The role of gastrointestinal vagal afferent fibres in obesity
SJ Kentish, AJ Page - The Journal of Physiology, 2015 - Wiley Online Library
SJ Kentish, AJ Page
The Journal of Physiology, 2015•Wiley Online LibraryGastrointestinal (GI) vagal afferents are a key mediatory of food intake. Through a balance of
responses to chemical and mechanical stimuli food intake can be tightly controlled via the
ascending satiety signals initiated in the GI tract. However, vagal responses to both
mechanical and chemical stimuli are modified in diet‐induced obesity (DIO). Much of the
research to date whilst in relatively isolated/controlled circumstances indicates a shift
between a balance of orexigenic and anorexigenic vagal signals to blunted anorexigenic …
responses to chemical and mechanical stimuli food intake can be tightly controlled via the
ascending satiety signals initiated in the GI tract. However, vagal responses to both
mechanical and chemical stimuli are modified in diet‐induced obesity (DIO). Much of the
research to date whilst in relatively isolated/controlled circumstances indicates a shift
between a balance of orexigenic and anorexigenic vagal signals to blunted anorexigenic …
Abstract
Gastrointestinal (GI) vagal afferents are a key mediatory of food intake. Through a balance of responses to chemical and mechanical stimuli food intake can be tightly controlled via the ascending satiety signals initiated in the GI tract. However, vagal responses to both mechanical and chemical stimuli are modified in diet‐induced obesity (DIO). Much of the research to date whilst in relatively isolated/controlled circumstances indicates a shift between a balance of orexigenic and anorexigenic vagal signals to blunted anorexigenic and potentiated orexigenic capacity. Although the mechanism responsible for the DIO shift in GI vagal afferent signalling is unknown, one possible contributing factor is the gut microbiota. Nevertheless, whatever the mechanism, the observed changes in gastrointestinal vagal afferent signalling may underlie the pathophysiological changes in food consumption that are pivotal for the development and maintenance of obesity.
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