Influence of dietary supplementation with olive oil on pyroglutamyl-beta-naphthylamide hydrolysing activity in serum and different tissues of mice.
Pyroglutamyl aminopeptidase is an omega peptidase which removes pyroglutamyl N-terminal residues from peptides and arylamide derivatives. To date, three distinct types of this enzyme have been described and called serum thyroliberinase, cytosolic pyroglutamyl aminopeptidase type I and membrane-bound pyroglutamyl aminopeptidase type II. The activity of all of them is thought to be involved in the regulation, more or less restricted in their substrate specificity, of various susceptible endogenous substrates such as TRH, GnRH, neurotensin, bombesin and anorexogenic peptide. It is well known that the type and amount of fat in the diet not only modify blood lipid concentrations, including cholesterol levels, but change the cell membrane lipid composition. Modifications in the composition and physical properties of the membrane lead to alterations in the activities of membrane-bound enzymes and carriers. The aim of this work was to compare the effect of a standard diet and a high fat diet (olive oil, 20% wt/wt) on pyroglutamyl-beta-naphthylamide hydrolysing activity, in serum and in soluble and membrane-bound fractions from different tissues of male mice. After ten weeks of feeding, pyroglutamyl-beta-naphthylamide hydrolysing activity was measured fluorometrically using pyroglutamyl-beta-naphthylamide as substrate. Mice fed the high fat diet had higher rates of body weight than controls starting from the second week of feeding. Serum total cholesterol concentrations were higher after feeding the high fat diet than after feeding the control diet. In serum, no changes were observed in the high fat group. In selected tissues, only pyroglutamyl-beta-naphthylamide hydrolysing activity was modified significantly in the soluble fraction, but not in the membrane-bound one, decreasing in the adrenal gland of high fat fed animals. The results may reflect functional modifications in susceptible endogenous substrates.