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Role of Insulin Resistance Associated With Compensatory Hyperinsulinemia in Ischemic Stroke

 

作者: Kazuya MD Shinozaki,   Hiroaki MD Naritomi,   Takao MD Shimizu,   Masaaki MD Suzuki,   Motoyoshi MD Ikebuchi,   Tohru MD Sawada,   Yutaka MD Harano,  

 

期刊: Stroke: A Journal of Cerebral Circulation  (OVID Available online 1996)
卷期: Volume 27, issue 1  

页码: 37-43

 

ISSN:0039-2499

 

年代: 1996

 

出版商: OVID

 

数据来源: OVID

 

摘要:

Background and PurposeAlthough insulin resistance and hyperinsulinemia play a crucial role in the pathogenesis of atherosclerosis, little is known about their roles in ischemic stroke. The purpose of this study was to clarify whether insulin resistance and hyperinsulinemia are causative factors in the pathogenesis of ischemic stroke.MethodsThirty-four consecutive patients with ischemic stroke, who were normotensive, nondiabetic, and not obese, were classified into three groups--atherothrombotic infarction (n = 16), lacunar infarction (n = 10), and cardioembolic infarction (n equals 8)--based on clinical findings, brain imaging, and cerebral angiography. Both oral glucose tolerance tests and lipid analyses were performed. Insulin sensitivity was determined by the steady state plasma glucose method with the use of octreotide acetate. Data were compared with those of healthy control subjects (n = 15).ResultsSteady state plasma glucose levels were significantly higher in the atherothrombotic infarction group compared with control subjects and the other two stroke groups, indicating the presence of insulin resistance in patients with atherothrombotic infarction. In the atherothrombotic infarction group, the 2-hour insulin area (area under the plasma insulin concentration curve) during a 75-g oral glucose tolerance test was significantly increased and dyslipidemic changes (increased triglyceride and apolipoprotein B, decreased high-density lipoprotein) were observed, whereas these changes were not found in the lacunar infarction and cardioembolic stroke groups.ConclusionsInsulin resistance in association with compensatory hyperinsulinemia and dyslipidemia may be an important pathogenetic factor underlying the development of athero-thrombotic infarction.(Stroke. 1996;27:37-43.)

 



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