DIABETIC-KETOACIDOSIS IN OBESE AFRICAN-AMERICANS
DIABETIC-KETOACIDOSIS IN OBESE AFRICAN-AMERICANS
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DOI：
10.2337/diabetes.44.7.790
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发表时间：
1995-07-01
期刊：
影响因子：
7.7
通讯作者：
PHILLIPS, LS
中科院分区：
文献类型：
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作者：
UMPIERREZ, GE;CASALS, MC;PHILLIPS, LS
我们的初步数据表明，15%的非洲裔美国糖尿病酮症酸中毒（DKA）患者是肥胖的。为探讨糖尿病酮症酸中毒的发病机制，我们对35例肥胖糖尿病酮症酸中毒患者和22例肥胖糖尿病酮症酸中毒患者的临床特点、胰岛素分泌和胰岛素敏感性指标进行了分析。10名瘦型DKA患者和10名肥胖非糖尿病受试者。在DKA消退后1天进行研究。以及12周的随访后。在就诊时，肥胖DKA和肥胖高血糖患者均未检测到对静脉注射葡萄糖的胰岛素反应，但他们对胰高血糖素给药有反应。肥胖DKA患者对胰高血糖素的急性胰岛素反应（AIR）（0.9 ± 0.1 ng/ml）低于肥胖高血糖患者（1.5 ± 0.1 ng/ml，P < 0.01），但显著高于消瘦DKA患者（0.1 ± 0.1 ng/ml，P < 0.01）。随访12周后，两组肥胖糖尿病患者的AIR对葡萄糖的反应均有所改善，但仍显著低于非糖尿病对照组（均P < 0.01）。与此相反，AIR对胰高血糖素的作用与肥胖对照组无显著差异。两组肥胖糖尿病患者的胰岛素敏感性在就诊时均降低，随访后改善至与肥胖非糖尿病对照组相似的水平。与胰岛细胞抗体的反应性没有检测到任何患者。在随访期间，35例肥胖DKA中的25例和22例高血糖患者中的16例能够停止胰岛素治疗，并继续保持良好的代谢控制。我们的结果表明，在非裔美国人中，患有DKA的肥胖患者代表了II型糖尿病的一个子集。虽然在就诊时发现胰岛素分泌和胰岛素作用受损，但胰腺胰岛素储备减少似乎是肥胖患者发生DKA的主要缺陷。
Our preliminary data indicate that 15% of African-American patients presenting with diabetic ketoacidosis (DKA) are obese. To determine underlying mechanisms, we analyzed the clinical characteristics and indexes of insulin secretion and insulin sensitivity in 35 obese patients with DKA, 22 obese patients with hyperglycemia. 10 lean patients with DKA, and 10 obese nondiabetic subjects. Studies were performed 1 day after resolution of DKA. and after 12 weeks of follow-up. At presentation, both obese DKA and obese hyperglycemic patients had no detectable insulin response to intravenous glucose, but they did respond to glucagon administration. The acute insulin response (AIR) to glucagon in obese DKA patients (0.9 +/- 0.1 ng/ml) was lower than in obese hyperglycemic subjects (1.5 +/- 0.1 ng/ml, P < 0.01), but significantly greater than in lean patients with DKA(0.1 +/- 0.1 ng/ml, P < 0.01). After 12 weeks of follow-up, the AIR to glucose improved in both groups of obese diabetic patients but remained significantly lower than in nondiabetic control subjects (both P < 0.01). In contrast, the AIR to glucagon was not significantly different from that in obese control subjects. Insulin sensitivity was decreased in both groups of obese diabetic patients at presentation and improved after follow-up to levels similar to those in obese nondiabetic control subjects. Reactivity with islet cell antibodies was not detected in any of the patients. During follow-up, 25 Of 35 obese DKA and 16 of 22 hyperglycemic patients were able to discontinue insulin therapy, with continued good metabolic control. Our results indicate that in African-Americans, obese patients with DKA represent a subset of type II diabetes. Although impaired insulin secretion and insulin action were found at presentation, decreased pancreatic insulin reserve appears to be the primary defect in the development of DKA in obese patients.