The Role of PYY in Eating Behavior and Diet
Peptide YY (PYY) is a gastrointestinal peptide secreted from the endocrine L cells of the intestine in response to food intake. PYY3–36 is the active form of PYY and is the major form of circulating PYY after a meal. PYY, once released from the intestine to the circulation, can cross the blood brain barrier and act centrally at the level of the arcuate nucleus in the hypothalamus to contribute to eating behavior. PYY3–36’s ability to bind to the Y2 receptor in the arcuate nucleus indicates the key pivotal role of this peptide in body weight regulation. Circulating PYY concentrations rise in response to a caloric load after a meal and peak PYY concentrations are achieved in proportion to the amount of calories ingested and are affected by the macronutrient content of the meal. Fasting and post-prandial PYY concentrations are chronically elevated in populations of energy-deficient women, including women with anorexia nervosa. Fasting PYY concentrations are also elevated in exercising women with functional hypothalamic amenorrhea (FHA). Elevated PYY in the presence of elevated ghrelin may cause a relative ghrelin resistance in women with anorexia nervosa or FHA. Fasting PYY concentrations are suppressed in most studies of obese patients and circulating PYY concentrations are consistently suppressed in obese individuals compared to lean individuals after a meal. Peripherally administered PYY3–36 decrease appetites and 24 h food intake in obese individuals and indicates that administration of PYY3–36 may be a future weight loss aid, by decreasing caloric intake during meal. The PYY response to macronutrients differs between lean and obese individuals and a high-protein diet may be beneficial for obese individuals, potentially increase satiety, and assist with weight control or weight loss.
KeywordsAnorexia Nervosa Energy Deficiency Caloric Load Obese Girl Functional Hypothalamic Amenorrhea
Body mass index
Cocaine- and amphetamine-regulate
Dipeptidly peptidease IV
Function hypothalamic amenorrhea
- Scheid JL, De Souza MJ, Leidy HJ, Williams NI. 2010, unpublished.Google Scholar