Energy/Endurance

Effect of Enterostatin

A peptide that acts similar to Cyclo (His-Pro) is enterostatin. Enterostatin is a pentapeptide that has been shown to be selective in inhibiting fat intake. It is formed following the cleavage of the enzyme procolipase by trypsin in the gastric juice of the intestinal lumen. Procolipase is an enzyme essential for fat digestion.

Following the cleavage of procolipase, enterostatin and colipase are produced. Colipase is an obligatory cofactor for pancreatic lipase digestion of fat. Enterostatin appears to act as a fat satiety factor that is believed to inhibit fat intake via receptors in the gut and brain. However, there may be a limitation to enterostatin administration.

Most of the research so far has investigated exogenously administered enterostatin in animals; only one study has administered it to humans. Therefore, it is difficult to know whether enterostatin will be functionally effective in humans.

Animal Studies

Several studies have shown that peripherally or centrally administered enterostatin inhibits the intake of dietary fat. Two mechanisms appear to be of action, depending on the location of administration. Peripherally, enterostatin reduces gastric emptying. The slow rate of gastric emptying could result in greater gastric distension increasing satiety Furthermore, enterostatin may also interact with gut receptors, regulating motility and satiety Centrally, enterostatin appears to interact with an opioid pathway for modulating selection and consumption of diets high in fat. Enterostatin does not delay the onset of feeding but appears to shorten the time spent eating.

An interesting aspect of enterostatin function in rats is that it appears to reduce fat intake only in animals that have been adapted to diets which are high in fat before testing. In animals that have been adapted to a standard diet or a high-carbohydrate diet, there appears to be no effect of enterostatin in reducing fat intake.

Human Studies

Enterostatin response to feeding in humans is similar to that in rats. Serum enterostatin increased in response to a large meal. However, some sensitivity and detection problems have been associated with the immunoreactive assay for measuring enterostatin.

Intravenous administration of enterostatin in obese men resulted in no significant effect on feeding behavior. However, other researchers have reported that the intravenous administration is not the most efficient method of administration. Animal studies have reported that intravenous administration results in a prolonged response delay. No other studies have been published which have orally administered enterostatin to humans.
Safety and Toxicity

Animal studies have not reported any adverse reactions associated with enterostatin administration, either peripherally or centrally The only human study to administer enterostatin reported no adverse reactions. The only potential problem that could be found with enterostatin relates to the dosage. The dose-response to enterostatin is U-shaped, exhibiting an inhibition of fat intake at lower doses, but stimulation of food intake at higher doses. Because of this dose response curve there could be a range of functional dosages which could depend on a number of physiological factors.

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