Beta-lactotensin and neurotensin rapidly reduce serum cholesterol via NT2 receptor.

Beta-lactotensin, a neurotensin NT2 agonist derived from beta-lactoglobulin, has hypocholesterolemic activity after administration for 2 days at a dose of 30 mg/kg (i.p.) or 100 mg/kg (p.o.) for 2 days in mice fed a high-cholesterol/cholic acid diet. The onset of hypocholesterolemic activity of beta-lactotensin was observed 90 min after a single i.p. or p.o. administration at the same dose as described above. Neurotensin also induced hypocholesterolemic activity 90 min after single i.p. administration at a dose of 2 microg per mouse but was ineffective after oral administration. The rapid onset of hypocholesterolemic activities of beta-lactotensin and neurotensin was blocked by levocabastine (50 microg/kg), an NT2 antagonist, and raclopride (0.5 mg/kg), a dopamine D2 antagonist.