A peptide that acts similar to Cyclo (His-Pro) is Enterostatin or APGPR.
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.
It 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 its use.
Most of the research so far has investigated exogenous process in animals! Only one study has administered it to humans.
Therefore, it is difficult to know whether to function effectively in humans.
Enterostatin Studies on Animal
Several studies have shown that peripheral or central enterostatin inhibits food fat intake.
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, it may also interact with gut receptors, regulating motility and satiety.
Centrally, it appears to interact with the opioid pathway. This process modulates the selection and consumption of high-fat diets.
Enterostatin does not delay the onset of feeding but appears to shorten the time spent eating.
An interesting aspect in rats! 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 appear to be no effects in reducing fat intake.
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 test to measure them.
Giving to obese men has no significant effect on eating behavior. However, other researchers have reported, this intravenous administration is not the most efficient method.
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. These associated with enterostatin administration, either peripherally or centrally. The only human study reported no adverse reactions.
The only potential problem that could be found relates to the dosage.
The dose-response is U-shaped. This 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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