Dopamine and opioid receptor pathways in the forebrain drive the desire for food reward, and ingestion of palatable food increases expression of opioid peptides. 4, 5 The forebrain, including the orbitofrontal cortex and nucleus accumbens, appears able to drive food intake despite a lack of hunger or physiologic need for food. Emerging research indicates that sensory properties of food and other pleasant factors involved with food intake stimulate parts of the forebrain recognized as “reward centers.” 1 – 3Īlthough the hypothalamus is the primary site for modulating hunger and satiety, the orbitofrontal cortex of the brain plays a key role in processing interacting sensory inputs including sight, smell, taste, and texture of food. In addition, environmental and sensory factors can disrupt or override physiologic controls of appetite. The ultimate control over chronic regulation of energy balance and body weight is not fully known.ĭisease and drugs can interfere with normal regulatory pathways, contributing to pathologic polyphagia. Such polyphagia can be recognized in patients with hyperadrenocorticism.Ĭhronic regulation of energy intake is driven, in part, by adipose-derived substances such as leptin and adiponectin. 1, 2 Glucocorticoids inhibit action of melanocortins and enhance appetite-stimulating effects of agouti-related peptide. Acting at the same hypothalamic neuroreceptor, melanocortins (α-melanocyte-stimulating hormone ) inhibit food intake and increase energy expenditure via stimulation of thyroid hormone and sympathetic nervous activity. Multiple peripheral signals combine to stimulate release of hypothalamic orexigenic neuropeptides, neuropeptide Y, and agouti-related peptide, which promote food intake as well as decrease energy expenditure. Gut hormones that promote food intake include ghrelin, which is stimulated by hypoglycemia. These effects can be observed in patients with insulinoma and diabetes mellitus. In addition hormones (e.g., insulin, glucagon-like peptide) suppress appetite, whereas insulin deficiency contributes to excessive food intake. Gastrointestinal hormones (e.g., cholecystokinin, peptide YY) initiate a cascade effect that among other changes inhibits appetite. 1, 2 Gastric and duodenal distention trigger inhibitory signals via the vagus nerve, reducing the desire for food. Neuronal and hormonal signals provide feedback to the brainstem and hypothalamic center that controls appetite.
Hunger, or the drive to eat, is the dominant effect that is inhibited by various satiety signals. Control over food intake and energy balance is regulated by multiple, redundant pathways.
0 kommentar(er)
