Ao. Akanji et I. Alshayji, THE RELATIONSHIPS BETWEEN INSULIN AND PLASMINOGEN-ACTIVATOR INHIBITOR-1 LEVELS - ASSESSMENT IN GROUPS OF SUBJECTS WITH DYSLIPIDEMIA AND HYPERTENSION, Clinica chimica acta, 274(1), 1998, pp. 41-52
Elevated plasminogen activator inhibitor-1 (PAI-1) levels have been de
scribed in some populations to associate with hyperinsulinaemia in the
metabolic syndrome which predisposes to coronary heart disease (CHD).
This association, if consistently present, could provide more evidenc
e for a synergistic role for insulin resistance and altered fibrinolys
is in the pathogenesis of CHD. To test the hypothesis further therefor
e. we explored the relationships between the fasting levels of insulin
and PAI-I and lipids in groups of non-diabetic Arab subjects classifi
ed as: A: normolipidaemic (II = 148); B: hyperlipidaemic: (n = 99), su
bdivided into - C: normotensive (n = 71) and D: hypertensive (n = 28);
and E: patients with CHD (n = 12). In Group A, fasting insulin (FI) w
as 7.2+/-(SD) 3.4 mU/l, PAI-1 30.6+/-9.7 ng/ml, both levels significan
tly lower (P < 0.05) than in Group B as a whole (FI 9.7+/-5.2, PAI-1 3
6.9+/-10.6), or as normotensive Group C (FI 9.4+/-5.4, PAI-1 36.7+/-10
.3) or hypertensive Group D (FI 10.9+/-4.8, PAI-1 37.2+/-11.5). These
values were highest in the hyperlipidaemic hypertensive Group D. There
were no significant differences relative to the hyperlipidaemic pheno
type of predominant hypercholesterolaemia, hypertriglyceridaemia or mi
xed hyperlipidaemia. PAI-1 (34.7+/-13.8) and Fl (7.0+/-2.4) levels in
Group E with CHD were similar to those of Group A but lower than Value
s seen in Groups B, C and D, Consistent positive correlations (r = 0.3
2-0.41, P < 0.01) were demonstrable in all the groups between PAI-1 an
d triglycerides levels. There were also significant correlations betwe
en insulin and PAI-1 (r = 0.20, P < 0.1) in all the subjects (grouped
as a whole, n = 259) and in normolipidaemic Group A (r = 0.29, P < 0.0
1) but not in any of the hyperlipidaemic groups or in patients with CH
D. This study therefore suggests that levels of insulin and PAI-1 are
increased in hyperlipidaemic subjects, particularly when also hyperten
sive. The further observation of significant correlations between insu
lin and PAI-1 levels only in normolipidaemic subjects and not those wh
o were hyperlipidaemic or with CHD is at variance with observations in
Caucasians in whom strong positive correlations between insulin and P
AI-1 had suggested that elevated PAI-I levels should constitute one mo
re component of the metabolic syndrome which strongly predisposes to C
HD. Whether this is a racial variation or an artifact of the insulin/P
AI-1 assay methodology is unclear and deserves further study. (C) 1998
Elsevier Science B.V. All rights reserved.