J Korean Soc Study Obes 2000; 9(2): 101-111
Published online July 1, 2000
Copyright © Korean Society for the Study of Obesity.
Seung-Joon Oh,Young-Seol Kim,Cheol-Young Park,Deog-Yoon Kim,Sung-Woon Kim,In-Myung Yang,Jin-Woo Kim,Young-Kil Choi,Jeng Ryung Paeng,Kyung-Chun Jeong1
Department of Internal Medicien, Department of Neurology1, School of Medicine, Kyung Hee University, Seoul, Korea
Plasminogen activator inhibitor-1 (PAI-1) is known be related to insulin resistance and several components of the large vascular disease. Notably, the high frequencies of diseases such as coronary heart disease or stroke are related to type 2 diabetes complications.
We studied to find out whether the PAI-1 promoter genotype could be a marker for cerebral infarction in type 2 patients. Subject patients were; 56 type 2 diabetics (age 58.3±12.6), 51 patients with cerebral infarction (age 63.1±13.2), 48 type 2 diabetics with cerebral infarction (age 64.8±9.3), and 76 healthy control (age 46.4±11.1).
The 4G/5G genotype of PAI-1 promoter was evaluated by polymerase chain reaction and endonuclease digestion. PAI-1 concentration and activity were assessed by EIA method (Biopool, CA, USA). PAI-1 promoter genotype frequency (4G/4G, 4G/5G, 5G/5G) was 23.7%, 75.0% and 1.3% in healthy control, 17.9%, 67.9% and 14.3% in type 2 diabetes patients, 19.6%, 66.7% and 13.7% in cerebral infarction patients, 33.3%, 58.3% and 8.3% in type 2 diabetics with cerebral infarction (X2=12.6, p=0.05). This finding is lower in frequency of 5G/5G homozygote than that reported in Caucasians.
The plasma PAI-1 concentrations according to the disease were 13.4, 1.8∼65.2 ng/mL (median, range) for healthy control, 14.4, 2.9∼47.8 ng/mL for type 2 diabetes, 21.9, 6.2∼154.7 ng/mL for cerebral infarction, and 28.8, 3.2∼139.3 ng/mL, for cerebral infarction with type 2 diabetes (p=0.000). In the all subjects, PAI-1 concentration and activity of PAI-1 promoter genotype did not show any significant difference. However, the PAI-1 activity was independently associated with serum triglyceride level, plasma proinsulin and BMI (p=0.000, p=0.000 and p=0.005 respectively).
We concluded that PAI-1 genotype is not a marker for the cerebral infraction; however, the genotype is related to PAI-1 concentration, and therefore it seems to be that metabolic factors such as triglyceride level or plasma proinsulin or BMI are more in relations with determining the PAI-1 concentration than the genotype.
Keywords: Plasminogen activator inhibitor 1, diabetes, Non-insuln dependene, Cerebral Infarction, Insulin resistance, Diabetis angiopathies