“…This result shows BconB to be a potent appetite suppressor via CCK release from EECs and also suggests the direct acceptance of these peptides by CCK-producing I-cells in the small intestine as those peptides already shown in previous studies. [9][10][11]14,15) Although the in vivo study gives no evidence for the suppression of appetite by BconB being CCK-dependent, the strong ability of BconB for CCK release from EECs in vitro suggests that BconB-induced appetite suppression was dependent on CCK secretion. We did not measure the release of CCK in vivo, so there is also a possibility that the BconBinduced appetite suppression was associated with the The rats (14-week-old male Sprague-Dawley animals weighing about 400 g) assigned to 3 groups (water, n ¼ 6), (BconB50, n ¼ 5) and (BconB200, n ¼ 5) were preloaded with either the active CCK-releasing and appetite-suppressing peptide, BconB, as 50 and 200 mg/1 mL of distilled water or with only water as a negative control.…”