understood.
The hypothesis tested in this study states that while individuals with atypical KPD are phenotypically similar to those with type 2 diabetes, metabolically, they behave more like individuals with autoimmune type 1 diabetes.
Thirty-seven individuals of Black, Hispanic, or White background and a diagnosis of diabetes mellitus for an average duration of 4 years participated in this cross-sectional study. Ten, 12, and 15 subjects had type 1, atypical, and type 2 diabetes, respectively. Insulin secretion was evaluated by a mixed-meal test. Insulin sensitivity and fuel oxidation were assessed by simultaneous euglycemic hyperinsulinemic clamp and indirect calorimetry. Lastly, a 12-h insulin withdrawal test was performed.
Insulin secretion, insulin sensitivity, and the insulin withdrawal tests yielded significant differences for type 1 vs. atypical diabetes and type 1 vs. type 2 diabetes, while there were no significant differences between atypical vs. type 2 diabetes. The indirect calorimetry showed higher-than-normal basal nonprotein respiratory quotients (RQs) and lower-than-normal insulin-stimulated nonprotein RQs across the three study groups.
After 4 years from diabetes diagnosis and while far from optimal glycemic control, atypical KPD resembles type 2 diabetes phenotypically and metabolically as well. Therefore, this study supports the classification of atypical KPD as ketosis-prone type 2 diabetes, and the concept that metabolic inflexibility occurs in the presence of insulin resistance in type 1 and type 2 diabetes.
非典型易发生酮症糖尿病(KPD)在糖尿病诊断时常见于肥胖个体,但其确切病理生理学尚不清楚。
本研究检验的假设是,虽然非典型KPD个体在表型上与2型糖尿病个体相似,但在代谢方面,他们的行为更类似于自身免疫性1型糖尿病个体。
37名具有黑人、西班牙裔或白人背景且糖尿病诊断平均病程为4年的个体参与了这项横断面研究。分别有10名、12名和15名受试者患有1型、非典型和2型糖尿病。通过混合餐试验评估胰岛素分泌。通过同步正常血糖高胰岛素钳夹和间接量热法评估胰岛素敏感性和燃料氧化。最后,进行了12小时胰岛素撤药试验。
胰岛素分泌、胰岛素敏感性和胰岛素撤药试验在1型与非典型糖尿病以及1型与2型糖尿病之间产生了显著差异,而非典型与2型糖尿病之间没有显著差异。间接量热法显示,在三个研究组中,基础非蛋白呼吸商(RQ)高于正常,胰岛素刺激后的非蛋白RQ低于正常。
糖尿病诊断4年后,尽管血糖控制远未达到最佳状态,但非典型KPD在表型和代谢方面也类似于2型糖尿病。因此,本研究支持将非典型KPD分类为易发生酮症的2型糖尿病,以及1型和2型糖尿病在存在胰岛素抵抗时会出现代谢灵活性受损的概念。