ENTEROSTATIN - A PEPTIDE REGULATING FAT INTAKE

A high fat intake, together with an inability to match lipid oxidation to fat intake, has been found to be correlated with obesity in humans , This review describes our current understanding of enterostatin, a p eptide that selectively reduces fat intake, Enterostatin is formed in the intestine by the cleavage of secreted pancreatic procolipase, the remaining colipase serving as an obligatory cofactor for pancreatic li pase during fat digestion, Enterostatin is also produced in the gastri c mucosa and the mucosal epithelia of the small intestine, Procolipase gene transcription and enterostatin release into the gastrointestinal lumen are increased by high-fat diets, After feeding, enterostatin ap pears in the lymph and circulation, Enterostatin will selectively inhi bit fat intake during normal feeding and in experimental paradigms tha t involve dietary choice, Its anorectic effect has been demonstrated i n a number of species, Both peripheral and central sites of action hav e been proposed, The peripheral mechanism involves an afferent vagal s ignaling pathway to hypothalamic centers, The central responses are me diated through a pathway that includes both serotonergic and opioiderg ic components, Chronically, enterostatin reduces fat intake, bodyweigh t, and body fat, This response may involve multiple metabolic effects of enterostatin, which include a reduction of insulin secretion, an in crease in sympathetic drive to brown adipose tissue, and the stimulati on of adrenal corticosteroid secretion, A possible pathophysiological role is suggested by studies that have linked low enterostatin product ion and/or responsiveness to strains of rat that become obese and pref er dietary fat. Humans with obesity also exhibit a lower secretion of pancreatic procolipase after a test meal, compared with persons of nor mal weight.