Oral sensory stimulation improves glucose tolerance in humans: Effects on insulin, C-peptide, and glucagon

Monell Chemical Senses Center, Philadelphia, Pennsylvania 19104, USA.
The American journal of physiology (Impact Factor: 3.28). 06/1996; 270(6 Pt 2):R1371-9.
Source: PubMed


In animals, bypassing the oropharyngeal receptors by intragastric administration of glucose results in glucose intolerance. To determine whether the absence of oral sensory stimulation alters glucose tolerance in humans, we monitored plasma levels of glucose and hormones after intragastric administration of glucose, with and without subjects tasting food. Plasma glucose area under the curve (AUC) was significantly lower 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 AUCs were higher during the first one-half of the sampling period (insulin, 5,771 +/- 910 vs. 4,295 +/- 712 microU. ml-1.75 min-1; P < 0.05; C-peptide, 86 +/- 10 vs. 66 +/- 9 75 min-1; P < 0.03) and lower during the second one-half of the sampling period compared with the control condition (1,010 +/- 233 vs. 2,106 120 min-1; P < 0.025; 31 +/- 8 vs. 56 +/- 18 120 min-1; P < 0.05; insulin and C-peptide, respectively). Oral sensory stimulation markedly increased plasma glucagon compared with the control condition (1,258 +/- 621 vs. -2,181 +/- 522 195 min-1; P < 0.002). These data provide evidence in humans that oral sensory stimulation influences glucose metabolism and suggest that the mechanisms elicited by this cephalic stimulation are necessary for normal glucose homeostasis.

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    • "To our best knowledge, no studies have been conducted on the effect of moderate alcohol consumption on the satiety or reward response of orally sensed food. A method to study orosensory stimulation is the modified sham feeding (MSF) technique, in which food is smelled, chewed and tasted, but not swallowed (Joosten, de Graaf, Rietman, Witkamp, & Hendriks, 2010; Teff & Engelman, 1996; Wijlens et al., 2012). By the use of MSF after alcohol consumption the role of orosensory stimulation in alcohol's effect on food intake and food reward can be investigated. "
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    ABSTRACT: The aim of this study was to investigate whether food reward plays a role in the stimulating effect of moderate alcohol consumption on subsequent food intake. In addition, we explored the role of oral and gut sensory pathways in alcohol's effect on food reward by modified sham feeding (MSF) or consumption of a preload after alcohol intake. In a single-blind crossover design 24 healthy men were randomly assigned to either consumption of vodka/orange juice (20 g alcohol) or orange juice only, followed by consumption of cake, MSF of cake or no cake. Food reward was evaluated by actual food intake measured by an ad libitum lunch 45 min after alcohol ingestion and by behavioural indices of wanting and liking of four food categories (high fat, low fat, sweet and savoury). Moderate alcohol consumption increased food intake during the ad libitum lunch by 11% (+338 kJ, P = 0.004). Alcohol specifically increased intake (+127 kJ, P < 0.001) and explicit liking (P = 0.019) of high-fat savoury foods. Moreover, moderate alcohol consumption increased implicit wanting for savoury (P = 0.013) and decreased implicit wanting for sweet (P = 0.017) before the meal. Explicit wanting of low-fat savoury foods only was higher after alcohol followed by no cake as compared to after alcohol followed by cake MSF (P =0.009), but not as compared to alcohol followed by cake consumption (P = 0.082). Both cake MSF and cake consumption had no overall effect on behavioural indices of food reward. To conclude, moderate alcohol consumption increased subsequent food intake, specifically of high-fat savoury foods. This effect was related to the higher food reward experienced for savoury foods. The importance of oral and gut sensory signalling in alcohol's effect on food reward remains largely unclear. Copyright © 2015. Published by Elsevier Ltd.
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    • "We had hypothesized that meal ingestion, which elicits incretin responses (33,34) and neurally mediated insulin release (35,36), would be more likely to unveil the effects of a centrally mediated psychiatric agent than glucose methodologies that bypass activation of the brain-gut-pancreas axis. Our findings of increases in postprandial insulin and the incretin hormone GLP-1 support this initial hypothesis. "
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    • "The primary metabolic changes occurring during this phase are gallbladder contraction (Witteman et al., 1993), gastric acid production (Feldman & Richardson, 1986), and stimulation of both the exocrine and endocrine pancreas (Konturek & Konturek, 2000). Its physiological relevance in response to meal ingestion becomes apparent when blocking (Ahren & Holst, 2001) or bypassing (Teff & Engelman, 1996a) the cephalic phase, which has detrimental effects on postprandial glycemia and insulinemia. Moreover, modified sham-feeding (MSF), a method to provoke cephalic phase responses, with fatty foods alters mobilization of free fatty acids (FFA), triglycerides and glucose in the postprandial state (Heath, Jones, Frayn, & Robertson, 2004; Mattes, 1996; Robertson, Jackson, Williams, Fielding, & Frayn, 2001; Robertson, Mason, & Frayn, 2002; Smeets & Westerterp-Plantenga, 2006a). "
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