The food-borne
trichothecene mycotoxins have been documented to cause human and animal
food poisoning.
Anorexia is a hallmark of the
trichothecene mycotoxins-induced adverse effects.
Type B trichothecenes have been previously demonstrated to elicit robust
anorectic responses, and this response has been directly linked to secretion of the gut satiety
hormones cholecystokinin (CCK) and
glucagon-like peptide-17-36
amide (GLP-1). However, less is known about the
anorectic effects and underlying mechanisms of the
type A trichothecenes, including
T-2 toxin (T-2),
HT-2 toxin (HT-2),
diacetoxyscirpenol (
DAS),
neosolaniol (NEO). The purpose of this study was to relate
type A trichothecenes T-2, HT-2,
DAS and NEO-induced
anorectic response to changes plasma concentrations of CCK and
GLP-1. Following both oral gavage and intraperitoneal (IP) administration of 1mg/kg bw T-2, HT-2,
DAS and NEO evoked robust
anorectic response and secretion of CCK and
GLP-1. Elevations of plasma CCK markedly corresponded to
anorexia induction by T-2, HT-2,
DAS and NEO. Following oral exposure, plasma CCK was peaked at 6h, 6h, 2h, 2h and lasted up to 24h, 24h, > 6h, > 6h for T-2, HT-2,
DAS and NEO, respectively. IP exposed to four toxins all induced elevation of CCK with peak point and duration at 6h and >24h, respectively. In contrast to CCK,
GLP-1 was moderately elevated by these toxins. Following both oral and IP exposure, T-2 and HT-2 evoked plasma
GLP-1 elevation with peak point and duration at 2h and 6h, respectively. Plasma
GLP-1 was peaked at 2h and still increased at 6h for IP and
oral administration with
DAS and NEO, respectively. In conclusion, CCK plays a contributory role in
anorexia induction but
GLP-1 might play a lesser role in this response.