Role of Intraduodenally Administered Enterostatin in Rats: Inhibition of Food

Mei, Jie; Erlanson–Albertsson, Charlotte

doi:10.1002/j.1550-8528.1996.tb00528.x

Cited by 28 publications

(17 citation statements)

References 27 publications

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“…Since enterostatin as well as its precursor molecule procolipase increased with high-fat diet it was suggested to act as a negative feedback regulator during fat intake [4]. The anorectic effect, originally observed after central and peripheral injection, was also observed after intra-intestinal administration, hence at a site where enterostatin is also produced [9,10]. For the transmission of the satiety effect of enterostatin intact vagus afferent innervation was important [11].…”

Section: Enterostatin -A Peptide Released From Procolipase During Fatmentioning

confidence: 99%

Enterostatin and its target mechanisms during regulation of fat intake

Berger

Winzell

Mei

et al. 2004

Physiology & Behavior

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A high-fat diet easily promotes hyperphagia giving an impression of an uncontrolled process. Fat digestion itself however provides control of fat intake through the digestion itself, carried out by pancreatic lipase and its protein cofactor colipase, and through enterostatin, a peptide released from procolipase during fat digestion. Procolipase (-/-) knockout mice have a severely reduced fat digestion and fat uptake, pointing to a major role of the digestive process itself. With a normal fat digestion enterostatin basically restricts fat intake by preventing the overconsumption of fat. The mechanism for enterostatin is an inhibition of a mu -opioidmediated pathway, demonstrated through binding studies on SK-N-MC-cells and crude brain membranes. Another target protein of enterostatin is the beta-subunit of F1F0-ATPase, displaying a distinct binding of enterostatin, established through an aqueous two-phase partition system. The binding of enterostatin to F1-ATPase was partially displaced by β-casomorphin, a peptide stimulating fat intake and acting competitively to enterostatin. We hypothetize that regulation of fat intake contains a reward component, which is an opioidergic pathway.

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Section: Enterostatin -A Peptide Released From Procolipase During Fatmentioning

confidence: 99%

Enterostatin and its target mechanisms during regulation of fat intake

Berger

Winzell

Mei

et al. 2004

Physiology & Behavior

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“…Similarly, enterostatin reduces intake of single diets when the diet is high, but not when it is low, in fat content (36). Enterostatin is effective intragastrically (91) and intraduodenally (48) and by intraperitoneal (38,55,56), intravenous (46), and intracerebroventricular (icv) (36,38,46) routes. With the exception of intravenous administration, when there is a delay in the response of 60 minutes to 120 minutes, the peptide has a rapid effect (<30 minutes) after administration by all other routes.…”

Section: Feeding Response Of Enterostatinmentioning

confidence: 99%

“…The potency of the action of enterostatin is reflected in its long duration of action and its effect on feeding, lasting up to 6 hours after a single injection in rats adapted to a 6-hour feeding schedule (48) or lasting up to 24 hours after a single injection in ad libitum-fed rats (56). During chronic OBESITY RESEARCH Vol.…”

Section: Feeding Response Of Enterostatinmentioning

confidence: 99%

“…Dietary fat intake is reduced by the intragastric, intraduodenal, or intraperitoneal administration of enterostatin (38,48,55,56,9 1 ). Because enterostatin is released peripherally either from the pancreas or the gastrointestinal tract, it is relevant to question how the response to peripheral enterostatin is transmitted to the brain.…”

Section: Peripheral Response To Enterostatinmentioning

confidence: 99%

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Enterostatin‐A Peptide Regulating Fat Intake

Erlanson–Albertsson

York

1997

Obesity Research

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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.

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“…The first relates to the site of the CCK-A receptors that modulate the response. After the initial observations that enterostatin given intraperitoneally would inhibit intake of dietary fat (28), localized infusions of enterostatin, initially into the stomach (45) or duodenum (24) and subsequently into the near-celiac artery (12), have suggested that the gastric-proximal duodenum region is a peripheral site of action. Both the procolipase precursor protein and enterostatin have been localized to mucosal layers in this region by using immunohistochemical approaches (23,39).…”

Section: Discussionmentioning

confidence: 99%

Enterostatin inhibition of dietary fat intake is dependent on CCK-A receptors

Thomas

Kilroy

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Enterostatin, a pentapeptide released from the exocrine pancreas and gastrointestinal tract, selectively inhibits fat intake through activation of an afferent vagal signaling pathway. This study investigated if the effects of enterostatin were mediated through a CCKdependent pathway. The series of in vivo and in vitro experiments included studies of 1) the feeding effect of peripheral enterostatin on Otsuka Long Evans Tokushima Fatty (OLETF) rats lacking CCK-A receptors, 2) the effect of CCK-8S on the intake of a two-choice high-fat (HF)/low-fat (LF) diet, 3) the effects of peripheral or central injection of the CCK-A receptor antagonist lorglumide on the feeding inhibition induced by either central or peripheral enterostatin, and 4) the ability of enterostatin to displace CCK binding in a 3T3 cell line expressing CCK-A receptor gene and in rat brain sections. The results showed that OLTEF rats did not respond to enterostatin (300 g/kg ip) in contrast to the 23% reduction in intake of HF diet in Long Evans Tokushima Otsuka (LETO) control rats. CCK (1 g/kg ip) decreased the intake of the HF diet in a two-choice diet regime with a compensatory increase in intake of the LF diet. Peripheral injection of lorglumide (300 g/kg) blocked the feeding inhibition induced by either near-celiac arterial or intracerebroventricular enterostatin, whereas intracerebroventricular lorglumide (5 nmol icv) only blocked the response to intracerebroventricular enterostatin but not to arterial enterostatin. Enterostatin did not bind on CCK-A receptors because neither enterostatin nor its analogs VPDPR and ␤-casomorphin lorglumide; cholecystokinin-A receptor; near-celiac arterial; intracerebroventricular OVER THE LAST DECADE, we and others have published substantial evidence to suggest that enterostatin, the NH 2 -terminal pentapeptide derived from the procolipase precursor protein, will selectively inhibit the intake of dietary fat in rodent models given a choice of diets (7, 12-18, 23, 28, 29). The procolipase gene is expressed in the exocrine pancreas, the stomach and duodenal mucosa (29), and in specific brain regions (13). Enterostatin-like immunoreactivity has been identified at similar locations, suggesting that procolipase is processed to colipase and enterostatin in these other sites in addition to the exocrine pancreas (13, 39).Like other gut peptides, enterostatin appears to have both a peripheral and a central site of action. Peripherally, it appears that enterostatin acts within the gastroduodenal region to activate vagal fibers that communicate through the brain stem regions to hypothalamic and extrahypothalamic forebrain regions to effect food intake (12, 42). Stereotaxic injections suggest that the amygdala is the central site of action of enterostatin (17) and that the feeding response is modulated through a pathway that involves both paraventricular serotonergic activity in the hypothalamus (19, 48) and -opioid activity in the nucleus tractus solitarius (NTS) (48). Despite evidence that -opioids displace enterostatin fr...

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Role of Intraduodenally Administered Enterostatin in Rats: Inhibition of Food

Cited by 28 publications

References 27 publications

Enterostatin and its target mechanisms during regulation of fat intake

Enterostatin and its target mechanisms during regulation of fat intake

Enterostatin‐A Peptide Regulating Fat Intake

Enterostatin inhibition of dietary fat intake is dependent on CCK-A receptors

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