Enterostatin‐A Peptide Regulating Fat Intake

Abstract

YORK. Enterostatin-a peptide regulating fat intake. Obes Res. 1997;5:360-372. 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 peptide 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 lipase during fat digestion. Enterostatin is also produced in the gastric 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 appears in the lymph and circulation. Enterostatin will selectively inhibit fat intake during normal feeding and in experimental paradigms that involve dietary choice. Its anorectic effect has been demonstrated in a number of species. Both peripheral and central sites of action have been proposed. The peripheral mechanism involves an afferent vagal signaling pathway to hypothalamic centers. The central responses are mediated through a pathway that includes both serotonergic and opioidergic components. Chronically, enterostatin reduces fat intake, bodyweight, and body fat. This response may involve multiple metabolic effects of enterostatin, which include a reduction of insulin secretion, an increase in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. A possible pathophysiological role is suggested by studies that have linked low enterostatin production andor responsiveness to strains of rat that become obese and prefer dietary fat. Humans with obesity also exhibit a lower secretion of pancreatic procolipase after a test meal, compared with persons of normal weight.

The effects of yoghurt containing a novel fat emulsion on energy and macronutrient intakes in non-overweight, overweight and obese subjects

“…Although to date we have no measurements of peptide hormone levels following the consumption of Olibra TM , it may be that Olibra TM is acting through an increased and prolonged release of known satiety peptides such as enterostatin 23,24 and glucagon-like peptide-1 (GLP-1). 25 Both have been shown to reduce energy intake and particularly fat intake in the long term which was observed in our previous and current work.…”

Short-term effects of yoghurt containing a novel fat emulsion on energy and macronutrient intakes in non-obese subjects

“…27 Since the decrease in the intake of fat was particularly pronounced following the consumption of Olibra TM , it may be that apolipoprotein A-IV or enterostatin are of particular relevance since they have been shown to inhibit the intake of dietary fat in a number of experimental protocols. 19,24,26 On the other hand, orosensory factors are important in appetite regulation 28 and subjects could have been responding to different sensory cues from the yoghurts. Although both yoghurts were judged to be equally palatable, full descriptive sensory analyses of the two yoghurts are not available.…”

Effect of Long-term High-Fat Feeding on the Expression of Pancreatic Lipases and Adipose Tissue Uncoupling Proteins in Mice

“…Colipase is secreted as a proform, procolipase, which is processed in the intestine to release colipase and a pentapeptide named enterostatin. Enterostatin has been shown to act as a specific satiety signal for fat (6). In rat and mouse pancreas there is twice as much lipase as colipase; hence colipase is the limiting factor for fat digestion (7).…”