Fig. 2.

Schematic diagram illustrating the mechanisms involved in regulating feeding behaviour. Nutrient entry into the GI tract causes stomach and intestine distension, secretion of pancreatic enzymes and BA, altered enteric and vagal nerve signalling and exposure of gut enteroendocrine cells to nutrients with altered circulating gut hormone levels (e.g. decrease in orexigenic hormone ghrelin and increase in anorectic hormones PYY3-36 and GLP-1). Gut-derived signals (nutrients, hormones, and neural) and adipokines (e.g. leptin, IL-6, TNF-alpha and adiponectin) act directly and indirectly upon brainstem and hypothalamic arcuate nuclei (first order neurons: orexigenic NPY/AgRP and anorexigenic POMC/CART). ARC neurons interact with second order neurons in the PVN, and to the LHA. All those mechanisms are involved in the regulation of homeostatic hunger. Social factors, emotion, reward, pleasure, increased food availability and sensory cues can influence brain reward and higher cognitive brain regions leading to altered feeding behaviour (hedonic hunger). Taste and olfactory signals can also influence energy intake acting on both homeostatic and brain reward systems. Insulin leptin, GLP-1, PYY and ghrelin are present in saliva with cognate receptors on taste buds and olfactory neurons. AgRP agouti-related peptide, ARC arcuate nucleus, CART cocaine and amphetamine-regulated transcript, FGF-19 fibroblast growth factor-19, GLP-1 glucagon-like peptide 1, IL-6 interleukin-6, LHA lateral hypothalamic area, NPY neuropeptide Y, PNS peripheral nervous system, PVN paraventricular nucleus, PYY3-36 peptide tyrosine–tyrosine 3-36, POMC pro-opiomelanocortin, SNS sympathetic nervous system