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Enterostatin is an endogenous pentapeptide fragment involved in the regulation of food intake.1 It is released from its precursor protein, procolipase, during digestion and acts in the peripheral and central nervous systems to reduce food, especially fat, intake through the vagus nerve in the periphery and κ-opioid-, serotonin (5-HT) receptor subtype 5-HT1B-, and cholecystokinin-mediated signaling pathways in the brain.1,2 Enterostatin binds to mitochondrial complex V, also known as F1F0 ATP synthase, in a cell-free assay and inhibits ATP production and increases thermogenesis in INS-1 insulinoma cells.3 It reduces body weight in rats fed a high-fat diet but not mice fed a chow diet. Enterostatin (1 nmol, i.c.v) reduces food intake in wild-type, but not melanocortin receptor 4 knockout (Mc4r-/-), mice.4 It also enhances memory consolidation in mice in a passive avoidance test when administered at a dose of 300 mg/kg, an effect that can be blocked by the cholecystokinin 1 (CCK1) receptor antagonist lorglumide

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