PANCREATIC GLUCAGON SUPPRESSES GUSTATORY RESPONSIVENESS TO GLUCOSE

被引:29
作者
GIZA, BK
DEEMS, RO
VANDERWEELE, DA
SCOTT, TR
机构
[1] SANDOZ PHARMACEUT CORP, E HANOVER, NJ 07936 USA
[2] OCCIDENTAL COLL, DEPT PSYCHOL, LOS ANGELES, CA 90041 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1993年 / 265卷 / 06期
关键词
TASTE; NUCLEUS TRACTUS SOLITARIUS; FEEDING; ELECTROPHYSIOLOGY; RAT;
D O I
10.1152/ajpregu.1993.265.6.R1231
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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 mug/kg pancreatic GGN on taste responses in the nucleus tractus solitarius of the rat. Taste activity was elicited by oral application of NaCl, glucose, HCI, and quinine HCI. 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 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.
引用
收藏
页码:R1231 / R1237
页数:7
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