Role of cholecystokinin in anorexia induction following oral exposure to the 8-Ketotrichothecenes de

来源 :中国畜牧兽医学会家畜内科学会2014年学术研讨会 | 被引量 : 0次 | 上传用户:coding_key
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  Cereal grain contamination by trichothecene mycotoxins is known to negatively impact human and animal health with adverse effects on food intake and growth being of particular concern.The head blight fungus Fusarium graminearum elaborates five closely related 8-ketotrichothecene congeners: (1) deoxynivalenol (DON), (2) 3-acetyldeoxynivalenol (3-ADON), (3) 15-acetyldeoxynivalenol (15-ADON), (4) fusarenon X (FX) ,and (5) nivalenol (NIV).While anorexia induction in mice exposed intraperitoneally to DON has been linked to plasma elevation of the satiety hormones cholecystokinin (CCK) and peptide YY3-36 (PYY3-36), the effects of oral gavage of DON or of other 8-keotrichothecenes on release of these gut peptides have not been established.The purpose of this study was to (1) compare the anorectic responses to the aforementioned 8-ketotrichothecenes following oral gavage at a common dose (2.5mg/kg bw) and (2) relate these effects to changes plasma CCK and PYY3-36 concentrations.Elevation of plasma CCK markedly corresponded to anorexia induction by DON and all other 8-ketotrichothecenes tested.Furthermore, the CCK1 receptor antagonist SR 27897 and the CCK2 receptor antagonist L-365,260 dose-dependently attenuated both CCK-and DON-induced anorexia, which was consistent with this gut satiety hormone being an important mediator of 8-ketotnchothecene-induced food refusal.In contrast to CCK, PYY3-36was moderately elevated by oral gavage with DON and NIV but not by 3-ADON, 15-ADON, or FX.Taken together, the results suggest that CCK plays a major role in anorexia induction following oral exposure to 8-ketotrichothecenes, whereas PYY3-36 might play a lesser, congener-dependent role in this response.
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