The rewarding attributes of foods containing fat are associated with the increase in fat consumption, but little is known of how the complex physical and chemical properties of orally ingested fats are represented and decoded in the brain nor how this impacts feeding behavior within the population. Here, functional MRI (fMRI) is used to assess the brain response to isoviscous, isosweet fat emulsions of increasing fat concentration and to investigate the correlation of behavioral and neuroimaging responses with taster status (TS). Cortical areas activated in response to fat, and those areas positively correlated with fat concentration, were identified. Significant responses that positively correlated with increasing fat concentration were found in the anterior insula, frontal operculum and secondary somatosensory cortex (SII), anterior cingulate cortex, and amygdala. Assessing the effect of TS revealed a strong correlation with self-reported preference of the samples and with cortical response in somatosensory areas [primary somatosensory cortex (SI), SII, and midinsula] and the primary taste area (anterior insula) and a trend in reward areas (amygdala and orbitofrontal cortex). This finding of a strong correlation with TS in somatosensory areas supports the theory of increased mechanosensory trigeminal innervation in high 6-n-propyl-2-thiouracil (PROP) tasters and has been linked to a higher risk of obesity. The interindividual differences in blood oxygenation level-dependent (BOLD) amplitude with TS indicates that segmenting populations by TS will reduce the heterogeneity of BOLD responses, improving signal detection power.

Due to unique characteristics, umami substances have gained much attention in the food industry during the past decade as potential replacers to sodium or fat to increase food palatability. Umami is not only known to increase appetite, but also to increase satiety, and hence could be used to control food intake. Therefore, it is important to understand the mechanism(s) involved in umami taste perception. This review discusses current knowledge of the mechanism(s) of umami perception from receptor level to human brain imaging. New findings regarding the molecular mechanisms for detecting umami tastes and their pathway(s), and the peripheral and central coding to umami taste are reviewed. The representation of umami in the human brain and the individual variation in detecting umami taste and associations with genotype are discussed. The presence of umami taste receptors in the gastrointestinal tract, and the interactions between the brain and gut are highlighted. The review concludes that more research is required into umami taste perception to include not only oral umami taste perception, but also the wider "whole body" signaling mechanisms, to explore the interaction between the brain and gut in response to umami perception and ingestion.

Thermal taster status refers to the finding that, in some individuals, thermal stimulation of the tongue elicits a phantom taste. Little is known regarding the mechanism for this, it is hypothesised to be a result of cross‐wiring between gustatory and trigeminal nerves whose receptors co‐innervate papillae on the tongue. To address this, we use functional magnetic resonance imaging to perform the first study of whether the cortical response to gustatory‐trigeminal samples is altered with thermal taster status. We study the response to cold (6°C) gustatory (sweet) samples at varying levels of trigeminal stimulation elicited by CO2 (no CO2, low CO2, high CO2) in thermal taster (TT) and thermal non‐taster (TnT) groups, and evaluate associated behavioural measures. Behaviourally, the TT group perceived gustatory and trigeminal stimuli significantly more intense than TnTs, and were significantly more discriminating of CO2 level. fMRI data revealed elevated cortical activation to the no CO2 sample for the TT group compared to TnT group in taste, oral somatosensory and reward areas. In TnTs, a significant positive modulation in cortical response with increasing level of CO2 was found across taste, somatosensory and reward areas. In contrast, in TTs, a reduced positive modulation with increasing level of CO2 was found in somatosensory areas (SI, SII), whilst a significant negative modulation was found in taste (anterior insula) and reward (ACC) areas. This difference in cortical response to trigeminal stimuli supports cross‐modal integration in TTs, with gustatory and trigeminal nerves highly stimulated by cold gustatory samples due to their intertwined nature. Hum Brain Mapp 37:2263–2275, 2016. © 2016 Wiley Periodicals, Inc.

Background: The consumption of fat is regulated by reward and homeostatic pathways, but no studies to our knowledge have examined the role of high-fat meal (HFM) intake on subsequent brain activation to oral stimuli.Objective: We evaluated how prior consumption of an HFM or water load (WL) modulates reward, homeostatic, and taste brain responses to the subsequent delivery of oral fat.Methods: A randomized 2-way crossover design spaced 1 wk apart was used to compare the prior consumption of a 250-mL HFM (520 kcal) [rapeseed oil (440 kcal), emulsifier, sucrose, flavor cocktail] or noncaloric WL on brain activation to the delivery of repeated trials of a flavored no-fat control stimulus (CS) or flavored fat stimulus (FS) in 17 healthy adults (11 men) aged 25 ± 2 y and with a body mass index (in kg/m2) of 22.4 ± 0.8. We tested differences in brain activation to the CS and FS and baseline cerebral blood flow (CBF) after the HFM and WL. We also tested correlations between an individual’s plasma cholecystokinin (CCK) concentration after the HFM and blood oxygenation level–dependent (BOLD) activation of brain regions.Results: Compared to the WL, consuming the HFM led to decreased anterior insula taste activation in response to both the CS (36.3%; P < 0.05) and FS (26.5%; P < 0.05). The HFM caused reduced amygdala activation (25.1%; P < 0.01) in response to the FS compared to the CS (fat-related satiety). Baseline CBF significantly reduced in taste (insula: 5.7%; P < 0.01), homeostatic (hypothalamus: 9.2%, P < 0.01; thalamus: 5.1%, P < 0.05), and reward areas (striatum: 9.2%; P < 0.01) after the HFM. An individual’s plasma CCK concentration correlated negatively with brain activation in taste and oral somatosensory (ρ = −0.39; P < 0.05) and reward areas (ρ = −0.36; P < 0.05).Conclusions: Our results in healthy adults show that an HFM suppresses BOLD activation in taste and reward areas compared to a WL. This understanding will help inform the reformulation of reduced-fat foods that mimic the brain’s response to high-fat counterparts and guide future interventions to reduce obesity.