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肥胖非裔美国人中的糖尿病酮症酸中毒

Diabetic ketoacidosis in obese African-Americans.

作者信息

Umpierrez G E, Casals M M, Gebhart S P, Mixon P S, Clark W S, Phillips L S

机构信息

Department of Medicine, Emory University School of Public Health, Atlanta, Georgia, USA.

出版信息

Diabetes. 1995 Jul;44(7):790-5. doi: 10.2337/diab.44.7.790.

Abstract

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, 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.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们的初步数据表明,因糖尿病酮症酸中毒(DKA)就诊的非裔美国患者中有15%为肥胖患者。为确定潜在机制,我们分析了35例肥胖DKA患者、22例肥胖高血糖患者、10例消瘦DKA患者和10例肥胖非糖尿病受试者的临床特征以及胰岛素分泌和胰岛素敏感性指标。研究在DKA缓解1天后及随访12周后进行。就诊时,肥胖DKA患者和肥胖高血糖患者对静脉注射葡萄糖均无可检测到的胰岛素反应,但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)为(0.9±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对葡萄糖的AIR均有所改善,但仍显著低于非糖尿病对照受试者(P均<0.01)。相比之下,对胰高血糖素的AIR与肥胖对照受试者无显著差异。两组肥胖糖尿病患者就诊时胰岛素敏感性均降低,随访后有所改善,达到与肥胖非糖尿病对照受试者相似的水平。所有患者均未检测到与胰岛细胞抗体的反应性。随访期间,35例肥胖DKA患者中的25例和22例高血糖患者中的16例能够停用胰岛素治疗,且代谢控制持续良好。我们的结果表明,在非裔美国人中,肥胖的DKA患者代表了II型糖尿病的一个亚组。(摘要截选至250词)

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