Pancreatic glucagon suppresses gustatory responsiveness to glucose

Abstract

Peripheral administration of the gut peptide pancreatic glucagon (GGN) alters hepatic metabolism and suppresses feeding. Other physical (gastric distension) and chemical factors (hyperglycemia, hyperinsulinemia) that reduce food intake also suppress taste-evoked activity. This may attenuate the reinforcement derived from feeding and so promote termination of the meal. To determine whether this mechanism was operative with GGN administration, we studied the effect of hepatic portal infusions of 40 micrograms/kg pancreatic GGN on taste responses in the nucleus tractus solitarius of the rat. Taste activity was elicited by oral application of NaCl, glucose, HCl, and quinine HCl. Responses were monitored before and after injections of GGN or a control vehicle. Blood glucose levels were measured in separate groups of GGN- and vehicle-injected rats. Blood glucose increased significantly after GGN infusion and returned to control levels within 35 min. Taste responsiveness to glucose was significantly reduced after the GGN injection and recovered to preinjection levels by 36 min. Activity evoked by NaCl, HCl, and quinine HCl 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.