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David A. York - One of the best experts on this subject based on the ideXlab platform.

  • Different metabolic responses to central and peripheral injection of Enterostatin
    2016
    Co-Authors: Ling Lin, David A. York, Miejung Park, Matt Hulver, David York A. Different
    Abstract:

    tapeptide cleaved from procolipase, suppresses fat intake after peripheral and central administration. Chronic treatment of rats with Enterostatin decreases body weight and body fat. The effect was greater than could be accounted by the reduction in food intake alone. Hence, we have investigated the effect of Enterostatin on energy metabolism. Male Sprague-Dawley rats adapted to a high-fat diet were implanted with lateral cerebral ventricular or amygdala cannulas. The metabolic effects were determined by indirect calorimetry. After habituation to the test cages, fasted rats were injected with either saline vehicle or Enterostatin given either intraperitoneally (100 nmol) or intracere-broventricularly (1 nmol) or into specific brain regions [amygdala (0.01 nmol) or paraventricular nucleus (PVN) (0.1 nmol)]. Respiratory quotient (RQ) and energy expenditure were monitored over 2 h. Intraperitoneal Enterostatin reduced RQ (saline: 0.81 0.02 vs. Enterostatin: 0.76 0.01) and increased energy expenditure by 44%. Intracerebroventricular enterosta-tin increased the energy expenditure without any effects on RQ, wherea

  • Effects of dietary fat and Enterostatin on dopamine and 5-hydroxytrytamine release from rat striatal slices
    Brain research, 2010
    Co-Authors: David A. York, Lihong Teng, Miejung Park-york
    Abstract:

    Studies have demonstrated defects of DA and 5HT neurotransmission in dietary fat induced obese animals. In the present study, we used a perfusion system to assay the release of DA and 5HT from striatal slices preloaded with [(3)H]-DA or [(3)H]-5HT. The release of both DA and 5HT from striatal slices of rats fed a high fat diet for 10 days, but not 3 days, was reduced when compared to striatal slices taken from rats fed a low fat diet. Enterostatin, an endogenous pentapeptide inhibits dietary fat intake when administered peripherally and centrally in animals. The central mechanism for the action of Enterostatin is not yet determined even though several mechanisms have been suggested. We have shown that Enterostatin enhanced [(3)H]-DA release, but not [(3)H]-5HT release from striatal slices of rats that had been adapted to high fat diet for 10 days. The Enterostatin-induced increase in [(3)H]-DA release was blocked by nomifensine. Enterostatin did not alter [(3)H]-DA or [(3)H]-5HT release from striatal slices of rats adapted to high fat or low fat diet feeding for 3 days. These findings suggest that Enterostatin may inhibit dietary fat intake by blocking dopamine reuptake transport to increase central striatal DA release from rats that have acquired diminished dopamine signal after an adaptive period of fat consumption.

  • Melanocortin activity in the amygdala controls appetite for dietary fat
    American journal of physiology. Regulatory integrative and comparative physiology, 2009
    Co-Authors: Stéphane Boghossian, Miejung Park, David A. York
    Abstract:

    The amygdala is rich in melanocortin 4 receptors. Because the reduction in dietary fat intake after Enterostatin is injected in the central nucleus of the amygdala (CeA) is blocked by a melanocorti...

  • Enterostatin alters protein trafficking to inhibit insulin secretion in Beta-TC6 cells
    Peptides, 2009
    Co-Authors: Miejung Park, Jeffery Farrell, Karalee Lemmon, David A. York
    Abstract:

    Enterostatin is a peptide that regulates dietary fat intake in rodents and inhibits insulin secretion from pancreatic beta cells. Microarray studies of the genomic response of both a human hepatoma cell line (HepG2 cells) and a mouse hypothalamic cell line (GT1-7 cells) to Enterostatin suggested that it might regulate protein trafficking. Using semi-quantitative real-time PCR and Western blot analysis, we confirmed that Enterostatin upregulated Scamp2 and down regulated Dynamin2 in these cell lines. The receptor for Enterostatin is the F1-ATPase beta subunit. We transfected HepG2 cells with either a green fluorescent protein (GFP) tagged F1-ATPase beta subunit or a red fluorescent protein (RFP) tagged F1-ATPase alpha subunit to study the effects of Enterostatin on translocation of its own receptor protein. Enterostatin induced movement of GFP-beta subunit to the cell periphery area but did not have any effect on the localization of RFP-alpha subunit protein in HepG2. As Scamp2 is involved in glucose uptake in mouse Beta-TC6 insulinoma cells we tested Enterostatin's effect in Beta-TC6 cells. Glucose stimulated insulin release was inhibited by Enterostatin as reported previously. Using siRNA to Scamp2 did not change glucose stimulated insulin release but siRNA to Dynamin2 and dominant negative Dynamin2 (Dyn K44A) inhibited glucose stimulated insulin release and abolished the response to Enterostatin. This suggests Enterostatin inhibits glucose stimulated insulin release in pancreatic beta cells through down regulation of Dynamin2. This study also suggests that Enterostatin might have a more generalized effect on protein trafficking in various cells.

  • Enterostatin affects cyclic AMP and ERK signaling pathways to regulate Agouti-related protein (AgRP) expression.
    Peptides, 2008
    Co-Authors: Miejung Park, David A. York
    Abstract:

    Enterostatin, a gut-brain peptide, inhibits dietary fat intake in rats. The purpose of this study was to identify the intracellular signaling pathways that are responsive to Enterostatin and that modulate the effects of Enterostatin on the expression of Agouti-related protein (AgRP). We used the hypothalamic GT1-7 neuronal cell line to identify the effects of Enterostatin on cyclic AMP and ERK signaling using conventional immunoassays or Western blots to assay the activity of these pathways. Enterostatin enhanced the level of cyclic AMP, PKA(RIIbeta) and phospho-CREB and increased pERK levels in GT 1-7 cells. The effects on pERK were rapid (7.5 min) and dose-dependent. These signaling responses were blocked by an antibody to the Enterostatin receptor (beta subunit of F1-ATPase), by the pERK inhibitor U0126 and by the P2Y receptor antagonist Suramin. Enterostatin showed a biphasic effect on AgRP mRNA, initially increasing but subsequently decreasing the levels. The cyclic AMP activator Sp-cAMP increased AgRP mRNA expression. Transfection of a wild type ERK construct reduced AgRP mRNA levels. Enterostatin inhibited expression of Kruppel-like factor 4 (KLF4), a transcriptional regulator of AgRP. KLF4 gene expression was increased by Sp-cAMP but decreased by wild-type ERK expression. U0126 blocked the effect of Enterostatin on KLF4 expression. We conclude that Enterostatin binding to its receptor activates the pERK pathway to inhibit AgRP gene expression but may enhance AgRP expression through activation of the cyclic AMP pathway. These pathways probably mediate the Enterostatin inhibition of dietary fat intake.

Charlotte Erlanson-albertsson - One of the best experts on this subject based on the ideXlab platform.

  • The Role of Enterostatin in Eating Behavior and Diet
    Handbook of Behavior Food and Nutrition, 2011
    Co-Authors: Charlotte Erlanson-albertsson
    Abstract:

    Enterostatin is the amino terminal pentapeptide produced by proteolytic cleavage of pancreatic procolipase and released into the small intestine during digestion of fat catalyzed by pancreatic lipase and its protein cofactor colipase. Enterostatin specifically suppresses fat intake or high-fat intake as opposed to high-carbohydrate diets. Procolipase and Enterostatin have also been localized to the gastric mucosa, as well as to certain brain regions, such as amygdala, hypothalamus, and cortex. The mechanism for the decreased fat intake is dependent on cholecystokinin pathways as well as melanocortin pathways, which involves an inhibition of gastric motility in the intestine, a release of serotonin centrally and a suppression of the fat-specific hunger hormone, agouti-related peptide (AgRP). The expression of Enterostatin is impaired by the presence of sucrose in the diet. Enterostatin also displays metabolic effects, such as inhibition of insulin secretion and lowering of serum cholesterol levels. Thermogenesis is likewise stimulated through an activation of sympathetic drive to brown adipose tissue with induced expression of uncoupling protein 1. The receptor for Enterostatin is the β-subunit of F1-ATPase being localized to the plasma membrane in target cells. Following activation of the receptor with Enterostatin various intracellular pathways are activated leading to a perturbed ATP/ADP ratio, an activation of cAMP, AMPkinase as well as MAPkinase. Enterostatin and fatty acids cause an increased expression of the receptor on the plasma membrane. No effect on food intake has been demonstrated in human beings when Enterostatin is given in single doses. With green plants proteins, which induce an endogenous release of Enterostatin, satiety is promoted in human beings. An Enterostatin-deficient mouse has elevated plasma cholesterol levels, pointing to the role of Enterostatin in reducing blood lipids. The fact that the production of Enterostatin and its receptor is strongly stimulated by dietary fat suggests that Enterostatin works as a feedback signal in promoting regulation of fat intake and utilization of fat as energy substrate.

  • Enterostatin deficiency increases serum cholesterol but does not influence growth and food intake in mice.
    American journal of physiology. Endocrinology and metabolism, 2009
    Co-Authors: Rita Miller, Charlotte Erlanson-albertsson, Dymphna D'agostino, Mark E. Lowe
    Abstract:

    A pentapeptide released from procolipase, Enterostatin, selectively attenuates dietary fat intake when administered peripherally or centrally. Enterostatin may act through the afferent vagus nerve and in the hypothalamus and amygdala, primarily in the central nucleus of the amygdala. To investigate the physiological role of endogenous Enterostatin, we created an Enterostatin-deficient, colipase-sufficient (Ent(-/-)) mouse. Ent(-/-) mice are viable, normally active, and fertile. They exhibit normal growth on low-fat and high-fat diets. Furthermore, Ent(-/-) mice develop diet-induced obesity, as do Ent(+/+) mice, and have normal responses to a two-macronutrient choice diet and to a switch from a high-fat to a low-fat diet. Levels of total serum (P = 0.004) and non-HDL (P

  • Enterostatin deficiency increases serum cholesterol but does not influence growth and food intake in mice
    American Journal of Physiology-endocrinology and Metabolism, 2009
    Co-Authors: Rita Miller, Charlotte Erlanson-albertsson, Dymphna D'agostino, Mark E. Lowe
    Abstract:

    A pentapeptide released from procolipase, Enterostatin, selectively attenuates dietary fat intake when administered peripherally or centrally. Enterostatin may act through the afferent vagus nerve ...

  • Enterostatin up-regulates the expression of the beta-subunit of F(1)F(o)-ATPase in the plasma membrane of INS-1 cells.
    Nutritional neuroscience, 2008
    Co-Authors: Andreas Lindqvist, Karin Berger, Charlotte Erlanson-albertsson
    Abstract:

    Exposure to high-fat diet easily promotes overeating while at the same time disrupting insulin secretion and islet function. Enterostatin is a peptide which is secreted from the pancreas in response to high-fat feeding and has been shown to inhibit fat intake as well as insulin secretion in experimental animal models. Until recently, there was no known receptor for Enterostatin. In 2002, Berger and co-workers found Enterostatin to target the beta-subunit of the F(1)-ATPase in rat brain membranes as well as in a clonal beta-cell line (INS-1). In this study, we found the beta-subunit of F(1)-ATPase to be ectopically expressed in the plasma membrane of INS-1 cells using both immunohistochemistry and Western blotting. Incubation with Enterostatin for 60 min resulted in a 3.5-fold increase of the protein expression of the beta-subunit of F(1)-ATPase in the plasma membrane. Furthermore, we found ATP to be able to displace the binding of Enterostatin to purified bovine F(1)-ATPase. This reported targeting of Enterostatin to the beta-subunit of F(1)-ATPase in insulin cells may provide a link between high-fat intake and islet function.

  • Enterostatin decreases postprandial pancreatic UCP2 mRNA levels and increases plasma insulin and amylin.
    American journal of physiology. Endocrinology and metabolism, 2005
    Co-Authors: Denis Arsenijevic, Charlotte Erlanson-albertsson, Eva Gallmann, William Moses, Thomas Lutz, Wolfgang Langhans
    Abstract:

    This study investigated the chronic effect of Enterostatin on body weight and some of the associated changes in postprandial metabolism. Rats were adapted to 6 h of food access/day and a choice of low-fat and high-fat (HF) food and then given Enterostatin or vehicle by an intraperitoneally implanted minipump delivering 160 nmol Enterostatin/h continuously over a 5-day infusion period. Enterostatin resulted in a slight but significant reduction of HF intake and body weight. After the last 6-h food access period, Enterostatin-treated animals had lower plasma triglyceride and free fatty acid but higher plasma glucose and lactate levels than control animals. Enterostatin infusion resulted in increased uncoupling protein-2 (UCP2) expression in various tissues, including epididymal fat and liver. UCP2 was reduced in the pancreas of Enterostatin-treated animals, and this was associated with increased plasma levels of insulin and amylin. Whether these two hormones are involved in the observed decreased food intake due to Enterostatin remains to be determined. As lipid metabolism appeared to be altered by Enterostatin, we measured peroxisome proliferator-activated receptor (PPAR) expression in tissues and observed that PPARalpha, -beta, -gamma1, and -gamma2 expression were modified by Enterostatin in epididymal fat, pancreas, and liver. This further links altered lipid metabolism with body weight loss. Our data suggest that alterations in UCP2 and PPARgamma2 play a role in the control of insulin and amylin release from the pancreas. This implies that Enterostatin changes lipid and carbohydrate metabolic pathways in addition to its effects on food intake and energy expenditure.

George A. Bray - One of the best experts on this subject based on the ideXlab platform.

  • Regulation of feeding behavior, gastric emptying, and sympathetic nerve activity to interscapular brown adipose tissue by galanin and Enterostatin: the involvement of vagal-central nervous system interactions
    Journal of Gastroenterology, 2002
    Co-Authors: Hajime Nagase, David A. York, Atsushi Nakajima, Hisahiko Sekihara, George A. Bray
    Abstract:

    Galanin and Enterostatin, which are distributed in both the central nervous system and the gastrointestinal tract, regulate the feeding behavior. In the first set of experiments, we investigated the effects of galanin and Enterostatin, injected into the third ventricle, on food intake, gastric emptying, and the sympathetic activity of nerves innervating interscapular brown adipose tissue in rats. Galanin dose-dependently increased the intake of a high-fat diet after overnight starvation, but it did not affect low-fat diet intake. In contrast, Enterostatin suppressed the intake of the high-fat diet, while intake of the low-fat diet was not affected. Galanin significantly and dose-dependently suppressed gastric emptying rate. However, gastric emptying showed no response to Enterostatin. Galanin produced a dose-dependent suppression of sympathetic firing rate. In rats fed a high-fat diet, the injection of Enterostatin showed a dose-dependent increase in firing rate. In contrast, animals fed a chow diet showed almost no response. In the second set of experiments, we investigated the role of the hepatic vagus nerve in modulating the peripheral response to Enterostatin in rats. Intraperitoneal (i.p.) Enterostatin reduced the intake of a high-fat diet. Immunohistochemical identification indicated that the Fos protein was present in the nucleus tractus solitarius, and parabrachial, paraventricular, and supraoptic nuclei after IP Enterostatin. These responses to i.p. Enterostatin were blocked by hepatic vagotomy. These results suggest that galanin and Enterostatin coordinate to regulate feeding behavior, gastric emptying, and sympathetic activity to interscapular brown adipose tissue via central and peripheral sites of action, one of which was the interaction which was found to exist through the vagal system.

  • regulation of feeding behavior gastric emptying and sympathetic nerve activity to interscapular brown adipose tissue by galanin and Enterostatin the involvement of vagal central nervous system interactions
    Journal of Gastroenterology, 2002
    Co-Authors: Hajime Nagase, David A. York, Atsushi Nakajima, Hisahiko Sekihara, George A. Bray
    Abstract:

    Galanin and Enterostatin, which are distributed in both the central nervous system and the gastrointestinal tract, regulate the feeding behavior. In the first set of experiments, we investigated the effects of galanin and Enterostatin, injected into the third ventricle, on food intake, gastric emptying, and the sympathetic activity of nerves innervating interscapular brown adipose tissue in rats. Galanin dose-dependently increased the intake of a high-fat diet after overnight starvation, but it did not affect low-fat diet intake. In contrast, Enterostatin suppressed the intake of the high-fat diet, while intake of the low-fat diet was not affected. Galanin significantly and dose-dependently suppressed gastric emptying rate. However, gastric emptying showed no response to Enterostatin. Galanin produced a dose-dependent suppression of sympathetic firing rate. In rats fed a high-fat diet, the injection of Enterostatin showed a dose-dependent increase in firing rate. In contrast, animals fed a chow diet showed almost no response. In the second set of experiments, we investigated the role of the hepatic vagus nerve in modulating the peripheral response to Enterostatin in rats. Intraperitoneal (i.p.) Enterostatin reduced the intake of a high-fat diet. Immunohistochemical identification indicated that the Fos protein was present in the nucleus tractus solitarius, and parabrachial, paraventricular, and supraoptic nuclei after IP Enterostatin. These responses to i.p. Enterostatin were blocked by hepatic vagotomy.

  • intragastric β casomorphin1 7 attenuates the suppression of fat intake by Enterostatin
    Peptides, 2000
    Co-Authors: Christy L. White, George A. Bray, David A. York
    Abstract:

    Abstract The current experiments were designed to compare the feeding response to Enterostatin and β-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. β-Casomorphin 1–7 stimulated the intake of the HF diet but had no effect on the LF diet. Finally, β-casomorphin 1–7 blocked the inhibitory effect of Enterostatin on HF intake in fasted rats.

  • Intragastric β-casomorphin1–7 attenuates the suppression of fat intake by Enterostatin☆
    Peptides, 2000
    Co-Authors: Christy L. White, George A. Bray, David A. York
    Abstract:

    Abstract The current experiments were designed to compare the feeding response to Enterostatin and β-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. β-Casomorphin 1–7 stimulated the intake of the HF diet but had no effect on the LF diet. Finally, β-casomorphin 1–7 blocked the inhibitory effect of Enterostatin on HF intake in fasted rats.

  • β-Casomorphins Stimulate and Enterostatin Inhibits the Intake of Dietary Fat in Rats
    Peptides, 1998
    Co-Authors: M Umahara, David A. York, George A. Bray
    Abstract:

    Abstract Lin, L., M. Umahara, D. A. York and G. A. Bray. β-casomorphins stimulate and Enterostatin inhibits the intake of dietary fat in rats. Peptides 19 (2) 325–331, 1998.—The effects of β-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) β-casomorphin 1–7 (β-CM 1–7 ) stimulated intake of HF diet in overnight fasted rats, but β-CM 1–5 and β-CM 1–4 were ineffective. Peripheral injection of β-CM 1–7 also increased the intake of a high fat diet, but reduced the intake of HC diet in satiated rats. Intracerebroventricular (ICV) β-CM 1–7 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 β-CM 1–7 stimulation of HF intake, as did the general opioid antagonist naloxone. Ligand binding studies with [ 3 H-pro] Enterostatin identified on low affinity binding site (Kd 100nM) on a crude brain membrane preparation. This binding was displaced by β-CM 1–7 , β-CM 1–5 and β-CM 1–4 . These data suggest that at high doses Enterostatin and β-CM 1–7 may interact with the same low affinity receptor to modulate intake of dietary fat.

Chandan Prasad - One of the best experts on this subject based on the ideXlab platform.

  • High-performance liquid chromatography–tandem mass spectrometry of Enterostatins in biological samples
    Analytica Chimica Acta, 2004
    Co-Authors: Yi-ming Liu, Kristina Vaughn, Yaru Song, Chandan Prasad
    Abstract:

    Abstract The three forms of Enterostatin (Ala–Pro–Gly–Pro–Arg, Val–Pro–Gly–Pro–Arg, and Val–Pro–Asp–Pro–Arg), pentapeptides known to inhibit fat-intake, were resolved on a C18 reversed-phase column using a ternary mobile phase consisting of methanol, acetonitrile, and water. Coupled with MS/MS detection, the method has been applied to identify Enterostatin sequences in human cerebrospinal fluid and rat brain tissue. Ala–Pro–Gly–Pro–Arg (APGPR) was found to be the predominant Enterostatin sequence in both cases. The levels of APGPR were 98.3±16.3 ng/ml in human cerebrospinal fluid and 30.1±12.6 ng/g wet tissue in rat brain, respectively.

  • Determination of Enterostatin in human cerebrospinal fluid by capillary electrophoresis with laser induced fluorescence detection
    Fresenius' Journal of Analytical Chemistry, 2001
    Co-Authors: Shulin Zhao, Chandan Prasad, Hugh J. F. Robertson, Y.-m. Liu
    Abstract:

    A capillary electrophoresis (CE) method with laser induced fluorescence (LIF) detection is described for quantification of Enterostatin (Val-Pro-Asp-Pro-Arg), a pentapeptide involved in appetite regulation and insulin secretion. Enterostatin and two other pentapeptides belonging to the Enterostatin family (i.e. Ala-Pro-Gly-Pro-Arg and Val-Pro-Gly-Pro-Arg) were well separated from each other. The peptides were fluorescently tagged with naphthalene-2,3- dicarboxaldehyde (NDA) and separated by micellar electrokinetic chromatography (MEKC) in the presence of methanol as an organic modifier. Coupled with LIF detection, the method had a detection limit of 4.8 × 10^–6 M for Enterostatin. The relative standard deviation was to be 4.0% from five determinations of Enterostatin at 37.2 μM in a human cerebrospinal fluid (CSF) sample. Twenty-three human CSF samples were analyzed. The level of Enterostatin ranged from 24 μM to 51 μM with a mean (± SEM) value of 41.7 ± 2.0 μM.

  • HyperEnterostatinemia in premenopausal obese women.
    The Journal of clinical endocrinology and metabolism, 1999
    Co-Authors: Chandan Prasad, Makoto Imamura, Chittaranjan Debata, Nasira Sumar, F. Svec, John Hermon-taylor
    Abstract:

    Enterostatins [Val-Pro-Asp-Pro-Arg (VPDPR), Val-Pro-Gly-Pro-Arg (VPGPR), and Ala-Pro-Gly-Pro-Arg (APGPR)] are pentapeptides derived from the NH2-terminus of procolipase after tryptic cleavage and belong to the family of gut-brain peptides. Although Enterostatin-like immunoreactivities exist in blood, brain, and gut, and exogenous Enterostatins decrease fat appetite and insulin secretion in rats, the roles of these peptides in human obesity remain to be examined. To determine whether VPDPR and APGPR secretion is altered in obesity, serum VPDPR and APGPR levels were measured in 38 overnight-fasted subjects (body mass index, 17.9–54.7 kg/m2) before and after a meal. The mean fasting VPDPR in the serum of lean subjects was significantly lower than that in obese subjects [lean = 603 ± 86 nmol/L (n = 17); obese, 1516 ± 227 nmol/L (n = 21); P = 0.0023]. In addition, the rise in serum APGPR after a meal (postmeal/fasting ratio) was significantly higher in lean than in obese subjects [lean, 1.71 ± 0.24 (n = 17); o...

  • On the nature and distribution of Enterostatin (Val-Asp-Pro-Asp-Arg)-like immunoreactivity in rat plasma.
    Peptides, 1999
    Co-Authors: Makoto Imamura, Chittaranjan Debata, Chandan Prasad
    Abstract:

    Enterostatins, pentapeptides represented at the amino-terminus of the procolipase molecule, are derived following tryptic cleavage of the procolipase molecule in the lumen of the gut. Val-Pro-Asp-Pro-Arg or VPDPR is one such Enterostatin. Despite pharmacologic studies suggesting a role for VPDPR in appetite regulation and insulin secretion, the function of this endogenous peptide has been impossible to discern due to the lack of a suitable assay. Using polyclonal antibodies raised against VPDPR and different chromatographic methods, we examined the nature and distribution of Enterostatin-like immunoreactivity in rat plasma. The results reported here show for the first time the presence of VPDPR-like immunoreactivity in rat plasma. Further characterization of the plasma VPDPR-like immunoreactivity revealed that a) it is not due to APGPR, VPGPR, or VPDPR but to another peptide similar to VPDPR, and b) plasma VPDPR-like immunoreactivity may circulate bound to large carrier proteins.

  • Hormones in Foods: Presence of Enterostatin-Like Immunoreactivities in Bovine Milk.
    Nutritional neuroscience, 1999
    Co-Authors: Chandan Prasad, Chittaranjan Debata, John U. Mcgregor
    Abstract:

    Enterostatins, pentapeptides (Val-Pro-Asp-Pro-Arg [VPDPR], Val-Pro-Gly-Pro-Arg, Ala-Pro-Gly-Pro- Arg [APGPR], and others) derived from the amino terminus of procolipase, are endogenous to a variety of tissues and body fluids including brain, gut, blood, cerebrospinal fluid, and urine. The administration of exogenous peptides has been shown to elicit a variety of biologic activities, including a decrease in dietary fat preference and pancreatic insulin secretion. Since milk is a rich source of a variety of bioactive substances, especially peptides, we investigated the presence of Enterostatin-like immunoreactivity in bovine milk. We measured Enterostatins-APGPR and VPDPR-in milk from a herd of 19 cows randomly selected from the Louisiana State University Department of Dairy Science Research Herd in Baton Rouge; the results of this study show a mean peptide concentration in raw milk of 33.7 ± 2.9 ng/ml for APGPR and of 104.5 ± 16.3 ng/ml for VPDPR. A further chromatographic characterization of the nature of APGPR- and VPDPR-like immunoreactivities suggested the endogenous peptides share a common epitope with APGPR or VPDPR but are not APGPR or VPDPR. Unlike APGPR or VPDPR, the endogenous peptides were heat-labile and therefore their values were much lower in pasteurized milk.

Masaaki Yoshikawa - One of the best experts on this subject based on the ideXlab platform.

  • Enterostatin reduces serum cholesterol levels by way of a CCK1 receptor-dependent mechanism
    Peptides, 2008
    Co-Authors: Yasuyuki Takenaka, Kousaku Ohinata, Tomoko Shimano, Takaaki Mori, I-ching Hou, Masaaki Yoshikawa
    Abstract:

    Abstract Enterostatin (APGPR), an anorectic pentapeptide derived from the amino terminus of procolipase, significantly reduced serum cholesterol levels after oral administration at a dose of 100 mg/kg for 3 days in mice fed a high-cholesterol-cholic acid diet. The hypocholesterolemic effect of APGPR was inhibited by pretreatment with lorglumide, an antagonist for cholecystokinin 1 (CCK 1 ) receptor, even though APGPR does not have any affinity for CCK 1 receptors. Similarly, the hypocholesterolemic activity of VPDPR, an APGPR analogue, was blocked by lorglumide. These results suggest that the hypocholesterolemic effects of APGPR and VPDPR are mediated by a CCK 1 receptor-dependent mechanism.

  • Enterostatin (APGPR) suppresses the analgesic activity of morphine by a CCK-dependent mechanism.
    Peptides, 2008
    Co-Authors: Yasuyuki Takenaka, Kousaku Ohinata, Tomoko Shimano, Yuko Yamada, Mariko Yoshida, Masaaki Yoshikawa
    Abstract:

    Enterostatin (APGPR) found in the gastrointestinal tract and brain is an anorectic pentapeptide. We found that APGPR inhibited morphine-induced analgesia after intracerebroventricular administration in mice at a dose of 10nmol/mouse. The anti-analgesic effect of APGPR was inhibited by pretreatment with lorglumide and LY225910, antagonists for cholecystokinin 1 (CCK1) and cholecystokinin 2 (CCK2) receptors, respectively. The anti-analgesic effect of APGPR may be mediated by CCK release, since APGPR does not have affinity for CCK receptors.

  • Enterostatin (APGPR) enhances memory consolidation in mice.
    Peptides, 2006
    Co-Authors: Kousaku Ohinata, Soushi Sonoda, Tomoko Shimano, Masaaki Yoshikawa
    Abstract:

    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.

  • Introduction of DPR, an Enterostatin Fragment Peptide, into Soybean β-Conglycinin α′ Subunit by Site-directed Mutagenesis
    Bioscience biotechnology and biochemistry, 2004
    Co-Authors: Yasuyuki Takenaka, Shigeru Utsumi, Naomi Doyama, Nobuyuki Maruyama, Masaaki Yoshikawa
    Abstract:

    DPR, a fragment peptide of Enterostatin (VPDPR) having hypocholesterolemic activity, was introduced into the three homologous sites, EPR, DYR, and DPI, in the soybean β-conglycinin α′ subunit by site-directed mutagenesis. The modified β-conglycinin was expressed in Escherichia coli and recovered in the soluble fraction. After purification on ion-exchange HPLC, the modified β-conglycinin was digested by trypsin to release integrated DPR. The yield of DPR from 1 mole of the modified β-conglycinin was 1.2 mole.

  • Anti-analgesic activity of Enterostatin (VPDPR) is mediated by corticosterone.
    Peptides, 2003
    Co-Authors: Yasuyuki Takenaka, Futoshi Nakamura, Hachiro Usui, Andrzej W. Lipkowski, G. Toth, Masaaki Yoshikawa
    Abstract:

    Although Enterostatin (VPDPR) inhibited morphine-induced analgesia, it had no affinity for μ-opioid receptors. VPDPR administration was reported to elevate serum corticosterone levels. We found that corticosterone exhibited a similar anti-analgesic effect selective for μ-opioid. Furthermore, the anti-analgesic effect of VPDPR was inhibited by RU486, an antagonist for the glucocorticoid receptor. The anti-analgesic effect of VPDPR was not observed in adrenalectomized mice. These results suggest that the anti-analgesic activity of VPDPR is mediated by corticosterone released from the adrenal cortex.