The taste of sugar elicits cephalic-phase insulin release (CPIR), which limits the rise in blood glucose associated with meals. Little is known, however, about the gustatory mechanisms that trigger CPIR. We asked whether oral stimulation with any of the following taste stimuli elicited CPIR in mice: glucose, sucrose, maltose, fructose, Polycose, saccharin, sucralose, AceK, SC45647, or a nonmetabolizable sugar analog. The only taste stimuli that elicited CPIR were glucose and the glucose-containing saccharides (sucrose, maltose, Polycose). When we mixed an α-glucosidase inhibitor (acarbose) with the latter three saccharides, the mice no longer exhibited CPIR. This revealed that the carbohydrates were hydrolyzed in the mouth, and that the liberated glucose triggered CPIR. We also found that increasing the intensity or duration of oral glucose stimulation caused a corresponding increase in CPIR magnitude. To identify the components of the glucose-specific taste-signaling pathway, we examined the necessity of Calhm1, P2X2+P2X3, SGLT1, and Sur1. Among these proteins, only Sur1 was necessary for CPIR. Sur1 was not necessary, however, for taste-mediated attraction to sugars. Given that Sur1 is a subunit of the ATP-sensitive K channel (K) channel and that this channel functions as a part of a glucose-sensing pathway in pancreatic β-cells, we asked whether the K channel serves an analogous role in taste cells. We discovered that oral stimulation with drugs known to increase (glyburide) or decrease (diazoxide) K signaling produced corresponding changes in glucose-stimulated CPIR. We propose that the K channel is part of a novel signaling pathway in taste cells that mediates glucose-induced CPIR.

Background Temperament and personality traits, including negative emotionality/neuroticism, may represent risk factors for eating disorders. Further, risk factors may differ by sex. We examined longitudinal temperament/personality pathways of risk for purging and binge eating in youth stratified by sex using data from a large-scale prospective study. Methods Temperament, borderline personality features, sensation seeking, ‘big five’ personality factors, and depressive symptoms were measured at five time points from early childhood to adolescence in 5812 adolescents (3215 females; 2597 males) in the Avon Longitudinal Study of Parents and Children. We conducted univariate analyses with these predictors of binge eating and purging at 14 and 16 years for total and sex-stratified samples. We used structural equation modeling (SEM) to fit data to a path analysis model of hypothesized associations. Results Of the total sample, 12.54% engaged in binge eating and 7.05% in purging by 16 years. Prevalence was much greater and increased dramatically for females from 14 years (7.50% binge eating; 2.40% purging) to 16 years (15.80% binge eating; 9.50% purging). For both sexes, borderline personality, depressive symptoms and lower emotional stability predicted eating disorder behaviors; sensation seeking and conscientiousness were also significant predictors for females. SEM identified an ‘emotional instability’ pathway for females from early childhood into adolescence (RMSEA = 0.025, TLI = 0.937 and CFI = 0.970). Conclusions Binge eating and purging are common in female and male adolescents. Early temperament/personality factors related to difficulty regulating emotions were predictive of later adolescent eating disorder behaviors. Results have important clinical implications for eating disorder prevention and intervention.

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Schizophrenia (Sz) is associated with deficits in fluent reading ability that compromise functional outcomes. Here, we utilize a combined eye-tracking, neurophysiological, and computational modeling approach to analyze underlying visual and oculomotor processes. Subjects included 26 Sz patients (SzP) and 26 healthy controls. Eye-tracking and electroencephalography data were acquired continuously during the reading of passages from the Gray Oral Reading Tests reading battery, permitting between-group evaluation of both oculomotor activity and fixation-related potentials (FRP). Schizophrenia patients showed a marked increase in time required per word (d = 1.3, P < .0001), reflecting both a moderate increase in fixation duration (d = .7, P = .026) and a large increase in the total saccade number (d = 1.6, P < .0001). Simulation models that incorporated alterations in both lower-level visual and oculomotor function as well as higher-level lexical processing performed better than models that assumed either deficit-type alone. In neurophysiological analyses, amplitude of the fixation-related P1 potential (P1f) was significantly reduced in SzP (d = .66, P = .013), reflecting reduced phase reset of ongoing theta-alpha band activity (d = .74, P = .019). In turn, P1f deficits significantly predicted increased saccade number both across groups (P = .017) and within SzP alone (P = .042). Computational and neurophysiological methods provide increasingly important approaches for investigating sensory contributions to impaired cognition during naturalistic processing in Sz. Here, we demonstrate deficits in reading rate that reflect both sensory/oculomotor- and semantic-level impairments and that manifest, respectively, as alterations in saccade number and fixation duration. Impaired P1f generation reflects impaired fixation-related reset of ongoing brain rhythms and suggests inefficient information processing within the early visual system as a basis for oculomotor dyscontrol during fluent reading in Sz.