Table 1.

anorexigenic or adipose-derives hormones in Prader-Willi syndrome (PWS)

Hormone	Site of production	Site of action	Physiological role	Patients with PWS	References
Obestatin	Stomach, derived from preproghrelin	AgRP in arcuate nucleus	Appetite ↓	Contradictory results	[43,45,48]
			Gastric emptying↓	Higher in young (<3 yr) PWS infants
			Body weight ↓	No difference between obese PWS and obese control
Adiponectin	Adipose tissue	β-cell in pancreas	Insulin sensitivity ↑	Higher in PWS than obese control	[42,44,46]
			Modulate appetite and energy homeostasis
Pancreatic polypeptide (PP)	PP cell in pancreas	Y4 receptors in hypothalamic feeding nuclei	Appetite ↓	Similar or lower in PWS than control	[47]
			Regulate pancreatic secretion	Decreased postprandial level in PWS
Peptide YY	Gastrointestinal tract	NPY receptor	Appetite ↓	Contradictory results	[41,47]
			Gastric motility ↓
			Pancreatic secretion ↓
Adropin	Liver, brain	Multiorgan	Insulin sensitivity ↑	Higher in PWS children	[48]
			Body weight, fat mass ↓
Glucagon like peptide-1	Intestine	Pancreas	Insulin sensitivity ↑	No difference between PWS and control	[46]
			Satiety ↑
Leptin	Adipose tissue	POMC and NPY in arcuate nucleus	Satiety ↑	No difference between obese PWS and obese control	[46,47,49]

AgRP, agouti-related peptide; NPY, neuropeptide Y; POMC, proopiomelanocortin.