Inhibition of insulin release by enterostatin

Ookuma, Mari; Da, York

doi:10.1038/sj.ijo.0800663

Cited by 19 publications

(11 citation statements)

References 26 publications

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“…Its ability to inhibit the intake of dietary fat, to activate sympathetically mediated brown adipose tissue thermogenesis and inhibit insulin secretion has been described (5,25,28,29). However, less is known about the neural network and the target effectors of these responses.…”

Section: Discussionmentioning

confidence: 99%

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

Lin¹,

Park²,

York³

2007

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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) knockout 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 icv blocked the feeding response to amygdala enterostatin in rats. Amygdala enterostatin induced fos activation in α-melanocyte stimulating hormone (α-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.

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Section: Discussionmentioning

confidence: 99%

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

Lin¹,

Park²,

York³

2007

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“…We reported that enterostatin inhibits angiogenesis in both Human Umbilical Vein Endothelial Cells (HUVEC) and fat cells [22] and promotes Myocellular fatty acid oxidation through its stimulation of the AMPK signaling pathway [22]. Enterostatin also inhibits forskolin induced insulin secretion in isolated pancreatic islets [20], and it has been reported to enhance memory and inhibit analgesia induced by the μ-opioid agonist morphine [28]. Recently it was reported the oral administration of enterostatin reduces blood cholesterol by inhibiting VLDL and LDL [30].…”

Section: Introductionmentioning

confidence: 99%

Enterostatin alters protein trafficking to inhibit insulin secretion in Beta-TC6 cells

et al. 2009

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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 F 1 -ATPase beta subunit. We transfected HepG2 cells with either a Green Fluorescent protein (GFP) tagged F 1 -ATPase beta subunit or a Red Fluorescent protein (RFP) tagged F 1 -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.

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“…Enteorstatin is produced in the pancreas, gastrointestinal tract and in specific regions of the brain. In addition to its effects on feeding, enterostatin directly regulates energy expenditure [39], and inhibits insulin secretion [40]. As rebamipide is a gastroprotective agent, we carefully presumed that mucosal protection by rebamipide treatment resulted in increasing level of enterostatin.…”

Section: δ1214mentioning

confidence: 99%

Metabolomics Approach to Explore the Effects of Rebamipide on Inflammatory Arthritis Using Ultra Performance Liquid Chromatography/Quadrupole Time-of-Flight Mass Spectrometry

et al. 2017

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Objective. Rebampide is a gastroprotective agent used to treat gastritis. It possesses anti-inflammatory and anti-arthritis effects, but the mechanisms of these effects are not well understood. The objective of this study was to explore mechanisms underlying the therapeutic effects of rebamipide in inflammatory arthritis. Methods. Collagen-induced arthritis (CIA) was induced in DBA/1J mice. DBA/1J mice were immunized with chicken type II collagen, then treated intraperitoneally with rebamipide (10 mg/kg or 30 mg/kg) or vehicle (10% carboxymethylcellulose solution) alone. Seven weeks later, plasma samples were collected. Plasma metabolic profiles were analyzed using ultra performance liquid chromatography/quadrupole time-of-flight mass spectrometry-based metabolomics study and metabolite biomarkers were identified through multivariate data analysis. Results. Low dose rebamipide treatment reduced the clinical arthritis score compared with vehicle treatment, whereas high dose rebamipide in CIA aggravated arthritis severity. Based on multivariate analysis, 17 metabolites were identified. The plasma levels of metabolites associated with fatty acids and phospholipid metabolism were significantly lower with rebamipide treatment than with vehicle. The levels of 15-deoxy-Δ12,14 prostaglandin J2 and thromboxane B3 decreased only in high dose-treated groups. Certain peptide molecules, including enterostatin (VPDPR) enterostatin and bradykinin dramatically increased in rebamipide-treated groups at both doses. Additionally, corticosterone increased in the low dose-treated group and decreased in the high dose-treated group. Conclusion. Metabolomics analysis revealed the anti-inflammatory effects of rebamipide and suggested the potential of the drug repositioning in metabolism-and lipid-associated diseases. (J Rheum Dis 2017;24:192-202)

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Inhibition of insulin release by enterostatin

Cited by 19 publications

References 26 publications

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

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

Enterostatin alters protein trafficking to inhibit insulin secretion in Beta-TC6 cells

Metabolomics Approach to Explore the Effects of Rebamipide on Inflammatory Arthritis Using Ultra Performance Liquid Chromatography/Quadrupole Time-of-Flight Mass Spectrometry

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