Centrally administered neuropeptide Y (NPY) inhibits gastric emptying and intestinal transit in the rat

Matsuda, Masayuki; Aono, Mitsuru; Moriga, Motoyuki; Okuma, Minoru

doi:10.1007/bf01295910

Cited by 30 publications

(25 citation statements)

References 23 publications

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“…This type of action is similar to that described recently for opioid peptides 20–22 and it may provide a mechanistic explanation for the opposing responses to in vivo DVC application of these polypeptides 6,8,14–18,55. In basal conditions, DVC microinjection of PYY and NPY increases motility.…”

Section: Discussionsupporting

confidence: 83%

Modulation of inhibitory neurotransmission in brainstem vagal circuits by NPY and PYY is controlled by cAMP levels

Browning¹,

Travagli²

2009

Neurogastroenterology Motil

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Pancreatic polypeptides such as neuropeptide Y (NPY) and peptide YY (PYY) exert profound, vagally mediated effects on gastrointestinal (GI) motility. Vagal efferent outflow to the GI tract is determined principally by tonic GABAergic synaptic inputs onto dorsal motor nucleus of the vagus (DMV) neurons, yet neither peptide modulates GABAergic transmission. We showed recently that opioid peptides appear similarly ineffective because of the low resting cAMP levels. Using whole cell recordings from identified DMV neurons, we aimed to correlate the influence of brainstem cAMP levels with the ability of pancreatic polypeptides to modulate GABAergic synaptic transmission. Neither NPY, PYY, nor the Y1 or Y2 receptor selective agonists [Leu,Pro]NPY or NPY(3-36) respectively, inhibited evoked inhibitory postsynaptic current (eIPSC) amplitude unless cAMP levels were elevated by forskolin or 8-bromo-cAMP, by exposure to adenylate cyclase-coupled modulators such as cholecystokinin octapeptide (sulfated) (CCK-8s) or thyrotropin releasing hormone (TRH), or by vagal deafferentation. The inhibition of eIPSC amplitude by [Leu,Pro]NPY or NPY(3-36) was stable for approximately 30 min following the initial increase in cAMP levels. Thereafter, the inhibition declined gradually until the agonists were again ineffective after 60 min. Analysis of spontaneous and miniature currents revealed that such inhibitory effects were due to actions at presynaptic Y1 and Y2 receptors. These results suggest that, similar to opioid peptides, the effects of pancreatic polypeptides on GABAergic transmission depend upon the levels of cAMP within gastric inhibitory vagal circuits.

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Section: Discussionsupporting

confidence: 83%

Modulation of inhibitory neurotransmission in brainstem vagal circuits by NPY and PYY is controlled by cAMP levels

Browning¹,

Travagli²

2009

Neurogastroenterology Motil

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“…To facilitate evaluation of enzyme compositions, formulations, and dosing regimens, we sought to develop a rodent model for gluten digestion. A number of studies (Robert et al, 1991;Matsuda et al, 1993;Burton-Freeman et al, 1997;Izbeki et al, 2001;Overhaus et al, 2004;Turan and Ozdemir, 2004) have exploited the intrinsic similarities between gastrointestinal metabolism of food in rats and hu-mans. Rats may be an effective model for gluten digestion because they are able to eat and digest a significant level of food (on the order of several grams, which would represent a physiological gluten load for a Celiac patient) in a suitable time frame (i.e., in approximately 5-8 h) (Kaneko et al, 1995).…”

mentioning

confidence: 99%

Effect of Barley Endoprotease EP-B2 on Gluten Digestion in the Intact Rat

Gass¹,

Vora²,

Bethune³

et al. 2006

J Pharmacol Exp Ther

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Celiac Sprue is a multifactorial disease characterized by an intestinal inflammatory response to ingested gluten. Proteolytically resistant gluten peptides from wheat, rye, and barley persist in the intestinal lumen and elicit an immune response in genetically susceptible individuals. Here, we demonstrate the in vivo ability of a gluten-digesting protease ("glutenase") to accelerate the breakdown of a gluten-rich solid meal. The proenzyme form of endoprotease B, isoform 2 from Hordeum vulgare (EP-B2), was orally administered to adult rats with a solid meal containing 1 g of gluten. Gluten digestion in the stomach and small intestine was monitored as a function of enzyme dose and time by high-performance liquid chromatography and mass spectrometry. In the absence of supplementary EP-B2, gluten was solubilized and proteolyzed to a limited extent in the stomach and was hydrolyzed and assimilated mostly in the small intestine. In contrast, EP-B2 was remarkably effective at digesting gluten in the rat stomach in a dose-and time-dependent fashion. At a 1:25 EP-B2/gluten dose, the gastric concentration of the highly immunogenic 33-mer gliadin peptide was reduced by more than 50-fold within 90 min with no overt signs of toxicity. Evaluation of EP-B2 as an adjunct to diet control is therefore warranted in celiac patients.

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“…Liquid gastric emptying was estimated by gavage of 0.5 ml of phenol red (1 mg/ml) into the stomach prior to sacrifice of the mouse, as has been described (1,20). After sacrifice, each stomach was removed and weighed; phenol red remaining in the stomach was recovered by rinsing out the stomach with water, and phenol red was measured by spectrophotometry at 560 nm as previously described (21).…”

Section: Methodsmentioning

confidence: 99%

Effects of Esomeprazole Magnesium on Nonsteroidal Anti-Inflammatory Drug Gastropathy

et al. 2005

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It has been proposed that tissue damage induced by nonsteroidal anti-inflammatory drugs is related to increased tissue free radical production with antioxidant depletion. We have shown that esomeprazole increases gastric total antioxidant capacity in mice and, therefore, hypothesized that the protective effect of esomeprazole during treatment with a nonsteroidal anti-inflammatory drug is related to increased gastric antioxidant capacity and decreased tissue free radical production. A/J mice received one of four treatments by daily gavage: saline in vehicle (control), indomethacin, esomeprazole, or indomethacin and esomeprazole. After 10 days, all mice were sacrificed and validated assays were used to measure gastric total antioxidant capacity, lipid peroxide levels, and myeloperoxidase activity. Indomethacin-treated mice developed weight loss and melena. No mice receiving indomethacin and esomeprazole died, but the death rate while receiving indomethacin was 38% (chi2, P = 0.05). Gastric lipid peroxide levels increased in mice receiving indomethacin treatment compared to treatment with esomeprazole and indomethacin (P = 0.03). There was a strong trend (P = 0.08) toward increased gastric total antioxidant capacity in mice receiving esomeprazole and indomethacin compared to mice receiving indomethacin. Gastric myeloperoxidase activities were not different among the four groups. Esomeprazole significantly improved survival in mice that received indomethacin, reduced free radical production, as estimated by lipid peroxide levels, and appeared to increase gastric total antioxidant capacity. The mechanisms for the beneficial effects of esomeprazole in the treatment of gastropathy are more complex than previously thought.

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Centrally administered neuropeptide Y (NPY) inhibits gastric emptying and intestinal transit in the rat

Cited by 30 publications

References 23 publications

Modulation of inhibitory neurotransmission in brainstem vagal circuits by NPY and PYY is controlled by cAMP levels

Modulation of inhibitory neurotransmission in brainstem vagal circuits by NPY and PYY is controlled by cAMP levels

Effect of Barley Endoprotease EP-B2 on Gluten Digestion in the Intact Rat

Effects of Esomeprazole Magnesium on Nonsteroidal Anti-Inflammatory Drug Gastropathy

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