Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Gastrointestinal Transit”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed2004

Effects of cannabinoid receptor-2 activation on accelerated gastrointestinal transit in lipopolysaccharide-treated rats.

The biological effects of cannabinoids (CB) are mediated by CB(1) and CB(2) receptors. The role of CB(2) receptors in the gastrointestinal tract is uncertain. In this study, we examined whether CB(2) receptor activation is involved in the regulation of gastrointestinal transit in rats. Basal and lipopolysaccharide (LPS)-stimulated gastrointestinal transit was measured after instillation of an Evans blue-gum Arabic suspension into the stomach, in the presence of specific CB(1) and CB(2) agonists and antagonists, or after treatment with inhibitors of mediators implicated in the transit process. In control rats a CB(1) (ACEA; 1 mg kg(-1)), but not a CB(2) (JWH-133; 1 mg kg(-1)), receptor agonist inhibited basal gastrointestinal transit. The effects of the CB(1) agonist were reversed by the CB(1) antagonist AM-251, which alone increased basal transit. LPS treatment increased gastrointestinal transit. This increased transit was reduced to control values by the CB(2), but not the CB(1), agonist. This inhibition by the CB(2) agonist was dose dependent and prevented by a selective CB(2) antagonist (AM-630; 1 mg kg(-1)). By evaluating the inhibition of LPS-enhanced gastrointestinal transit by different antagonists, the effects of the CB(2) agonist (JWH-133; 1 mg kg(-1)) were found to act via cyclooxygenase, and to act independently of inducible nitric oxide synthase (NOS) and platelet-activating factor. Interleukin-1 beta and constitutive NOS isoforms may be involved in the accelerated LPS transit. The activation of CB(2) receptors in response to LPS is a mechanism for the re-establishment of normal gastrointestinal transit after an inflammatory stimulus.

Animals↗
PubMed1998

Acute blood volume expansion delays the gastrointestinal transit of a charcoal meal in awake rats.

The present study evaluates the effect of blood volume expansion on the gastrointestinal transit of a charcoal meal (2.5 ml of an aqueous suspension consisting of 5% charcoal and 5% gum arabic) in awake male Wistar rats (200-270 g). On the day before the experiments, the rats were anesthetized with ether, submitted to left jugular vein cannulation and fasted with water ad libitum until 2 h before the gastrointestinal transit measurement. Blood volume expansion by i.v. infusion of 1 ml/min Ringer bicarbonate in volumes of 3, 4 or 5% body weight delayed gastrointestinal transit at 10 min after test meal administration by 21.3-26.7% (P < 0.05), but no effect was observed after 1 or 2% body weight expansion. The effect of blood volume expansion (up to 5% body weight) on gastrointestinal transit lasted for at least 60 min (P < 0.05). Mean arterial pressure increased transiently and central venous pressure increased and hematocrit decreased (P < 0.05). Subdiaphragmatic vagotomy and yohimbine (3 mg/kg) prevented the delay caused by expansion on gastrointestinal transit, while atropine (0.5 mg/kg), L-NAME (2 mg/kg), hexamethonium (10 mg/kg), prazosin (1 mg/kg) or propranolol (2 mg/kg) were ineffective. These data show that blood volume expansion delays the gastrointestinal transit of a charcoal meal and that vagal and yohimbine-sensitive pathways appear to be involved in this phenomenon. The delay in gastrointestinal transit observed here, taken together with the modifications of gastrointestinal permeability to salt and water reported by others, may be part of the mechanisms involved in liquid excess management.

Animals↗
PubMed1997

Gastric emptying and gastrointestinal transit during lactation in rats.

Female sex hormones can influence gastrointestinal function. To understand whether postpartum changes in female sex hormones may affect such function, gastric emptying and gastrointestinal transit were measured in rats on days 1-2, 10, 15, and 21 of lactation, on day 7 postweaning, and at the nonpregnant diestrous stage. Gastric emptying and gastrointestinal transit were assessed in conscious rats 15 min after intragastric instillation of a test meal containing charcoal and (51)Cr. The results showed that gastric emptying was increased throughout the first 2 wk of lactation, with a gradual decrease as lactation proceeded toward weaning, and returned to the level of the virgin rats by 1 wk postweaning. Gastrointestinal transit was greater in the early stage of lactation and was related to gastric emptying (P < 0.001). Increases in gastric emptying and intestinal length were correlated with lactation (P < 0.001) and plasma prolactin levels (P < 0.05) but not with plasma progesterone or estradiol levels. We concluded that the sex steroid hormones associated with lactation do not mediate a change in gastric emptying and gastrointestinal transit during lactation.

Animals↗
PubMed1998

Interactive effect of morphine and dexmedetomidine on gastric emptying and gastrointestinal transit in the rat.

We studied the interactive effect of dexmedetomidine and morphine on gastric emptying and gastrointestinal transit in the rat. In one group of rats, to examine the interactive effect on gastrointestinal transit, the two drugs were injected i.p. in a fixed ratio (30: 1)--that of their ED50 values--in six doses (0.062-1.075 mg kg-1), each to a different group of 5-8 male rats for each dose. In another group, to examine the interactive effect on gastric emptying, either dexmedetomidine or saline was injected with saline or with the ED25 or ED50 of morphine (0.22 and 2.8 mg kg-1, respectively). In both groups, at 30 min, radiolabelled saline 1 ml was infused into the stomach; at 1 h, gastric emptying or gastrointestinal transit was calculated by measuring the radioactivity in the gastrointestinal tract. Morphine and dexmedetomidine produced a supra-additive inhibitory effect on gastrointestinal transit (P = 0.02). Dexmedetomidine 0.01 mg kg-1, which itself significantly inhibited gastric emptying (P < 0.01), did not significantly alter the inhibitory effect of morphine on gastric emptying. Therefore, in rats, dexmedetomidine markedly enhanced the inhibitory effect of morphine on gastrointestinal transit, but it did not significantly alter the effect on gastric emptying.

Adrenergic alpha-Agonists↗
PubMed2004

A new method using flow cytometry to measure the effects of drugs on gastric emptying and gastrointestinal transit in mice.

The use of radiolabelled markers is considered to be a gold standard for assessing gastric emptying and gastrointestinal transit in mice and rats, but their use has increasingly been restricted due to health concern. Therefore, a new method using fluorescent polystyrene microbeads and flow cytometry was devised. Saline containing fluorescent markers (together with non-fluorescent microbeads) was infused into the stomach of each mouse and gastric emptying and gastrointestinal transit were calculated by measuring the quantity of the fluorescent microbeads in the gastrointestinal tract using flow cytometer. The effects of saline (as a control), morphine (CAS 52-26-6) and dexmedetomidine (CAS 113775-47-6) were tested. Both gastric emptying and gastrointestinal transit measured with this method (after i.p. injection of saline) were similar to those reported previously using the conventional radiolabelled methods. Morphine significantly inhibited both gastric emptying and gastrointestinal transit in a dose-dependent manner. Dexmedetomidine did not significantly inhibit gastric emptying but inhibited gastrointestinal transit. These results were also similar to those obtained using the conventional radiolabelled method. The method using fluorescent microbeads and flow cytometry may be a reliable alternative to the methods using radioisotope for studying the effects of drugs on gastric emptying and gastrointestinal transit.

Analgesics, Non-Narcotic↗
PubMed1985

Stereospecific opiate receptors in the actions of thyrotropin releasing hormone and morphine on gastrointestinal transit.

Studies in these laboratories have shown that morphine and thyrotropin releasing hormone (TRH) inhibit gastrointestinal transit in the mouse. Administration of morphine sulfate (5 mg/kg, s.c.) or TRH (10 microgram i.c.v.) to mice inhibited gastrointestinal transit as measured by the charcoal meal test. In order to determine whether the effects of TRH and morphine were mediated via stereospecific opiate receptors, the effects of two stereoisomers of an antagonist, (-) alpha -5,9-diethyl-2'-hydroxy-2-(3-furylmethyl)6,7-benzomorphan (MR2266), the active isomer and (+) alpha-5,9-diethyl-2'-hydroxy-2-(3-furylmethyl)6,7-benzomorphan (MR 2267), the inactive isomer, on morphine and TRH induced changes in gastrointestinal transit were determined. Morphine and THR induced inhibition of gastrointestinal transit was antagonized by MR 2266 (1 and 3 mg/kg, s.c.) but was unaffected by MR 2267. These studies provide evidence for the involvement of opiate receptors in the actions of morphine and TRH on gastrointestinal transit, and further suggest that the receptors are stereospecific in nature.

Animals↗
PubMedDate not supplied

The role of dopamine (D2), alpha and beta-adrenoceptor receptors in the decrease in gastrointestinal transit induced by dopamine and dopamine-related drugs in the rat.

This study analyses the effects of dopamine receptor agonists and antagonists on rat gastrointestinal transit (GIT) in an attempt to identify the mechanisms involved. Dopamine (DA), apomorphine, quinpirole, bromocriptine and fenoldopam were given by subcutaneous (s.c.), intrathecal (i.t.), intracisternal (i.c.) and/or intraperitoneal (i.p.) routes. In general, DA (200 micrograms, i.t.), apomorphine (3, 5 and 10 mg/kg, s.c.; or 10, 30 and 100 micrograms, i.t.), and bromocriptine (1, 5 and 10 mg/kg, s.c.) elicited decreases in gastrointestinal transit which were significantly antagonized by the D2 receptor antagonists domperidone or alizapride (both 5 mg/kg, s.c.), but remained unaffected by the D1 receptor antagonist SCH 23390 (5 mg/kg, s.c.). Similarly, DA (50, 100 and 200 micrograms, i.c.) and apomorphine (12 and 50 micrograms; i.c.) produced dose-dependent decreases in gastrointestinal transit amenable to blockade by the classical DA receptor antagonist haloperidol (10 micrograms, i.c.). The responses to apomorphine (3, 5 and 10 mg/kg, s.c.) were unaltered by 6-hydroxydopamine (100 mg/kg, i.p.)-induced sympathectomy but were antagonized by both propranolol (1 mg/kg, s.c.) and phentolamine (5 mg/kg, s.c.). Significantly, after bilateral (cervical) vagotomy, gastrointestinal transit was markedly reduced, but apomorphine (5 mg/kg, s.c.) apparently further reduced gastrointestinal transit. The D1 agonists fenoldopam (5, 10 and 20 mg/kg, s.c.) significantly reduced GIT. Fenoldopam-induced antitransit effects were markedly modified by the D1 receptor antagonist, SCH 23390 (5 mg/kg, s.c.); only the response induced by 5 mg/kg of fenoldopam was apparently antagonized by SCH 23390. The mixed D2 and D3 receptor agonist quinpirole (4 and 8 mg/kg, s.c.; or 8 mg/kg, i.p.; 200 micrograms, i.t.) did mimic DA eliciting significant reductions in gastrointestinal transit which, however, were not antagonized by domperidone (5 mg/kg, s.c.). Taken together, the present results support the contention that the decrease in rat gastrointestinal transit induced by DA and apomorphine may be mediated by an interaction with central and/or peripheral D2 receptors. The presence of dopamine receptors (D2) in the alimentary canal are strengthened by antitransit effect of fenoldopam and bromocriptine in the gastrointestinal tract.

Animals↗
PubMed2002

Modulation of gastric emptying and gastrointestinal transit in rats through intestinal cannabinoid CB(1) receptors.

We studied the delay in gastric emptying and gastrointestinal transit induced by the cannabinoid receptor agonists (+)-WIN 55,212-2 (R(+)-[2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazin-yl]-(1-naphthalenyl)methanone mesylate) and CP 55,940 ((-)-cis-3[2-hydroxy-4-(1,1-dimethylheptyl)phenyl]-trans-4-(3-hydroxypropyl) cyclohexanol), as prevented by the selective cannabinoid CB(1)-receptor antagonist SR141716 ((N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide)) in rats after systemic or central drug administration. Oral SR141716 showed comparable potency (ID(50) range 1.0-3.9 mg/kg) in antagonizing gastric emptying and gastrointestinal transit delay by (+)-WIN 55,212-2 or CP 55,940. Gastric emptying and gastrointestinal transit delay after intracerebroventricular (i.c.v.) (+)-WIN 55,212-2 was prevented by oral or i.c.v. SR141716, but i.c.v. SR141716 did not significantly reduce the effect of i.p. (+)-WIN 55,212-2. Pertussis toxin prevented the delaying action of i.c.v. (+)-WIN 55,212-2 on both gastric emptying and gastrointestinal transit, but had no effect on (+)-WIN 55,212-2 i.p. These findings are consistent with a primary role of peripheral cannabinoid CB(1) receptor mechanisms in gastrointestinal transit delay by specific agonists.

Administration, Oral↗
PubMed1998

Effects of nalbuphine, pentazocine and U50488H on gastric emptying and gastrointestinal transit in the rat.

We studied the effect of mixed agonist-antagonist opioids (nalbuphine and pentazocine) and a kappa opioid agonist (U50488H) on gastric emptying and gastrointestinal transit, and their interactions with morphine in rats. In each group, nalbuphine (0.01-30 mg kg-1), pentazocine (1-30 mg kg-1), U50488H (1-100 mg kg(-1)1) or saline was injected i.p. at 0 min. Another four groups of rats received morphine 13.4 mg kg-1 (ED75) and one of the following substances: saline, nalbuphine, pentazocine or U50488H. In both groups, at 30 min, radiolabelled saline 1 ml was infused into the stomach; at 1 h, gastric emptying and gastrointestinal transit were calculated by measuring the radioactivity in the gastrointestinal tract. Slopes for dose-response curves were determined. Nalbuphine significantly, but only weakly, delayed gastric emptying (P < 0.0005) and gastrointestinal transit (P < 0.01). Pentazocine markedly inhibited both, whereas U50488H did not significantly inhibit either. The slopes of the dose-response curves for nalbuphine, but not for pentazocine, on both gastric emptying and gastrointestinal transit were significantly less steep than those for morphine. Nalbuphine significantly antagonized the inhibitory effect of morphine on gastric emptying (P = 0.005) and gastrointestinal transit (P = 0.02), whereas pentazocine and U50488H did not. Nalbuphine and pentazocine delay gastric emptying and gastrointestinal transit, possibly by different mechanisms.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2004

Propofol and midazolam inhibit gastric emptying and gastrointestinal transit in mice.

We studied the effect of propofol and midazolam on gastric emptying and gastrointestinal transit in mice. Ten minutes after intraperitoneal injection of propofol or midazolam, 0.2 mL of saline containing fluorescent microbeads was infused into the stomach. Thirty minutes later, the gastrointestinal tract was excised, and gastric emptying and gastrointestinal transit were calculated by measuring the quantity of fluorescent microbeads in the gastrointestinal tract by using a flow cytometer. At a dose that produced a light level of sedation (mice righted themselves within 2 s), both drugs significantly, but weakly, inhibited gastric emptying to a similar degree (propofol: P < 0.001 versus control value; 95% confidence interval [CI] for difference, 4.9%-20.2%; midazolam: P < 0.001 versus control value; 95% CI for difference, 7.8%-14.7%). Midazolam, but not propofol, delayed gastrointestinal transit (P < 0.001). At a larger dose that produced a deeper level of sedation (absence of righting reflex >10 s), both drugs significantly inhibited gastric emptying (propofol: P < 0.001; 95% CI for difference, 31.4%-61.2%; midazolam: P < 0.001; 95% CI for difference, 30.8%-61.1%) and gastrointestinal transit (P < 0.001 for both drugs).

Algorithms↗
PubMed2001

Gastrointestinal transit of dosage forms in the pig.

The gastrointestinal transit of liquid, pellet and tablet formulations was measured under fasted conditions in the domestic pig (n = 4) using the technique of gamma scintigraphy. The mean times for 50% gastric emptying for liquid and pellet systems were 1.4 and 2.2 h, respectively; tablets emptied between 1.5 and 6.0 h. Total transit times were in the order of 50 h. These data conform well to published values for the transit of liquid and solid food materials in the pig. The times are much shorter than those previously published for the transit of solid dosage forms in the pig. We conclude that the domestic pig would be a good model to study the gastrointestinal transit of pharmaceutical formulations and the absorption of drug compounds.

Animals↗
PubMed1993

The effect of some alpha 2-adrenoceptor agonists and antagonists on gastrointestinal transit in mice: influence of morphine, castor oil and glucose.

1. The effects of graded doses of the alpha 2-adrenoceptor agonists clonidine, tizanidine and BHT-920, and the alpha 2-adrenoceptor antagonists yohimbine and idazoxan, on gastrointestinal transit were investigated in mice using the charcoal meal test. 2. The agonists produced significant and dose-dependent decreases in gastrointestinal transit, and the antagonists produced the opposite effect. In affecting the gastrointestinal transit, clonidine (1 mg/kg) was as effective as tizanidine (12 mg/kg) and BHT-920 (40 mg/kg), while yohimbine (2 mg/kg) was as effective as idazoxan (1 mg/kg). 3. Morphine (2, 4 and 8 mg/kg) significantly inhibited gastrointestinal transit. This effect was significantly reversed by the co-administration of yohimbine (2 mg/kg) and idazoxan (1 mg/kg). 4. The acute administration of glucose (5.04 g/kg, i.p.) potentiated the inhibition of gastrointestinal transit produced by clonidine (1 mg/kg) and BHT-920 (40 mg/kg). Glucose treatment, however, had no significant effect on the increase in gastrointestinal transit induced by yohimbine (2 mg/kg) or idazoxan (1 mg/kg). 5. Castor oil (0.25 mL/mouse, orally) induced diarrhoea in saline-treated animals within about 45 min. Clonidine (1 mg/kg), tizanidine (12 mg/kg) and BHT-920 (40 mg/kg) delayed the occurrence of diarrhoea to 2.1, 1.2 and 1.4 h, respectively.

Adrenergic alpha-Agonists↗
PubMed1988

Calcitonin and CGRP inhibit gastrointestinal transit via distinct neuronal pathways.

This study compares the central nervous system effects of rat calcitonin and rat calcitonin gene-related peptide (CGRP) on gastrointestinal transit in freely moving rats. Calcitonin and CGRP (0.01-1.0 nmol) injected into the lateral cerebral ventricle significantly inhibited gastric emptying and small bowel transit but did not affect large bowel transit. These biological actions were abolished by ganglionic blockade with chlorisondamine but not by noradrenergic blockade with bretylium. Truncal vagotomy abolished the inhibitory effects of CGRP but not those of calcitonin. Neither adrenalectomy nor hypophysectomy prevented the inhibitory actions of calcitonin and CGRP on gastric emptying and small bowel transit. Intraperitoneal administration of calcitonin and CGRP (1 nmol) produced inhibition of gastric emptying only, and this was not abolished by ganglionic blockade. These results indicate that calcitonin and CGRP exhibit similar central nervous system effects, producing inhibition of gastric emptying and small bowel transit but not altering large bowel transit. Calcitonin inhibits gastrointestinal transit via nonvagal, nonnoradrenergic autonomic efferents, yet CGRP inhibits gastrointestinal transit via vagal efferent fibers.

Animals↗
PubMed1997

Differential effects of clonidine and dexmedetomidine on gastric emptying and gastrointestinal transit in the rat.

We have studied the effect of clonidine, dexmedetomidine and morphine on gastric emptying and gastrointestinal transit in the rat. In one group, each agonist was injected i.p. in 6-12 male Wistar rats. In another group of rats, yohimbine, naloxone or saline was injected with an agonist. At 30 min, radiolabelled saline 1 ml was infused into the stomach. At 1 h, gastric emptying and gastrointestinal transit were calculated by measuring the radioactivity in the gastrointestinal tract. We found that clonidine and dexmedetomidine strongly inhibited gastrointestinal transit (ED50 0.08 and 0.04 mg kg-1, respectively). They also significantly inhibited gastric emptying (P < 0.05), but the effect was weak (95% confidence intervals for difference from saline 8.2-34.9% with clonidine 1 mg kg-1 and 3.4-15.4% with dexmedetomidine 0.03 mg kg-1). Morphine strongly inhibited both gastric emptying and gastrointestinal transit (ED50 2.8 and 1.2 mg kg-1, respectively). Yohimbine significantly antagonized the inhibitory effects of clonidine and dexmedetomidine (P < 0.05), whereas naloxone, which significantly antagonized the effect of morphine (P < 0.01), did not antagonize the effect of either of the other agonists.

Adrenergic alpha-Agonists↗
PubMed1997

Nitric oxide modulates the acute increase of gastrointestinal transit induced by endotoxin in rats: a possible role for tachykinins.

Because of the evidence that endogenous nitric oxide (NO) plays an essential role in the physiological regulation of gastrointestinal motility we have investigated, by use of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), the role of endogenous NO in the acute endotoxin-induced changes of gastrointestinal transit. Pre-treatment with E. coli endotoxin (100 micrograms kg-1, i.v.) induced a significant increase in the gastrointestinal transit of a charcoal suspension in anaesthetized rats. Previous administration of the NO synthase inhibitor, L-NAME (10 mg kg-1, i.v.) significantly prevented the effects of endotoxin. L-arginine (200 mg kg-1, i.v.) and the substance P antagonist [D-Pro2, D-Trp7,9]-substance P (SPA), significantly reversed the effects of L-NAME on gastrointestinal transit in rats treated with endotoxin. Pre-treatment with dexamethasone (5 mg kg-1, s.c., twice), an inhibitor of the expression of inducible NO synthase, did not affect the increase in the gastrointestinal transit through constitutive NO synthesis. The results suggest that constitutive nitric oxide is involved in the increase of gastrointestinal transit induced by endotoxin and that the reduction in transit induced by L-NAME in endotoxin-treated rats is mediated by endogenous tachykinins.

Animals↗
PubMed1984

Pituitary-adrenal mediation of bombesin-induced inhibition of gastrointestinal transit in rats.

Centrally administered bombesin (0.1-3.5 micrograms, i.c.v.) inhibits gastrointestinal transit of a charcoal meal in a dose-related manner in rats. The roles of pituitary and adrenal glands in the mediation of this effect were assessed. The inhibition of gastrointestinal transit associated with bombesin (0.5 microgram, i.c.v.) was prevented by either hypophysectomy or adrenalectomy. Bombesin-induced inhibition of gastrointestinal transit is therefore mediated through the pituitary-adrenal axis. This is in contrast to bombesin-induced scratching and inhibition of gastric acid secretion which are not markedly influenced by either hypophysectomy or adrenalectomy.

Animals↗
PubMed1990

Fractional gastrointestinal transit time: intra- and interindividual variation.

The intra- and interindividual variation in the gastrointestinal transit times was measured in 12 healthy adult test subjects using a scintigraphic method with 111In marked single unit tablets. Test conditions were semi-standardized. The variation within the same individual was as large as the variation between different subjects regarding the transit times through both the small and the large intestines. The small intestine transit time was 5 h (median) with an interquartile range of 4-7 h. The median transit time through the large intestine was 23.5 h (interquartile range 19.0-40.5 h). The coefficient of repeatability for the small intestinal and large intestinal transit time was 4 h and 33 h respectively. Our conclusion is that the 111In single unit capsule method can be used for measuring the fractional gastrointestinal transit times, but the intra- and interindividual variations are rather large and similar. From a radiation-hygienic point of view the 111In single unit capsule method is acceptable. The large inter- and intraindividual variation in gastrointestinal transit time might be an important factor in the absorption of certain drugs.

Adult↗
PubMed1977

Ovarian hormones and meal patterns in rats: effects of progesterone and role of gastrointestinal transit.

Three experiments determined: (1) whether progesterone treatment would reverse the effects of estradiol benzoate (EB) on meal patterns of ovariectomized (OVX) rats, and (2) whether changes in gastrointestinal transit were responsible for the EB-induced changes in meal patterns. Progesterone (5 mg/day) reversed the effects of EB by increasing meal size and decreasing meal frequency in OVX, EB-treated rats. Progesterone had no effect on these measures in OVX rats that were not given EB. In a comparison of the rate of gastrointestinal transit, the rate of gastrointestinal transit was found to be faster in OVX rats injected with EB daily for two weeks than in OVX, oil-treated controls as measured under anesthesia with infusion of ten ml of liquid diet. However, this alteration in gastrointestinal transit does not appear to be responsible for the decreased meal size of EB-treated, OVX-rats, because the gastrointestinal changes are not observed 34-38 hr after an EB injection, a time at which meal size is already affected.

Animals↗