Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

It is not clear whether elevated levels of the fibrinolytic inhibitor, plasminogen activator inhibitor-1 (PAl-1) in Type 2 diabetes mellitus are the result of obesity or coexistent atherosclerosis. Therefore the relationship between PAl-1 and insulin resistance, determined by the homeostasis model assessment (HOMA) was investigated in a group of 26 insulin-resistant, normotensive newly diagnosed Type 2 diabetic patients with a low probability of atherosclerosis. Compared with a normal control group, closely matched for body mass index (BMI), fibrinolytic activity was depressed in the diabetic patients due to elevated levels of the inhibitor PAl-1, 17.6 (11.1-28) vs 8.4 (4.9-14.1) IU ml-1, p < 0.001. PAl-1 was related to BMI, r = 0.59, p < 0.001 plasma insulin, r = 0.66, p < 0.001; insulin resistance, r = 0.54, p < 0.005 and urinary albumin excretion, r = 0.48, p < 0.01, but not HbA1c or fasting glucose. PAl-1 was not related to blood pressure or plasma triglyceride levels. This study suggests that at the time of diagnosis of Type 2 diabetes mellitus, elevated PAl-1 levels are already linked to other risk factors for vascular disease including hyperinsulinaemia, insulin resistance, and urinary albumin excretion, and this is not the result of obesity or coexistent atherosclerosis.

Type

Journal article

Journal

Diabet Med

Publication Date

08/1993

Volume

10

Pages

638 - 642

Keywords

Blood Glucose, Blood Pressure, Cholesterol, Diabetes Mellitus, Type 2, Female, Fibrinolysis, Glycated Hemoglobin A, Homeostasis, Humans, Insulin, Insulin Resistance, Islets of Langerhans, Male, Middle Aged, Models, Biological, Plasminogen Activator Inhibitor 1, Reference Values, Sex Factors, Tissue Plasminogen Activator, Triglycerides