Enterostatin (APGPR), an anorectic pentapeptide derived from the amino terminus of procolipase, significantly reduced serum cholesterol levels after oral administration at a dose of 100 mg/kg for 3 days in mice fed a high-cholesterol-cholic acid diet. The hypocholesterolemic effect of APGPR was inhibited by pretreatment with lorglumide, an antagonist for cholecystokinin 1 (CCK(1)) receptor, even though APGPR does not have any affinity for CCK(1) receptors. Similarly, the hypocholesterolemic activity of VPDPR, an APGPR analogue, was blocked by lorglumide.
View Article and Find Full Text PDFResistance exercise intensity is commonly prescribed as a percent of 1 repetition maximum (1RM). However, the relationship between percent 1RM and the number of repetitions allowed remains poorly studied, especially using free weight exercises. The purpose of this study was to determine the maximal number of repetitions that trained (T) and untrained (UT) men can perform during free weight exercises at various percentages of 1RM.
View Article and Find Full Text PDFThe purpose of this study was to determine the impact of a very slow (VS) velocity and a self-selected volitional (VOL) velocity at varying intensities on repetition number, peak force, peak power, and total volume in the squat and shoulder press exercises. On separate testing days, 9 resistance trained men (age: 23.9 +/- 2.
View Article and Find Full Text PDFEnterostatin (APGPR) is a pentapeptide released from its precursor protein, procolipase. We found for the first time that enterostatin has memory-enhancing activity. Enterostatin enhanced memory consolidation after central or oral administration at a dose of 10 nmol/mouse or 300 mg/kg, respectively, in a step-through type passive avoidance test in mice.
View Article and Find Full Text PDFNeurotensin (NT), a tridecapeptide found in the mammalian brain and peripheral tissues, induces a decrease in food intake after central administration. In this investigation, we examine whether the histaminergic system is involved in NT-induced suppression of feeding. Intracerebroventricular injection of NT (0.
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