Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Colipases”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMed2006

Enterostatin (APGPR) enhances memory consolidation in mice.

Enterostatin (APGPR) is a pentapeptide released from its precursor protein, procolipase. We found for the first time that enterostatin has memory-enhancing activity. Enterostatin enhanced memory consolidation after central or oral administration at a dose of 10 nmol/mouse or 300 mg/kg, respectively, in a step-through type passive avoidance test in mice. The memory-enhancing activity of enterostatin was inhibited by pretreatment with lorglumide, an antagonist for cholecystokinin 1 (CCK1) receptor. However, enterostatin had no affinity for CCK receptors. These results suggest that enterostatin improves memory retention through CCK release.

Administration, Oral↗
PubMed2006

Appetite suppression through delayed fat digestion.

High-fat diets are often associated with greater caloric intake and weight gain. Since satiety during fat intake is induced by fat in the intestine we investigated the efficiency of a lipid compound that retards fat digestion to regulate fat intake. We found this compound to reduce high-fat food intake, body weight and blood lipids in Sprague-Dawley rats, without causing steatorrhea. The absence of steatorrhea is explained by an increased pancreatic lipase/colipase secretion, compensating the impaired lipolysis by the added compound. The animals also had an elevated CCK secretion. The satiety for fat may be the consequence of elevated CCK and procolipase/enterostatin levels. We conclude that compounds can be found that delay intestinal fat digestion and control high-fat food intake through the release of satiety signals, without causing steatorrhea. The absence of steatorrhea makes such compounds advantageous over lipase inhibitors in the treatment of obesity.

Animals↗
PubMed1997

Comparisons of the effects of enterostatin on food intake and gastric emptying in rats.

The effects of central and peripheral administration of enterostatin (ENT) on food intake and gastric emptying of a non-nutrient liquid meal have been studied in rats. Intraperitoneal and intragastric administration of ENT at a dose of 120 nmol suppressed the intake of a high-fat diet but failed to inhibit gastric emptying in Sprague-Dawley (SD) rats. Intracerebroventricular (i.c.v.) ENT (1 nmol) reduced intake of a high-fate diet in Osborne-Mendel (OM) and SD rats but not in S5B/Pl rats, whereas it decreased gastric emptying in S5B/P1 and SD rats but not in OM rats. The data suggest that although central ENT may reduce gastric emptying rate, this effect is not related to the inhibitory effect of ENT on food intake.

Animals↗
PubMed1996

The inhibition of intestinal dipeptidylaminopeptidase-IV promotes the absorption of enterostatin and des-arginine-enterostatin across rat jejunum in vitro.

Transport of enterostatin (VPDPR) across rat jejunum was investigated using Grass-Sweetana diffusion chambers. The rate of absorption of enterostatin and its metabolites were studied in absence and in presence of diisopropylfluorophosphate (DFP), a serine protease inhibitor. An extensive hydrolysis of enterostatin was observed during incubation with brush border membranes and when exposed to the mucosal side of the jejunal epithelium. No accumulation of enterostatin occurred in serosal tissue. Addition of DFP delayed enterostatin disappearance and abolished des-arg-enterostatin degradation. Under these conditions, a low amount of enterostatin was able to cross the epithelium intact. Moreover, a substantial amount of des-arg-enterostatin is absorbed across the jejunal epithelium, probably through passive diffusion. Thus, a decreased metabolic activity increased the absorption of a tetrapeptide (VPDP). Dipeptidylaminopeptidase IV, remains a limiting step in transfer of intact enterostatin and its metabolite des-arg-enterostatin across intestinal wall.

Animals↗
PubMed1998

Enterostatin (Val-Pro-Asp-Pro-Arg)-like immunoreactivity in rat urine: relationship to corticosterone output.

Numerous studies have documented a role for enterostatins in appetitive behavior. However, due to the lack of knowledge about the distribution of enterostatins in tissues and body fluids, it has not been possible to examine the role of endogenous enterostatin in this process. To this end, using a polyclonal antibody raised against enterostatin -- Val-Pro-Asp-Pro-Arg (VPDPR), we examined the nature and distribution of enterostatin-like immunoreactivity in the rat urine by ELISA and chromatography. The results reported here show for the first time the presence of VPDPR-like immunoreactivity (VPDPR-LI) in rat urine. Further characterization of rat urine VPDPR-LI revealed that it is not due to VPDPR but to another peptide similar to VPDPR. Furthermore, as urinary excretion of corticosterone increases, the level of VPDPR-LI in urine decreases.

Amino Acid Sequence↗
PubMed2002

Uptake across the blood-brain barrier and tissue distribution of enterostatin after peripheral administration in rats.

Enterostatin, the N-terminal activation pentapeptide of procolipase that is produced by the pancreas, reduces food intake from high-fat diet when injected either peripherally or centrally to rats. We investigated uptake across the blood-brain barrier (BBB) and tissue distribution of enterostatin by giving radioactive-labeled enterostatin (3H-VPDPR) intravenously. Low levels of 3H-VPDPR were detected in many areas of the brain, with greatest radioactivity in the frontal cortex, hippocampus and cerebellum. Radioactivity was found in the plasma and all tissues, with the highest amount detected in the pancreas.

Animals↗
PubMed1998

Effects of enterostatin in non-food-deprived rats with limited or continuous access to oil or sucrose.

The peptide enterostatin has been proposed to function as a selective signal for fat-induced satiety. In the majority of enterostatin studies, however, rats were food-deprived, and the test food was also the maintenance diet. The present study sought to determine if enterostatin would selectively reduce consumption of oil that was provided in addition to a standard diet in non-food-deprived rats. Rats had either continuous (24-h/day) or limited access (120-min/day) to either a 32% sucrose solution or 100% corn oil. In addition to the sucrose and the oil, rats also had 22-h access to a standard pelleted rodent diet. Control rats had unlimited access to the standard diet but no access to oil or sucrose. Rats were maintained on their respective diets for 3 weeks before enterostatin testing. Food intake and body weight were monitored. Rats with continuous access to oil or sucrose consumed more calories and gained more weight than control rats. Caloric intake and body weight of the rats with limited access to oil or sucrose did not differ significantly from controls. Enterostatin, administered intraperitoneally (i.p.) at doses of 0 (vehicle), 89, 178, and 356 microg/kg, had no effect on consumption of oil, sucrose, or standard diet in these non-food-deprivation paradigms; however, 356 microg/kg reduced standard-diet intake when rats were overnight food-deprived, thus verifying peptide activity. These results do not support a role for enterostatin in the regulation of fat intake when optional high-fat foods are provided in addition to a readily available standard diet.

Animals↗
PubMed2000

Intragastric beta-casomorphin(1-7) attenuates the suppression of fat intake by enterostatin.

The current experiments were designed to compare the feeding response to enterostatin and beta-casomorphin(1-7) injected intragastrically. Sprague-Dawley rats with a gastric cannula were allowed to chose from high-fat diet (HF) or low-fat diet (LF) in separate jars. Enterostatin injected intragastrically into overnight fasted rats caused a U-shaped dose-dependent reduction in the intake of the HF diet for the first two hours after infusion but had no effect on the LF intake. beta-Casomorphin(1-7) stimulated the intake of the HF diet but had no effect on the LF diet. Finally, beta-casomorphin(1-7) blocked the inhibitory effect of enterostatin on HF intake in fasted rats.

Animals↗
PubMed2002

Comparative study of enterostatin sequence in five rat strains and enterostatin binding proteins in rat and chicken serum.

Enterostatin, a pentapeptide derived from the precursor protein procolipase has been shown to inhibit dietary fat intake and to reduce body fat after chronic administration in rats. We repeat that the enterostatin amino acid sequence from the genomic DNA of 5 different rat strains is APGPR. 125I-APGPR bound to three proteins (300, 205 and 60 kDa) in rat serum and one 60 kDa protein in chicken serum. These serum binding proteins were also eluted by APGPR affinity chromatography. Western blot analysis of serum protein identified enterostatin-like immunoreactivity associated with the same molecular weight bands. Our results demonstrate the enterostatin sequence in rat is APGPR and suggest the presence of enterostatin binding proteins in rat and chicken serum.

Animals↗
PubMed1996

Intracerebroventricular enterostatin stimulates food intake in non-food-deprived rats.

Previous studies reported that ICV enterostatin reduced high-fat food intake in food-deprived rats. The present study sought to determine if ICV enterostatin would decrease intake of a high-fat food in non-food-deprived rats. Eight doses (0-32 micrograms) were tested. Enterostatin (32 micrograms) significantly stimulated cookie intake at 30 min. Enterostatin did not reduce food intake at any dose. These results conflict with previous reports and suggest that central enterostatin does not play a role in suppressing, but may play a role in stimulating, high-fat food consumption in non-food-deprived rats.

Animals↗
PubMed1997

Effect of enterostatin and kappa-opioids on macronutrient selection and consumption.

Enterostatin, the activation peptide of pancreatic procolipase, suppresses consumption of high-fat diets and selectively suppresses fat consumption over carbohydrate consumption. Kappa-opioid subtype agonists stimulate feeding whereas antagonists suppress feeding. We investigated the effects of enterostatin, the kappa-opioid agonist U50488, and the kappa-opioid antagonist nor-binaltorphimine (nor-BNI) on macronutrient selection and food consumption in rats adapted to choose between a high-fat (HF) diet or a low-fat-high-carbohydrate (LF) diet. In fasted rats, lateral cerebro-ventricular injection (LV) of enterostatin selectively suppressed consumption of the HF diet, with no effect on LF diet consumption. Nor-BNI also selectively suppressed consumption of the HF diet without affecting LF diet consumption. Additionally, U50488 prevented the suppression of consumption of the HF diet in response to enterostatin. In food-sated rates, U50488 preferentially increased consumption of the HF diet and had no effect on consumption of the LF diet. Combined infusions of subthreshold doses of enterostatin and nor-BNI also inhibited consumption of the HF but not the LF diet, whereas combined infusions of maximal doses of enterostatin and nor-BNI had no additive effects. Collectively, these data suggest that a kappa-opioid pathway modulates selection and consumption of diets high in fat and that enterostatin modulates consumption of dietary fat by interacting with this pathway.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1997

Inhibition of insulin release by intraduodenally infused enterostatin-VPDPR in rats.

Enterostatin, an amino-terminal pentapeptide produced in the intestinal lumen after cleavage of pancreatic procolipase, has been shown to suppress fat intake in rats after intraduodenal infusion. In this study, female Sprague-Dawley rats fitted with a duodenal catheter were intestinally infused with enterostatin (Val-Pro-Asp-Pro-Arg, 11.3 and 22.6 nmol/kg/min) plus 20% Intralipid for 30 min. Plasma insulin levels were significantly reduced, whereas plasma glucose concentrations were not altered by enterostatin-VPDPR. The tripeptide Asp-Pro-Arg was also found to decrease the levels of plasma insulin. However, the pentapeptide with the sequence Val-Pro-Gly-Pro-Arg, des-Arg-enterostatin Val-Pro-Asp-Pro and the tripeptide Pro-Asp-Pro failed to cause the reduction of plasma insulin levels in rats following intestinal infusion of these peptides. Radiolabeled enterostatin ([3H]VPDPR) was identified in plasma by HPLC following intraduodenal infusion of the peptide, indicating that the appearance of an intact enterostatin-VPDPR in blood. It is concluded that intestinally administered enterostatin-VPDPR and its metabolites reduce plasma levels of insulin stimulated by Intralipid.

Animals↗
PubMed1997

Chronic ICV enterostatin preferentially reduced fat intake and lowered body weight.

The pancreatic peptide enterostatin will acutely reduce fat intake in rats provided a choice of diets. Chronic ICV infusions of enterostatin suppress the intake of high fat diet. However, the effects of chronic ICV enterostatin on diet choice has not previously been studied. To investigate this, enterostatin (0.5 microgram/h) or artificial cerebrospinal fluid (CSF) was infused for 9 days into the lateral ventricle of rats adapted to a two-choice high-fat (HF) and low-fat (LF) diet regime. Enterostatin reduced intake of HF diet with the maximum depression at day 4, but there was no compensatory increase in LF intake. The body weight of enterostatin-infused rats declined. This was associated with a reduction in fat pad and liver weights compared to the CSF-infused control rats. Serum triglycerides and insulin were decreased and corticosterone was elevated in enterostatin-infused rats. The data show that enterostatin will chronically reduce fat intake and body weight and suggest that enterostatin may attenuate the appetite for fat.

Animals↗
PubMed1997

Enterostatin actions in the amygdala and PVN to suppress feeding in the rat.

The pentapeptide enterostatin (ENT) inhibits feeding after injection into the cerebral ventricles. To localize the central sites of action of ENT, the peptide (0.01 to 3.3 nM) was microinjected into several brain regions and the intake of a high fat diet was measured. The results show that ENT injection in the paraventricular nucleus (PVN) or the amygdala (AMYG) produced a bi-phasic dose related feeding response, low doses of ENT inhibited feeding while higher dose had no effect. The effective dose to inhibit feeding in the AMYG was 10 fold lower than that in the PVN. No changes in food intake were observed after ENT injection into the ventromedial hypothalamus and nucleus tractus solitarius. The data provide further support that there are targets in the CNS for ENT and suggest that central ENT function is site specific.

Adaptation, Physiological↗
PubMed1998

Beta-casomorphins stimulate and enterostatin inhibits the intake of dietary fat in rats.

The effects of beta-casomorphins 1-7, 1-5 and 1-4 on food intake of rats adapted to either a high fat (HF) or high carbohydrate (HC) diet have been studied and compared to the effects of enterostatin. Intracerebroventricular (icv) beta-casomorphin1-7 (beta-CM1-7) stimulated intake of HF diet in overnight fasted rats, but beta-CM1-5 and beta-CM1-4 were ineffective. Peripheral injection of beta-CM1-7 also increased the intake of a high fat diet, but reduced the intake of HC diet in satiated rats. Intracerebroventricular (ICV) beta-CM1-7 caused a dose-dependent increase in the intake of HF diet, but a dose-dependent inhibition of HC ingestion in satiated rats. Enterostatin (ICV) inhibited the beta-CM1-7 stimulation of HF intake, as did the general opioid antagonist naloxone. Ligand binding studies with [3H-pro] enterostatin identified on low affinity binding site (Kd 100nM) on a crude brain membrane preparation. This binding was displaced by beta-CM1-7, beta-CM1-5 and beta-CM1-4. These data suggest that at high doses enterostatin and beta-CM1-7 may interact with the same low affinity receptor to modulate intake of dietary fat.

Amino Acid Sequence↗
PubMed1998

Changes in the microstructure of feeding after administration of enterostatin into the paraventricular nucleus and the amygdala.

The effects of enterostatin (ENT) injected into the paraventricular nucleus (PVN) and the amygdala (AMYG) on the microstructure of feeding was studied by using an automated feeding apparatus. In rats adapted to a 6-h meal feeding regime, ENT reduced the size and duration of the first meal after injection in both the PVN and the AMYG. Similar effects were observed when ENT was given at the beginning of the dark cycle in rats fed ad libitum although the onset of feeding was also delayed in this situation. The number of meals and the size of subsequent meals was unaffected by ENT but the eating rate within the first meal was reduced after ENT injection into the AMYG of meal-fed rats. Enterostatin injected into the AMYG at a dose that suppressed feeding did not produce a conditioned taste aversion. ENT given centrally therefore appears to reduce food intake by delaying the initiation of feeding and/or advancing meal termination suggesting that it affects both appetite and satiation mechanisms.

Amygdala↗
PubMed1998

Distribution and characterization of enterostatin-like immunoreactivity in human cerebrospinal fluid.

Enterostatins belong to a family of peptides (e.g., Val-Pro-Asp-Pro-Arg, VPDPR; Ala-Pro-Gly-Pro-Arg, APGPR; and Val-Pro-Gly-Pro-Arg, VPGPR) derived from the tryptic cleavage of amino-terminal pentapeptide from procolipase. Pharmacologic studies have suggested a role for these peptides in appetite regulation and insulin secretion. Studies into the distribution of enterostatins or the role of endogenous peptides have not been possible until now due to the lack of a suitable method for assay. Using two polyclonal antibodies raised against VPDPR and APGPR and different chromatographic methods, we have examined the nature and distribution of enterostatin-like immunoreactivity in human cerebrospinal fluid. The results reported here show for the first time the presence of enterostatin-like immunoreactivity in the human cerebrospinal fluid. Further characterization of cerebrospinal fluid enterostatin-like immunoreactivity revealed that it is not due to APGPR, VPGPR, or VPDPR but to another peptide similar to VPDPR.

Adult↗