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 469 records · Page 26Linked to original sources
PubMed1991

Enterostatin (Val-Pro-Asp-Pro-Arg), the activation peptide of procolipase, selectively reduces fat intake.

Valine-proline-aspartate-proline-arginine (VPDPR), the amino terminal pentapeptide of pancreatic procolipase, produced a dose-dependent reduction in food intake when injected intraperitoneally into Osborne-Mendel rats that had been starved overnight. This inhibition of feeding was observed when the rats were fed a high-fat diet but not in rats fed a high-carbohydrate, low-fat diet. At higher doses of VPDPR, the inhibition of feeding was maintained for over 6 hours. An equimolar mixture of the free amino acids had no effect on food intake. In rats adapted to a three-choice macronutrient diet, VPDPR inhibited fat intake but had no effect on carbohydrate or protein intake. This selective inhibition of fat intake was observed in both overnight-fasted rats presented with food and in ad-lib-fed rats at the beginning of the dark-onset feeding period. It is suggested that this peptide may be a feedback signal to regulate the intake of dietary fat.

Animals↗
PubMed1993

Chronic effects of intracerebral ventricular enterostatin in Osborne-Mendel rats fed a high-fat diet.

Enterostatin, a pentapeptide found in the procolipase molecule of the pancreas, has been infused chronically into the lateral ventricle of Osborne-Mendel rats for 11 days. Treatment with enterostatin acutely lowered food intake more in the treated animals than in the vehicle-treated controls. Weight gain and serum insulin were significantly reduced by enterostatin. Corticosterone was significantly increased in rats receiving chronic infusions of enterostatin into the lateral ventricle and was also increased following an acute ICV injection of enterostatin. CRH antagonist did not block the acute feeding response to enterostatin in Sprague-Dawley rats. The elevation of corticosterone during chronic infusion of enterostatin reduced the level of hepatic glucocorticoid receptor as measured by Western blot. We conclude that body weight gain of OM rats is reduced by centrally administered enterostatin, and that the acute effects of enterostatin on food intake are not mediated through stimulation of CRH secretion.

Animals↗
PubMed1993

The peptide enterostatin may produce early satiety.

The time course of feeding, grooming, exploration, and sleeping behaviors has been measured following treatment with enterostatin, the signal pentapeptide from procolipase. The peptide was injected intraperitoneally prior to presenting food, and the frequency of feeding and grooming activity, drinking, and rest or sleeping were observed at 10-s intervals for 60 min. Enterostatin did not delay the onset of feeding but shortened the time spent eating compared to saline injected controls. Conversely, grooming activity appeared earlier following enterostatin, activity was reduced, and resting behavior occurred earlier with this peptide. There were no changes in the drinking behavior. For the first hour following enterostatin, eating represented 20.8% of the time, grooming 9.2%, activity 18.3%, and rest or sleep 47.2%, with drinking making up the other 4.4%. In contrast, saline-injected animals ate for 27.1% of the time, groomed for 12.4%, were active 28.5% of the time, had sleep or rest time equal to 27.9%, and drank for 4.1% of the time. In fasted animals, the onset of grooming, the decrease in activity, and the increase in time sleeping occurred earlier than with saline. These studies support the concept that enterostatin decreases food intake by producing early satiety.

Animals↗
PubMed1992

Effect of enterostatin given intravenously and intracerebroventricularly on high-fat feeding in rats.

The effect of enterostatin, the amino-terminal pentapeptide of pancreatic procolipase, on high-fat food intake has been investigated after intracerebroventricular as well as after intravenous injection. After an overnight fast enterostatin given i.c.v. at doses of 167 pmol and 333 pmol produced a significant and dose-dependent reduction in high-fat food intake, while a higher dose of 667 pmol had no effect. Following intravenous injection of enterostatin the intake of high-fat food was suppressed at doses of 8.3 nmol and 16.7 nmol, while no effect was observed at higher doses. The inhibition of feeding started 3 h after the initiation of feeding and persisted to the end of the test period (6 h). Enterostatin at a dose of 16.7 nmol gave no sign of aversion in an aversion test comparing the effect of enterostatin, lithium chloride and saline on liquid intake. The data suggest that enterostatin may exert its satiety effect on high-fat feeding by being absorbed into the bloodstream.

Animals↗
PubMed1994

The in vitro intestinal absorption of enterostatin is limited by brush-border membrane peptidases.

The intestinal metabolism and absorption of enterostatin was studied using brush-border membrane vesicles and an in vitro model of intestinal segments from rabbit ileum mounted in Sweetana-Grass diffusion chamber. Hydrolysis of enterostatin was observed with both epithelial sheets and brush-border membranes. The main metabolite was found to be des-arginine-enterostatin. Dipeptidylpeptidase IV was found to play a minor role in enterostatin degradation, whereas carboxypeptidase P activity accounted for the initial step of peptide hydrolysis. More than 50% of the amount of enterostatin added to the mucosal compartment of the Sweetana-Grass diffusion chamber was degraded after 30 min. Enterostatin was mainly absorbed as degradation products but a small transepithelial passage of des-arginine-enterostatin and immunoreactive enterostatin was also detected. Although immunoreactive enterostatin exhibits a low apparent permeability coefficient in rabbit ileum, the luminal production of this peptide may be of physiological importance in the control of appetite.

Amino Acid Sequence↗
PubMed1984

One-step purification of procolipase from human pancreatic juice by immobilized antibodies against human colipase86.

Purified antibodies to human colipase86 were coupled to CNBr-activated Sepharose 4B. The immunoadsorption column thus obtained was used to purify procolipase from human pancreatic juice in one step by immunoaffinity chromatography. A single form of procolipase was obtained, having similar biological properties as previously characterized procolipases from horse and pig. The sequence of the N-terminal propeptide was determined to be Ala-Pro-Gly-Pro-Arg. In bovine, equine and porcine procolipases the corresponding N-terminal sequence is Val-Pro-Asp-Pro-Arg.

Amino Acids↗
PubMed1995

Metabolism of enterostatin in rat intestine, brain membranes, and serum: differential involvement of proline-specific peptidases.

The degradation of enterostatin (VPDPR), a potent inhibitor of food intake, by intestinal brush-border membranes, brain membranes, and rat serum has been investigated in the presence of specific inhibitors. Hydrolysis by intestinal membranes was found to be 10 and 100 times faster than in serum and brain membranes, respectively. Enterostatin hydrolysis by intestinal and brain membranes involves the removal of C-terminal arginine by carboxypeptidase P, leading to the production of des-Arg-enterostatin, and the splitting of the Pro2-Asp3 bond by dipeptidyl aminopeptidase IV (DPP IV). A small amount of the potent anorectic peptide Pro2-Asp3-Pro4 was released during hydrolysis of des-Arg-enterostatin by brain membranes and rat serum. In rat serum, enterostatin degradation was mainly due to DPP IV.

Amino Acid Sequence↗
PubMed1994

Structural requirements for the biological activity of enterostatin.

A series of enterostatin analogues were tested to investigate the minimal structure required for activity to suppress the intake of high-fat (HF) diets. The dose-response curve to intracerebroventricular (ICV) enterostatin was U-shaped (maximal inhibition at 1 nmol). Removal or modification of the N-terminal valine from enterostatin (Val-Pro-Asp-Pro-Arg) abolished activity, as did C-terminal amidation. The tripeptide (Pro-Asp-Pro) and the cyclo-diketopiperazine cyclo-Asp-Pro retained activity whereas the linear Asp-Pro dipeptide was inactive. In rats adapted to a three-choice macronutrient diet, cyclo-Asp-Pro specifically inhibited fat intake and had near maximal inhibition (50%) at the 0.03 nmol dose. The enterostatin inhibitory effect on fat intake may reside in the cyclo-diketopiperazine molecule, cyclo-Asp-Pro.

Amino Acid Sequence↗
PubMed1994

Corticosterone facilitation of inhibition of fat intake by enterostatin (Val-Pro-Asp-Pro-Arg).

Enterostatin or Val-Pro-Asp-Pro-Arg (VPDPR) is the amino-terminal pentapeptide of procolipase; VPDPR is generated during tryptic activation of procolipase to lipase. In rodents, exogenous VPDPR has been shown to cause a selective decrement in fat appetite. To understand the mechanism(s) underlying the action of this peptide, we have studied the effects of corticosterone, an adrenal hormone known to modulate caloric intake, on VPDPR-mediated inhibition of appetite. The results of this study show a significant increase in the inhibition of total caloric intake by 250 micrograms/kg VPDPR following corticosterone treatment (control, 2.3%; corticosterone treated, 22.7%). Furthermore, the decrement in the caloric intake in corticosterone-treated rats was exclusively due to the loss of fat intake.

Amino Acid Sequence↗
PubMed1996

Enterostatin in gut endocrine cells--immunocytochemical evidence.

The presence of enterostatin, a pentapeptide acting as a potential satiety signal in rats, was investigated in rat intestine by immunocytochemical methods. Using antibodies directed against the C-terminal part of enterostatin, the peptide was identified in endocrine cells in the antral part of the stomach and in the small intestine of rat. The immunoreactive cells were more frequent in the antrum and duodenum and became gradually fewer towards the distal small intestine. In some of the labeled endocrine cells, a coexistence of enterostatin with serotonin was revealed by immunocytochemical double staining, implying that the cells were enterochromaffin cells. In the pancreas, no enterostatin-immunoreactive cells were detected, indicating enterostatin to be included in its parent molecule, procolipase. In addition, the existence of procolipase in the gastrointestinal tract, including the pancreas, was investigated. Procolipase immunoreactivity was also identified, except in the pancreas, in chief cells in the fundus region of the stomach. The number of labeled cells declined distally in the stomach, finally being absent in the intestine. Immunoreactive enterostatin was measured with a specific ELISA method. Intestinal content and serum were found to average 540 +/- 70 and 50 +/- 4 nM, respectively. Pancreatic duct ligation strongly reduced the levels of enterostatin in intestinal content to 5.4 +/- 1.5 nM (p < 0.001), and also reduced the serum enterostatin level to 35 +/- 5 nM (p < 0.05). It is concluded that the peptide enterostatin in the rat is produced both in the exocrine pancreas, as part of pancreatic procolipase, and in gut endocrine cells, both sources of peptide being important for the circulating enterostatin.

Amino Acid Sequence↗
PubMed1993

Enterostatin: a gut-brain peptide regulating fat intake in rat.

The effect of enterostatin on high-fat food intake has been investigated. After 18 h of food deprivation, rats were injected intravenously with enterostatin (VPGPR). A dose of 38 nmol of enterostatin gave a significant inhibition of high-fat food intake, while at a higher dose of 76 nmol the inhibiting effect was lost. During the first hour, after injection of enterostatin, there was even a slight increase in food intake. Binding studies of tritiated enterostatin to crude brain membranes indicated one binding site with high affinity (Kd = 0.5 nM) and one with low affinity (Kd = 170 nM). The two dissociation constants suggest different receptor subtypes and could explain why enterostatin both can inhibit and, at high doses, stimulate fat intake in rats.

Animals↗
PubMed2005

Real-time measurement of solute partitioning to lipid monolayers.

The interaction of a peripheral protein with a lipid-water interface can show a pronounced dependence on the composition and two-dimensional packing density of the lipids that comprise the interface. We report a novel optical method for measuring the adsorption of macromolecules, such as proteins and nucleic acids, and smaller solutes, such as drugs, to lipid monolayers at the gas-liquid interface. Using fluorescence emission from proteins and a small molecule, we demonstrate that the emissions from these solutes when in the aqueous phase and when associated with the monolayer can be temporally separated. Such separation allows measurement of the extent of solute adsorption, spectral characterization of the adsorbed solute, and characterization of lipid organization using adsorption kinetics. The method does not require, but is compatible with, the solute having different spectral properties in the bulk and surface phases. Indeed, if optical signals from adsorbed and soluble solute are the same or their relationship is known, absolute surface excess of adsorbed solute can be calculated without independent calibration. With appropriate instrumental configuration, the method should be adaptable for screening solutes for interaction with planar monolayers having both well-defined composition and adjustable lipid packing density.

Adsorption↗
PubMed2004

Amygdala enterostatin induces c-Fos expression in regions of hypothalamus that innervate the PVN.

Enterostatin selectively inhibits the intake of the dietary fat after both central and peripheral administration. Our previous studies have shown that a central site of action is the central nucleus of amygdala. Serotonergic agonists administered into the paraventricular nucleus (PVN) inhibit fat intake and serotonergic antagonists block the feeding suppression induced by amygdala enterostatin, suggesting that there are functional connections between the PVN and amygdala that affect the feeding response to enterostatin. Our purpose was to identify the anatomic and functional projections from the amygdala to the PVN and hypothalamic area that are responsive to enterostatin, by using a retrograde tracer fluorogold (FG) and c-Fos expression. Rats were injected with fluorogold unilaterally into the PVN and a chronic amygdala cannula was implanted ipsilaterally. After 10 days recovery, rats were injected with either enterostatin (0.1 nmol) or saline vehicle (0.1 microl) into the amygdala and sacrificed 2 h later by cardiac perfusion under anesthesia. The brains were subjected to dual immunohistochemistry to visualize both FG and c-Fos-positive cells. FG/c-Fos double-labeled cells were found in forebrain regions including the PVN, amygdala, lateral hypothalamus (LH), ventral medial hypothalamus (VMH) and arcuate nucleus (ARC). The data provides the first anatomical evidence that enterostatin activates amygdala neurons that have functional and anatomic projections directly to the PVN and also activates neurons in the arcuate, LH and VMH, which innervate the PVN.

Amygdala↗
PubMed2005

5-HT1B receptors modulate the feeding inhibitory effects of enterostatin.

Serotonin (5-HT) is considered to play an important role in control of appetite. Enterostatin has been shown to alter 5-HT release in the brain, and non-specific 5-HT antagonists blocked the anorectic response to icv enterostatin. The aim of this study was to further identify which 5-HT receptor subtype mediates the enterostatin feeding behavior and whether this effect occurs due to action in the PVN. Wild-type and 5-HT2C receptor-/- (KO) mice and normal Sprague-Dawley rats were used in these experiments. All animals were fed a high fat diet. Enterostatin (120 nmol, i.p.) reduced the intake of high fat diet in 5-HT2C receptor mutant mice (saline 4.54 +/- 0.47 kcal vs. Ent 2.53 +/- 0.76 kcal) 1 h after injection. A selective 5-HT1B antagonist (GR55526, 40 mg/kg body weight, i.p.) blocked the enterostatin hypophagic effects in these KO mice. Rats were implanted with cannulas into the amygdala and the ipsilateral PVN. The 5-HT receptor antagonists metergoline (non-specific receptor subtypes 1 and 2), or ritanserin (selective 2C), or GR55562 (selective l B) was injected into the PVN prior to enterostatin (0.01 nmol) injection into the amygdala. Enterostatin reduced food intake (saline: 5.80 +/- 0.59 g vs. enterostatin 3.47 +/- 0.56 g, P < 0.05 at l h). Pretreatment with either metergoline (10 nmol) or GR55526 (10 nmol) but not ritanserin (10 nmol) into the PVN attenuated the anorectic response to amygdala enterostatin. The data imply that the enterostatin anorectic response may be modulated by 5-HT1B receptors and that a neuronal pathway from the amygdala to the PVN regulates the enterostatin response through activation of 5-HTlB receptors in PVN.

Amygdala↗
PubMed2006

Procolipase gene expression in the rat brain: source of endogenous enterostatin production in the brain.

Enterostatin is a pentapeptide released from its precursor protein procolipase, which is synthesized in the exocrine pancreas and gastric mucosa. As central injection of enterostatin has potent effects on feeding, we hypothesized that the procolipase may also be expressed in the brain. We confirmed the presence of preprocolipase gene expression in amygdala by reverse transcription-polymerase chain reaction and Northern blot analysis and of protein expression by Western blots. Immunohistochemical analysis using antibodies for procolipase and enterostatin identified their immunoreactivity (IR) in rat brain. Procolipase IR was present in the cytoplasm of paraventricular, amygdala, and the dorsal thalamus nucleus. Enterostatin IR was evident in the fibers of the dorsal thalamus and arcuate nucleus. In vivo injection of enterostatin antibody into rat amygdala increased food intake. These data suggest that procolipase and enterostatin are synthesized within specific regions of the brain that function in the regulation of food intake centrally.

Analysis of Variance↗
PubMed2004

The F1-ATPase beta-subunit is the putative enterostatin receptor.

It has been suggested that the F1-ATPase beta-subunit is the enterostatin receptor. We investigated the binding activity of the purified protein with a labeled antagonist, beta-casomorphin1-7, in the absence and presence of cold enterostatin. 125I-beta-casomorphin1-7 weakly binds to the rat F1-ATPase beta-subunit. Binding was promoted by low concentrations of cold enterostatin but displaced by higher concentrations. To study the relationship between binding activity and feeding behavior, we examined the ability of a number of enterostatin analogs to affect beta-casomorphin1-7 binding to the F1-ATPase beta-subunit. Peptides that suppressed food intake promoted beta-casomorphin1-7 binding whereas peptides that stimulated food intake or did not affect the food intake displaced beta-casomorphin1-7 binding. Surface plasmon resonance measurements show that the beta-subunit of F1-ATPase binds immobilized enterostatin with a dissociation constant of 150 nM, where no binding could be detected for the assembled F1-ATPase complex. Western blot analysis showed the F1-ATPase beta-subunit was present on plasma and mitochondrial membranes of rat liver and amygdala. The data provides evidence that the F1-ATPase beta-subunit is the enterostatin receptor and suggests that enterostatin and beta-casomorphin1-7 bind to distinct sites on the protein.

Animals↗
PubMed2006

Enterostatin inhibition of dietary fat intake is modulated through the melanocortin system.

Enterostatin injected into the amygdala selectively reduces dietary fat intake by an action that involves a serotonergic component in the paraventricular nucleus. We have investigated the role of melanocortin signaling in the response to enterostatin by studies in melanocortin 4 receptor (MC4R) knock out mice and by the use of the MC4R and MC3R antagonist SHU9119, and by neurochemical phenotyping of enterostatin activated cells. We also determined the effect of enterostatin in vivo on the expression of AgRP in the hypothalamus and amygdala of rats and in culture on a GT1-7 neuronal cell line. Enterostatin had no effect on food intake in MC4R knock out mice. SHU9119 i.c.v. blocked the feeding response to amygdala enterostatin in rats. Amygdala enterostatin induced fos activation in alpha-melanocyte stimulating hormone (alpha-MSH) neurons in the arcuate nucleus. Enterostatin also reduced the expression of AgRP in the hypothalamus and amygdala and in GT1-7 cells. These data suggest enterostatin inhibits dietary fat intake through a melanocortin signaling pathway.

Agouti-Related Protein↗