title: Amelioration of the inhibition of fibrinolysis in elderly, obese subjects by moderate energy intake restriction.
abstract: A possible cause of accelerated atherothrombosis in the syndrome of insulin resistance appears to be an elevated blood concentration of plasminogen activator inhibitor type-1 (PAI-1). Insulin resistance occurs with aging, attributable partly to increased adiposity. Scarce information exists regarding the effects of weight loss in elderly, obese individuals on PAI-1 concentrations. Consequently, weight loss (9 +/- 1 kg) was induced by energy intake restriction in 19 elderly, obese individuals, and its effect on fibrinolytic system peptides was measured. Initially elevated PAI-1 concentrations decreased by 50%, with a simultaneous decrease in the concentration of tissue-type plasminogen activator (t-PA)/PAI-1 complexes but no significant change in t-PA suggested a decrease in inhibition of the fibrinolytic system. The concentration of plasmin/antiplasmin complexes (PAP complex) increased by approximately 20%, indicating augmented fibrinolytic system activity. The decline in PAI-1 correlated with that of the decrease in body weight (r = 0.5, P < 0.05) and fat mass losses (r = 0.46, P < 0.05). The increase in PAP complexes correlated with weight and fat mass losses (r = 0.4 and r = 0.46, respectively; P < 0.05 for both). No correlation was seen between fibrinolytic system variables and baseline concentrations of substrates or insulin, but the change in PAI-1 correlated with the change in plasma triacylglycerols (r = 0.58, P < 0.05). Results indicate that energy restriction sufficient to induce moderate weight loss leads to diminution of elevated plasma PAI-1 and relief of inhibition of the fibrinolytic system in elderly, obese subjects. To the extent that these changes are associated with a decrease in the progression of vasculopathy, weight loss in elderly, obese individuals may be a useful means to reduce cardiovascular morbidity and mortality.
authors.affiliation: Sims Obesity/Nutrition Research Center, University of Vermont, Burlington 05405-0068, USA.
authors.forename: J
authors.initials: J
authors.lastname: Calles-Escandon
authors.forename: D
authors.initials: D
authors.lastname: Ballor
authors.forename: J
authors.initials: J
authors.lastname: Harvey-Berino
authors.forename: P
authors.initials: P
authors.lastname: Ades
authors.forename: R
authors.initials: R
authors.lastname: Tracy
authors.forename: B
authors.initials: B
authors.lastname: Sobel
mesh_terms: D000368:Aged; D000375:Aging; D001161:Arteriosclerosis / Q000209:etiology; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004038:Diet, Reducing; D002149:Energy Intake; D005342:Fibrinolysis; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008875:Middle Aged; D009765:Obesity / Q000097:blood* / Q000178:diet therapy*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D007328:Insulin; D017395:Plasminogen Activator Inhibitor 1