Polyphagia and Hyperphagia

Chapter 19 Polyphagia and Hyperphagia

Appetite Control

Control over food intake and energy balance is regulated by multiple, redundant pathways. Hunger, or the drive to eat, is the dominant effect that is inhibited by various satiety signals. Neuronal and hormonal signals provide feedback to the brainstem and hypothalamic center that controls appetite.1,2 Gastric and duodenal distention trigger inhibitory signals via the vagus nerve, reducing the desire for food. Gastrointestinal hormones (e.g., cholecystokinin, peptide YY) initiate a cascade effect that among other changes inhibits appetite. In addition hormones (e.g., insulin, glucagon-like peptide) suppress appetite, whereas insulin deficiency contributes to excessive food intake. These effects can be observed in patients with insulinoma and diabetes mellitus.

Gut hormones that promote food intake include ghrelin, which is stimulated by hypoglycemia. 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. Acting at the same hypothalamic neuroreceptor, melanocortins (α-melanocyte-stimulating hormone [MSH]) inhibit food intake and increase energy expenditure via stimulation of thyroid hormone and sympathetic nervous activity.1,2 Glucocorticoids inhibit action of melanocortins and enhance appetite-stimulating effects of agouti-related peptide. Such polyphagia can be recognized in patients with hyperadrenocorticism.

Chronic regulation of energy intake is driven, in part, by adipose-derived substances such as leptin and adiponectin. The ultimate control over chronic regulation of energy balance and body weight is not fully known.

Disease and drugs can interfere with normal regulatory pathways, contributing to pathologic polyphagia. In addition, environmental and sensory factors can disrupt or override physiologic controls of appetite. 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.”13

Although 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.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. Dopamine and opioid receptor pathways in the forebrain drive the desire for food reward, and ingestion of palatable food increases expression of opioid peptides.3,4 Signals from this reward center can override satiety factors and stimulate food consumption.

Sensory-specific satiety is a decrease in appetite for a particular food rather than for food in general,5 and is controlled by the orbitofrontal cortex. Recognition of sensory-specific satiety helps explain increased intake that often follows introduction of new foods or new flavors. Dogs and cats, like humans, tend to overeat when presented with a variety of foods.6 After a time intake will decrease toward or even below energy needs, probably due to sensory-specific satiety as well as physiologic controls of energy balance. However, if novel foods are frequently introduced this stabilization does not take place, and the animal continues to gain weight.7

Stress and boredom are additional external factors that can increase food intake. Stress may stimulate appetite via increased release of endogenous corticosteroids or other orexigenic peptides.8 The role of boredom is less understood but may increase appetite via forebrain mechanisms. Alternate, nonfood stimuli of the reward center may be helpful in managing this type of hyperphagia.

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Jul 10, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Polyphagia and Hyperphagia

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