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.
"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. "
"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. "
[Show abstract][Hide abstract] ABSTRACT: Atypical antipsychotic (AAP) medications that have revolutionized the treatment of mental illness have become stigmatized by metabolic side effects, including obesity and diabetes. It remains controversial whether the defects are treatment induced or disease related. Although the mechanisms underlying these metabolic defects are not understood, it is assumed that the initiating pathophysiology is weight gain, secondary to centrally mediated increases in appetite. To determine if the AAPs have detrimental metabolic effects independent of weight gain or psychiatric disease, we administered olanzapine, aripiprazole, or placebo for 9 days to healthy subjects (n = 10, each group) under controlled in-patient conditions while maintaining activity levels. Prior to and after the interventions, we conducted a meal challenge and a euglycemic-hyperinsulinemic clamp to evaluate insulin sensitivity and glucose disposal. We found that olanzapine, an AAP highly associated with weight gain, causes significant elevations in postprandial insulin, glucagon-like peptide 1 (GLP-1), and glucagon coincident with insulin resistance compared with placebo. Aripiprazole, an AAP considered metabolically sparing, induces insulin resistance but has no effect on postprandial hormones. Importantly, the metabolic changes occur in the absence of weight gain, increases in food intake and hunger, or psychiatric disease, suggesting that AAPs exert direct effects on tissues independent of mechanisms regulating eating behavior.
"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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