In order to investigate the source of the additional circulating cholesterol in hypercholesterolemia induced by neurotensin (NT), 12.5 pmol/100 g body weight NT was injected into the tail veins of rats which received by the same route 1 X 10(6) dpm/100 g body weight cholesterol-4-14C 24 hours earlier. Fifteen minutes later the concentration of the labeled plasma cholesterol was the same in the treated animals and in the controls. However, specific activity of plasma cholesterol significantly decreased in rats that received NT, while it remained unchanged in the controls. These data suggest that the additional circulating cholesterol after the intravenous administration of NT was either newly formed or originated in some tissue where equilibrium between endogenous and exogenous cholesterol has not yet been established.
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