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

ArticleinThe American journal of physiology 270(6 Pt 2):R1371-9 · June 1996with12 Reads
Source: PubMed
Abstract
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 ng.ml-1. 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 microU.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 stimulation markedly increased plasma glucagon compared with the control condition (1,258 +/- 621 vs. -2,181 +/- 522 pg.ml-1. 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.
    • "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). "
    Dataset · Apr 2016 · Journal of food and nutrition research
    • "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. "
    [Show abstract] [Hide abstract] 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.
    Full-text · Article · Jan 2015
    • "These authors also found that subjects with higher amylase activity showed significantly lower area under the postprandial blood glucose curve, lower peak blood glucose concentrations and higher serum insulin concentrations than baseline during the preabsorptive period (<10 minutes after starch ingestion) compared to subjects with low salivary amylase activity. Then, it was proposed that the release of starch digestion products in the oral cavity may signal the body to prepare for incoming starch through vagal activation, resulting in an early insulin release termed preabsorptive insulin or cephalic phase of insulin secretion [9,17,18,19]. Interestingly, Butterworth et al. [20] suggest that sweet receptors in the gastrointestinal tract may detect maltose derived from starch, possibly affecting intestinal peptides release that influence Central Nervous System (CNS)mediated control of gastric emptying, insulin secretion and appetite. "
    [Show abstract] [Hide abstract] ABSTRACT: Salivary amylase activity is partially determined by genetic factors and is possibly related with postprandial plasma glucose levels. The aim of this study is to evaluate the association of salivary amylase activity with plasma glucose and insulin levels after consumption of a gelatinized starchy model food (80% amylopectin; 70% gelatinization), as well as to assess the influence of the salivary amylase gene (AMY1) copy-number variation in amylase activity and concentration. Our results show a strong and significant relation between copy-number variation of AMY1 gene measured through qPCR with salivary amylase concentration, with an enhanced correlation with amylase activity when corrected by salivary flow (r = 0.83, P-value = 0.003). Subjects with high salivary amylase activity tend to have a higher early increase in plasma insulin concentration and a lower glycemic response after starch ingestion compared to subjects with low salivary amylase activity, although these observations did not achieve statistical significance (r = 0.41; P-value = 0.23). In conclusion, we found a strong association between copy-number of AMY1 gene with salivary amylase activity and concentration. However, we did not find evidences for a major role of salivary amylase activity on glycemic response after starch consumption.
    Full-text · Article · Jan 2015
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