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

Lin, Ling; Park, MieJung; York, David A.

doi:10.1016/j.peptides.2006.10.003

Cited by 26 publications

(20 citation statements)

References 43 publications

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“…Dietary fat intake can be reduced by injections of either enterostatin (33,34) or NPY (41) while Mu-opioid agonists will enhance fat intake (51). In this manuscript, we provide evidence for melanocortin signaling to affect dietary fat intake in a similar manner to that previously demonstrated within the hypothalamus (21,23,26,42).…”

Section: Perspectives and Significancesupporting

confidence: 57%

“…It plays an important role in the development of conditioned taste aversion and the reward response to ingested food (19,54). Previous research from our group has shown the importance of the amygdala in modulating food preferences whether it was through the administration of enterostatin (32,33) or NPY (41) in rats given a two-choice diet paradigm. In the study presented here, we have examined the role of the melanocortin system in the amygdala control of food intake and macronutrient selection using the melanocortin agonist MTII, the melanocortin antagonist SHU-9119, and the reverse agonist AgRP.…”

Section: Discussionmentioning

confidence: 99%

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Melanocortin activity in the amygdala controls appetite for dietary fat

Boghossian

Park

York

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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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 melanocortin 4 receptor antagonist, we investigated the role of melanocortin activity in the CeA in regulating food intake and macronutrient choice. Sprague-Dawley rats, fitted with CeA cannulas, were fed either chow, a high-fat (HF) diet, or adapted to a two-choice HF or low-fat (LF) diet. Injections of the MC4R agonist melanotan II (MTII) in the CeA had a dose-dependent inhibitory effect on food intake that lasted for at least 24 h. This response was greater in rats fed a HF diet. The inverse agonist agouti-related protein (AgRP) and antagonist SHU-9119 increased food intake in a dose-dependent manner, with the hyperphagia lasting for 60 h. In rats adapted to a two-choice HF/LF diet, MTII decreased HF consumption but had no effect on LF consumption, resulting in a long-lasting decrease in total calorie intake (Ϫ35.5% after 24 h, P Ͻ 0.05). Total calorie intake increased in both AgRP-and SHU-9119-treated rats (32 and 109% after 24 h, respectively) as the result of increased intake of HF diet. There was no modification of LF consumption with AgRP treatment and a transient nonsignificant decrease with SHU-9119 treatment. Amygdala brain-derived neurotrophic factor expression was increased by AgRP in fed rats. These results identify the amygdala as a site of action for the melanocortin system to control food intake and dietary preferences.agouti-related protein; melanotan II; SHU-9119; brain derived neurotrophic factor, food intake FOR YEARS, HYPOTHALAMIC CENTERS have been considered as the major brain centers regulating food intake and/or macronutrient selection (45). The neural circuits involved in the regulation of feeding behavior are complex, and more recent studies implicate other parts of the brain in the regulation of ingestive behaviors. Areas such as the nucleus accumbens, the amygdala, the brain stem, and many others form together with the hypothalamic areas a complex circuitry regulating all levels of feeding behavior (6,8,55). Indeed, the paraventricular nucleus (PVN) is not essential for either neuropeptide Y (NPY)-induced feeding or the anorexic response to melanocortin activity (16) since both are evident in PVN-lesioned rats. Furthermore, the anorectic response to melanotan II (MTII) is evident in the dorsovagal complex of the brain stem (52,58).A number of neuropeptides and compounds are known to selectively affect macronutrient intake when administered centrally. For example, the orexigenic NPY (47, 48, 50) , norepinephrine (30, 50), or agouti-related protein (AgRP) (23) have been reported to induce specific selection of macronutrients. Enterostatin, a satiety factor secreted in the gastrointestinal tract and expressed also in the central nervous system, induces an immediate reduction in food intake and inhibits appetite specifically for dietary fat when injected peripherally or centrally (31,37,39).It has been hy...

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Section: Perspectives and Significancesupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Melanocortin activity in the amygdala controls appetite for dietary fat

Boghossian

Park

York

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Enterostatin is recognized as a satiety peptide that selectively suppresses fat intake [38]. Enteorstatin is produced in the pancreas, gastrointestinal tract and in specific regions of the brain.…”

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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“…[1][2][3] Enterostatin, a pentapeptide, is released from its parent procolipase molecule by proteolysis. It is produced in the exocrine pancreas, gastrointestinal tract and in specific regions of the brain.…”

Section: Introductionmentioning

confidence: 99%

“…It is produced in the exocrine pancreas, gastrointestinal tract and in specific regions of the brain. 1,4,5 In addition to its effects on feeding behavior, enterostatin also has metabolic effects, directly promoting fatty acid oxidation in muscle 6 and inhibiting insulin secretion. 7 The enterostatin receptor has been identified as the b-subunit protein of the F1-ATPase complex.…”

Section: Introductionmentioning

confidence: 99%

Enterostatin inhibition of angiogenesis: possible role of pAMPK and vascular endothelial growth factor A (VEGF-A)

Park

Lyons

et al. 2008

Int J Obes

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Introduction:We utilized a genomic analysis of the response of neuronal GT1-7 cells to enterostatin to identify pathways responsive to this peptide. This information, together with reported properties of the enterostatin receptor, suggested that enterostatin may have an effect on angiogenesis. Method: To investigate this hypothesis, we studied the effect of enterostatin as an antiangiogenic agent in two angiogenic tissue culture model systems.Results: Enterostatin induced a 50% or greater inhibition in the angiogenic response of human fat cells and had a U-shaped bimodal dose-response effect in inhibiting angiogenesis in a human placental vein angiogenesis model. To further understand this response, we tested enterostatin's effect in a human hepatoma cell line (HepG2 cells) that was subjected to glucose deprivation, a condition known to induce angiogenesis in other tumor cell lines. Phosphorylated AMP kinase (pAMPK) levels and vascular endothelial growth factor A (VEGF-A) mRNA expression were elevated robustly after incubation of HepG2 cells in the absence of glucose for 4 h, but 15 min incubation with enterostatin dramatically inhibited this pAMPK activation and reduced VEGF-A gene expression after 1 h incubation with enterostatin. The AMPK activator 5-aminoimidazole-4-carboximide ribonucleoside (AICAR) induced VEGF-A expression. Summary: These data suggest that enterostatin has an antiangiogenic effect and suggest that it regulates VEGF-A gene expression through inhibition of AMPK activity.

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

Cited by 26 publications

References 43 publications

Melanocortin activity in the amygdala controls appetite for dietary fat

Melanocortin activity in the amygdala controls appetite for dietary fat

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

Enterostatin inhibition of angiogenesis: possible role of pAMPK and vascular endothelial growth factor A (VEGF-A)

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