Enterostatins
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Enterostatins

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E07002 Enterostatin (human, mouse, rat) Inquiry
E07001 Enterostatin (bovine, canine, porcine) Inquiry

Enterostatin is a pentapeptide produced by cleavage of the N terminal of pancreatic prolipase in the small intestine. As a protein cofactor of pancreatic lipase, trypsin is necessary for intestinal fat digestion. Enterostatin is absorbed from the intestinal tract and acts as a powerful anorexia peptide function to reduce fat consumption in rodent selectivity. Three enterostatin amino acid sequences have been identified in rats and humans. Their amino acids are abbreviated as VPDPR (rat and human), APGPR (human) and VPGPR (rat). Although all three peptides can reduce food intake, little is known about the receptors that mediate these effects.

Mode of Action

Enterostatin is a pentapeptide that specifically suppresses fat or high-fat intake rather than a high-carbohydrate diet. Unlike most regulatory peptides, enterostatin is formed in the intestinal cavity and is therefore comparable to peptides from food sources. The mechanism of fat intake reduction depends on the cholecystokinin pathway, opioid pathway, and melanocortin pathway. Enterostatin also has metabolic effects, such as inhibiting insulin secretion, reducing serum cholesterol levels, and enhancing memory. Plasma cholesterol levels increased in a mouse lacking enterostatin, suggesting that enterostatin plays a role in reducing blood lipids. An enterostatin receptor is the β subunit of F1-ATP enzyme, which is located in the target.

Function of Enterostatins

Its effects include reducing insulin secretion, increasing sympathetic stimulation of brown adipose tissue, and stimulating adrenal corticosteroid secretion. At the last level, it triggers a sense of fullness in the stomach, which may be responsible for regulating fat intake and weight loss. The utilization of enterostatin requires the presence of CCK-A receptor. Studies based on rats lacking these receptors found that they did not respond to enterostatin. When the rats were injected with a high dose of enterostatin, the food intake of rats decreased with the increase of the dose. Although there is intestinal inhibin-like immune response in blood, brain, and intestine, exogenous enterostatin can reduce fat appetite and insulin secretion in rats, the role of these peptides in human obesity remains to be studied.

References:
1.  Erlanson‐Albertsson, C., & Yorkf, D. (1997). Enterostatin‐a peptide regulating fat intake. Obesity research5(4), 360-372.
2.  Nagaoka, S. (2019). Structure–function properties of hypolipidemic peptides. Journal of Food Biochemistry43(1), e12539.

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