ORAL SENSORY STIMULATION IMPROVES GLUCOSE-TOLERANCE IN HUMANS - EFFECTS ON INSULIN, C-PEPTIDE, AND GLUCAGON

In animals, bypassing the oropharyngeal receptors by intragastric admi nistration of glucose results in glucose intolerance. To determine whe ther the absence of oral sensory stimulation alters glucose tolerance in humans, we monitored plasma levels of glucose and hormones after in tragastric administration of glucose, with and without subjects tastin g food. Plasma glucose area under the curve (AUG) was significahtly lo wer after oral sensory stimulation (3,433 +/- 783 vs. 5,643 +/- 1,397 mg . dl(-1) . 195 min(-1); P < 0.03; n = 8). Insulin and C-peptide AUC s were higher during the first one-half of the sampling period (insuli n, 5,771 +/- 910 vs. 4,295 +/- 712 mu U . ml(-1) . 75 min(-1); P < 0.0 5; C-peptide; 86 +/- 10 vs. 66 +/- 9 ng . ml(-1) . 75 min(-1); P < 0.0 3) and lower during the second one-half of the sampling period compare d with the control condition (1,010 +/- 233 vs. 2,106 mu U . ml(-1) . 120 min(-1); P < 0.025; 31 +/- 8 vs. 56 +/- 18 ng . ml(-1) . 120 min(- 1); P < 0.05; insulin and C-peptide, respectively). Oral sensory stimu lation markedly increased plasma glucagon compared with the control co ndition (1,258 +/- 621vs. -2,181 +/- 522 pg . ml(-1) . 195 min(-1); P < 0.002). These data provide evidence in humans that oral sensory stim ulation influences glucose metabolism and suggest that the mechanisms elicited by this cephalic stimulation are necessary for normal glucose homeostasis.