Orally administered soymorphins, soy-derived opioid peptides, suppress feeding and intestinal transit via gut μ1-receptor coupled to 5-HT1A, D2, and GABABsystems

2010 ◽  
Vol 299 (3) ◽  
pp. G799-G805 ◽  
Author(s):  
Kentaro Kaneko ◽  
Masashi Iwasaki ◽  
Masaaki Yoshikawa ◽  
Kousaku Ohinata
Keyword(s):  
Food Intake ◽  
Oral Administration ◽  
Opioid Receptor ◽  
Intraperitoneal Administration ◽  
Inhibitory Effect ◽  
Intestinal Transit ◽  
Opioid Agonist ◽  
Small Intestinal Transit ◽  
Small Intestinal Motility ◽  
Small Intestinal

We previously reported that soymorphins, μ-opioid agonist peptides derived from soy β-conglycinin β-subunit, have anxiolytic-like activity. The aim of this study was to investigate the effects of soymorphins on food intake and gut motility, along with their mechanism. We found that soymorphins decreases food intake after oral administration in fasted mice. Orally administered soymorphins suppressed small intestinal transit at lower dose than that of anorexigenic activity. Suppression of food intake and small intestinal transit after oral administration of soymorphins was inhibited by naloxone or naloxonazine, antagonists of μ- or μ1-opioid receptor, respectively, after oral but not intraperitoneal administration. The inhibitory activities of small intestinal transit by soymorphins were also inhibited by WAY100135, raclopride, or saclofen, antagonists for serotonin 5-HT1A, dopamine D2, or GABABreceptor, respectively. We then examined the order of activation of 5-HT1A, D2, and GABABreceptors, using their agonists and antagonists. The inhibitory effect of 8-hydroxy-2-dipropylaminotetralin hydrobromide, a 5-HT1Aagonist, after oral administration on small intestinal transit was blocked by raclopride or saclofen. Bromocriptine, a D2agonist-induced small intestinal transit suppression, was inhibited by saclofen, but not by WAY100135. Baclofen, a GABABagonist-induced small intestinal transit suppression, was not blocked by WAY100135 or raclopride. These results suggest that 5-HT1Aactivation elicits D2followed by GABABactivations in small intestinal motility. We conclude that orally administered soymorphins suppress food intake and small intestinal transit via μ1-opioid receptor coupled to 5-HT1A, D2, and GABABsystems.

Excitatory effects of synchronized intestinal electrical stimulation on small intestinal motility in dogs

2007 ◽  
Vol 293 (6) ◽  
pp. G1190-G1195 ◽  
Author(s):  
Jieyun Yin ◽  
Jiande DZ Chen
Keyword(s):  
Electrical Stimulation ◽  
Intestinal Motility ◽  
Therapeutic Potential ◽  
Intestinal Transit ◽  
Excitatory Effect ◽  
Small Intestinal Transit ◽  
Small Bowel Motility ◽  
Small Intestinal Motility ◽  
Intestinal Electrical Stimulation ◽  
Small Intestinal

The aim of this study was to investigate effects of synchronized intestinal electrical stimulation (SIES) on small intestinal motility in dogs. Seventeen dogs were equipped with a duodenal cannula for the measurement of small bowel motility using manometry; an additional cannula was equipped in six of the dogs with 1.5 m distal to the first one for the measurement of small intestinal transit. Two pairs of bipolar electrodes were implanted on the small intestinal serosa with an interval of 5 cm; glucagon was used to induce postprandial intestinal hypomotility. Eleven dogs were used for the assessment of the small intestinal contractions in both fasting and fed states. The other six dogs were used for the measurement of small intestinal transit. We found that 1) SIES induced small intestinal contractions during phase I of the migrating motor complex (MMC) (contractile index or CI: 5.2 ± 0.6 vs. 10.3 ± 0.7, P = 0.003); 2) in the fed state, SIES significantly improved glucagon-induced small intestinal postprandial hypomotility (CI: 3.4 ± 0.5 vs. 6.0 ± 0.3, P = 0.03); 3) SIES significantly accelerated small intestinal transit delayed by glucagon (70.4 ± 3.1 vs. 44.5 ± 3.1 min, P < 0.01); 4) there was a negative correlation between the CI and transit time ( r = −0.427, P = 0.048); and 5) the excitatory effect of SIES was blocked by atropine. SIES may have a therapeutic potential for treating patients with small intestinal disorders.

scholarly journals The relation between food intake and abomasal emptying and small intestinal transit time in sheep

1985 ◽  
Vol 53 (2) ◽  
pp. 373-380 ◽  
Author(s):  
P. C. Gregory ◽  
S. J. Miller ◽  
A. C. Brewer
Keyword(s):  
Small Intestine ◽  
Food Intake ◽  
Transit Time ◽  
Intestinal Transit ◽  
Phenol Red ◽  
Intestinal Transit Time ◽  
Small Intestinal Transit ◽  
Nichrome Wire ◽  
Small Intestinal ◽  
Small Intestinal Transit Time

1. The relation between the level of food intake and gastrointestinal motility and digesta flow in the abomasum and small intestine was studied in sheep fitted with nichrome-wire electrodes in the gut wall, an abomasal and a duodenal catheter and a terminal ileal cannula.2. Abomasal volume and outflow were calculated from CrEDTA dilution in six sheep and small intestinal transit time by the passage of Phenol Red in ten sheep.3. The frequency of the migrating myoelectric complex of the small intestine was not altered by the level of food intake but the duration of the periods of irregular spiking activity, the amplitude of abomasal activity and the frequency of duodenal rushes were decreased as the level of food intake was decreased.4. There was a linear relation between the level of food intake (FI) and abomasal outflow (mean with SEM: 327 (69) ml/h for each kg FI/d; P < 0.01), and abomasal volume (mean with SEM: 344 (50) ml/kg FI per d; P < 0.001), without any significant change in the half-time of marker dilution in the abomasum. Small intestinal transit time decreased with an increase in food intake (mean with SEM: - 54.9 (5.6) min/kg FI per d; P < 0.001).5.It is concluded that abomasal volume and the rate of digesta flow from the abomasum and along the small intestine are linearly related to the level of food intake.

scholarly journals Modulation of High-Voltage Activated Ca2+ Channels in the Rat Periaqueductal Gray Neurons by μ-Type Opioid Agonist

1997 ◽  
Vol 77 (3) ◽  
pp. 1418-1424 ◽  
Author(s):  
Chang-Ju Kim ◽  
Jeong-Seop Rhee ◽  
Norio Akaike
Keyword(s):  
G Proteins ◽  
Opioid Receptor ◽  
High Voltage ◽  
Inhibitory Effect ◽  
Periaqueductal Gray ◽  
Dependent Manner ◽  
Opioid Agonist ◽  
Voltage Clamp Condition ◽  
Voltage Dependent ◽  
Clamp Condition

Kim, Chang-Ju, Jeong-Seop Rhee, and Norio Akaike. Modulation of high-voltage activated Ca2+ channels in the rat periaqueductal gray neurons by μ-type opioid agonist. J. Neurophysiol. 77: 1418–1424, 1997. The effect of μ-type opioid receptor agonist, D-Ala2,N-MePhe4,Gly5-ol-enkephalin (DAMGO), on high-voltage-activated (HVA) Ca2+ channels in the dissociated rat periaqueductal gray (PAG) neurons was investigated by the use of nystatin-perforated patch recording mode under voltage-clamp condition. Among 118 PAG neurons tested, the HVA Ca2+ channels of 38 neurons (32%) were inhibited by DAMGO (DAMGO-sensitive cells), and the other 80 neurons (68%) were not affected by DAMGO (DAMGO-insensitive cells). The N-, P-, L-, Q-, and R-type Ca2+ channel components in DAMGO-insensitive cells shared 26.9, 37.1, 22.3, 7.9, and 5.8%, respectively, of the total Ca2+ channel current. The channel components of DAMGO-sensitive cells were 45.6, 25.7, 21.7, 4.6, and 2.4%, respectively. The HVA Ca2+ current of DAMGO-sensitive neurons was inhibited by DAMGO in a concentration-, time-, and voltage-dependent manner. Application of ω-conotoxin-GVIA occluded the inhibitory effect of DAMGO ∼70%. So, HVA Ca2+ channels inhibited by DAMGO were mainly the N-type Ca2+ channels. The inhibitory effect of DAMGO on HVA Ca2+ channels was prevented almost completely by the pretreatment of pertussis toxin (PTX) for 8–10 h, suggesting that DAMGO modulation on N-type Ca2+ channels in rat PAG neurons is mediated by PTX-sensitive G proteins. These results indicate that μ-type opioid receptor modulates N-type HVA Ca2+ channels via PTX-sensitive G proteins in PAG neurons of rats.

Blockade of GRP receptors inhibits gastric emptying and gallbladder contraction but accelerates small intestinal transit in humans

2000 ◽  
Vol 94 (1-3) ◽  
pp. 9
Author(s):  
Pius Hildebrand ◽  
Lukas P. Degen ◽  
Annette Collet ◽  
Livio Rossi ◽  
Fuping Peng ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Intestinal Transit ◽  
Gallbladder Contraction ◽  
Small Intestinal Transit ◽  
Small Intestinal ◽  
Grp Receptors
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