The avoidance of wheat-and gluten-containing products is a worldwide phenomenon. While coeliac disease is wellestablished, much remains unknown about whether gluten can be a trigger of gastrointestinal and/or extra-intestinal symptoms in patients without coeliac disease. In this article, we discuss the latest scientific evidence and our current understanding for the possible mechanisms of this largely ambiguous group, termed 'non-coeliac gluten sensitive' (NCGS). We can conclude that NCGS should be regarded as an independent disease outside of coeliac disease and wheat allergy, and that the number of patients affected is likely to be limited. Many questions remain unanswered and it needs to be verified whether the elimination of dietary gluten alone is sufficient for the control of symptoms, and to understand the overlap with other components of wheat.

Intragastric QHCl decreases prospective and actual food intake in healthy women by interfering with homeostatic and hedonic brain circuits in a ghrelin- and motilin-mediated fashion. These findings suggest a potential of bitter tastants to reduce appetite and food intake, through the gut-brain axis.

Over the past few years, scientific interest in the gut-brain axis (i.e., the bidirectional communication system between the gastrointestinal tract and the brain) has exploded, mostly due to the identification of the gut microbiota as a novel key player in this communication. However, important progress has also been made in other aspects of gut-brain axis research, which has been relatively underemphasized in the review literature. Therefore, in this review, we provide a comprehensive, although not exhaustive, overview of recent research on the functional neuroanatomy of the gutbrain axis and its relevance toward the multidisciplinary field of health neuroscience, excluding studies on the role of the gut microbiota. More specifically, we first focus on irritable bowel syndrome, after which we outline recent findings on the role of the gut-brain axis in appetite and feeding regulation, primarily focusing on the impact of subliminal nutrient-related gut-brain signals. We conclude by providing future perspectives to facilitate translation of the findings from gut-brain axis neuroscientific research to clinical applications in these domains.

This study shows that associative fear learning biases intensity judgements of visceral sensations toward perceiving such sensations as more intense. Learning-induced alterations in visceroception might therefore contribute to the development or maintenance of visceral pain.

The motilin agonist, erythromycin, induces gastric phase III of the migrating motor complex, which in turn generates hunger peaks. To identify the brain mechanisms underlying these orexigenic effects, 14 healthy women participated in a randomized, placebo-controlled crossover study. Functional magnetic resonance brain images were acquired for 50 minutes interprandially. Intravenous infusion of erythromycin (40 mg) or saline started 10 minutes after the start of scanning. Blood samples (for glucose and hormone levels) and hunger ratings were collected at fixed timepoints. Thirteen volunteers completed the study, without any adverse events. Brain regions involved in homeostatic and hedonic control of appetite and food intake responded to erythromycin, including pregenual anterior cingulate cortex, anterior insula cortex, orbitofrontal cortex, amygdala, caudate, pallidum and putamen bilaterally, right accumbens, hypothalamus, and midbrain. Octanoylated ghrelin levels decreased, whereas both glucose and insulin increased after erythromycin. Hunger were higher after erythromycin, and these differences covaried with the brain response in most of the abovementioned regions. The motilin agonist erythromycin increases hunger by modulating neurocircuitry related to homeostatic and hedonic control of appetite and feeding. These results confirm recent behavioural findings identifying motilin as a key orexigenic hormone in humans, and identify the brain mechanisms underlying its effect.The bidirectional neural and hormonal communication system between the brain and the gastrointestinal (GI) tract is known as the 'brain-gut axis' 1 . It is part of an integrated interoceptive system which continuously conveys homeostatic information about the physiological state of the body to the brain.GI hormones are important mediators of these gut-brain interactions 1 . One of these hormones, motilin, is a 22-amino-acid gut peptide secreted by endocrine M cells in the small intestine 2 . Motilin is a physiological regulator of the migrating motor complex (MMC), a cyclical contraction pattern with different phases of activity (phase I-III) originating in the stomach or duodenum and migrating distally in the fasted state 3,4 . Phase III is characterized by strong contractile activity. In healthy humans, gastric but not duodenal phase IIIs are preceded by a motilin peak and exogenous administration of motilin induces a premature gastric phase III 5,6 , which has recently been associated with increases in hunger ratings and with the occurrence of hunger peaks during fasting 7 .Although motilin has thus been associated with the induction of these so-called hunger contractions 8 , the brain mechanisms underlying the putative role of motilin in regulating appetite and eating behavior have not