PANCREATIC GLUCAGON SUPPRESSES GUSTATORY RESPONSIVENESS TO GLUCOSE

Peripheral administration of the gut peptide pancreatic glucagon (GGN) alters hepatic metabolism and suppresses feeding. Other physical (gas tric distension) and chemical factors (hyperglycemia, hyperinsulinemia ) that reduce food intake also suppress taste-evoked activity. This ma y attenuate the reinforcement derived from feeding and so promote term ination of the meal. To determine whether this mechanism was operative with GGN administration, we studied the effect of hepatic portal infu sions of 40 mug/kg pancreatic GGN on taste responses in the nucleus tr actus solitarius of the rat. Taste activity was elicited by oral appli cation of NaCl, glucose, HCI, and quinine HCI. Responses were monitore d before and after injections of GGN or a control vehicle. Blood gluco se levels were measured in separate groups of GGN- and vehicle-injecte d rats. Blood glucose increased significantly after GGN infusion and r eturned to control levels within 35 min. Taste responsiveness to gluco se was significantly reduced after the GGN injection and recovered to preinjection levels by 36 min. Activity evoked by NaCl, HCl, and quini ne HCI was unaffected. The suppression of responsiveness to sugars may reduce the hedonic appeal of tastants and so serve as a mechanism by which GGN could contribute to postprandial satiety.