The Influence Of Nesfatin-1 And Exendin(9-39) Injected Into The Centre On Food Intaking And Gastrointestinal Regulation In Rats

Objective To investigate the influences and mechanisms of intracerebrov entricular injection with Exendin(9-39) on the changes of food intake and gastrointestinal dy namics induced by Nesfatin-1 in rats.Methods Sixty Wistar rats were randomly divid ed into four group s: normal control group(NC), Nesfatin-1 combined with salin e treated group(NS), Nesfatin-1 combin ed with Exendin(9-39) treated group(NE), Exendin(9-39) combin ed with saline treated group(ES). All the animals wer e surgically imp lanted with indwellin g cannulas in the PVN, then Nesfatin-1 or Exendin(9-39) was deliver ed to the PVN, food and water intake as well as body weight were measured before the in jection, the same data were measured at 12 hour and 24 hour after the injection. Gastric emp ty ing was measured by intragastric admin istration of methy l cellulose-p henol red solution. The exp ression levels of GLP-1 recep tor m RNA in the hyp othalamus and stomach were measured by RT-PCR.Results Comp ared with basal food intake, NS group rats exh ibited mark edly food intake decrease 12 h、24 h after injection(P<0.05), NE group exhib ited food incr ease co mp ared with NS group(P<0.05), but an opp osite result comp ared with NC group 12h、24h after injection(P<0.05). NS and NE group showed water intake decrease 12h、24h after injection co mp ared wit h basal water intake(P<0.05). Comp ared with basal body weight, NS group rats exh ibited body weight decr ease 12 h、24 h after injection(P<0.05), NE group exh ibited body weight decr ease 12 h after injection(P<0.05), but an opp osite result comp ared with NS group(P<0.05); NS group rats exhib ited lower gastric emp ty ing comp ared with NC and NE group after injection(P<0.05). The levels of hy p othalamic GLP-1Rm RNA were increased comp ared with NC group(P<0.05). Conclusions: GLP-1 recep tor antagonist could abate the inhib ition of f eedin g and gastrointestinal motility caused by Nesfatin-1. This result suggested CNS GLP-1 neurons may be a target for the satiety hormone Nesfatin-1. Nesfatin-1 may interact with GLP-1 neurons to involved in f eedin g and the regulation of gastrointestinal motility.