Feeding Pathways

Hunger vs. Satiety Neuroscience (Bears, Connors, Paradiso) Controlled by communication between the gut and parasympathetic nervous system

Some Basic Feeding Terminology Feeding Behavior: –Hyperphagy: increase in food intake (often used to explain pathological eating) –Hypophagy: decrease in food intake Feeding Physiology: –Orexigenic: release of a drug or hormone that increases food intake –Anorexigenic: release of a drug or hormone that decrease food intake

Peripheral Regulation of Food Intake Leptin (anorexigenic; satiety) Ghrelin (orexigenic; hunger)

Dysregulation of leptin leads to… The ob/ob mouse: do not have circulating leptin levels, but this does not mean that they are insensitive to leptin –In fact, they are hypersensitized to exogenously administered leptin. WHY? animal model of Type II diabetes

Central Regulation of Food Intake Hypothalamic Interactions The BIG THREE hypothalamic areas regulating food intake are: 1)Lateral hypothalamus 2)Ventromedial hypothalamus 3)Arcuate Nucleus

Central Regulation of Hyperphagy NPY/AgRP- containing neurons in the arcuate nucleus project onto the other hypothalmic nuclei that inhibit stress- and metabolic- hormone production and enhance feeding behavior

Central Regulation of Hypophagy αMSH/CART- containing neurons in the arcuate nucleus project onto the other hypothalmic nuclei that increase stress- and metabolic-hormone production and inhibit feeding behavior

Balance Between Two Pathways Competitive antagonism for MC4 receptors expressed in lateral hypothalamus is regulated by leptin

Central Regulation of Thirst Communication between neurons in the pituitary (organum vasculosum of lamina terminalis [OVLT] neurons and vasopressin-secreting neurons) and kidneys Diabetes Insipidus arises from dysregulation of this circuitry