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Biomedical subjects

R De Giorgio

Publications and source records attributed to R De Giorgio.

At least 73 records · Page 4Linked to original sources
PubMed1996

Upper gastrointestinal motor activity in patients with slow-transit constipation. Further evidence for an enteric neuropathy.

Recent evidence indicates that patients complaining of severe chronic idiopathic constipation may have motor abnormalities not limited to the colon. We studied by manometric means gastric and small bowel motility in a homogeneous group of patients with chronic idiopathic constipation, ie, the slow transit type. Twenty-one patients were recruited for the study and compared to 33 healthy subjects. Manometric examination was carried out for about 5 hr fasting and 1 hr after a standard meal. Analysis of the manometric tracings revealed during fasting no abnormalities in number and configuration of migrating motor complex with respect to controls. However, in 70% of patients motor abnormalities were detected, represented by bursts of nonpropagated contractions and discrete clustered contractions. After feeding, the patient group displayed a significantly shorter antral motor response to the meal with respect to controls; moreover, intestinal bursts of nonpropagated contractions were found in 19% of patients, and 14% of them had an early return of the activity fronts. We conclude that patients with slow transit constipation frequently display motor abnormalities of the upper gut. These findings further strengthen the concept that this condition may represent a panenteric disorder.

Adult↗
PubMed1996

Functional, biochemical and anatomical changes in the rat urinary bladder induced by perigangliar injection of colchicine.

The aim of this study was to assess the effect of blocking the axonal transport of sensory neuropeptides, by local injection of colchicine at pelvic ganglia level, on the sensory and efferent functions mediated by capsaicin-sensitive primary afferent neurons innervating the rat urinary bladder. Bilateral injection of colchicine in the prostatic tissue underneath the pelvic ganglia of male rats induced a time-dependent reduction (maximal at 72 h, 100% reduction) of the in vitro contraction of the bladder strips induced by capsaicin (1 microM). The response to electrical field stimulation was also reduced, although to a lesser extent. The direct contractions induced by substance P (100 nM) or KCl (80 mM) were not affected by colchicine pretreatment. In vivo, perigangliar injection of colchicine (72 h before) greatly increased bladder capacity, and reduced the amplitude of micturition contractions and micturition frequency. Capsaicin-induced plasma protein extravasation was abolished in the urinary bladder and reduced in the distal, but not the proximal ureter of colchicine-treated rats. Topical application of capsaicin onto the urinary bladder or onto the stomach induced a cardiovascular pressor reflex in urethane-anaesthetized, spinalized rats. Colchicine pretreatment reduced (by about 50%) the pressor response elicited by chemonociceptive stimulation of the bladder but not that arising from the stomach. Colchicine pretreatment did not produce overt changes of nerve profiles immunoreactive for calcitonin gene-related peptide- or tachykinin-like material in the rat urinary bladder. A more intense staining of nerve fibres positive for calcitonin-gene related peptide-like immunoreactivity and tachykinin-like immunoreactivity was observed in pelvic ganglia of colchicine-pretreated rats. No changes were detected in the dorsal horns of spinal cord segments where pelvic bladder afferents project (L6-S1). Colchicine pretreatment reduced, but did not abolish, bladder levels of substance P-, neurokinin A-, calcitonin gene-related peptide- and neuropeptide Y-like immunoreactivity. However, vasoactive intestinal peptide-like immunoreactivity levels were not changed. The capsaicin-evoked (1 microM) release of calcitonin gene-related peptide was abolished in capsaicin as well as in colchicine-pretreated animals. The present findings demonstrate that local treatment of pelvic ganglia with colchicine totally eliminates the "efferent" functions of capsaicin-sensitive afferent nerves in the urinary bladder. Although reduced, tissue levels of sensory neuropeptides are not completely depleted, thus indicating the existence of a releasable versus non-releasable pool. The chemically induced blockade of axoplasmic transport also induces a limited impairment of the sensory function of capsaicin-sensitive afferents, and of the parasympathetic efferent system.

Animals↗
PubMed1996

Monoclonal antibody to VIP: production, characterization, immunoneutralizing activity, and usefulness in cytochemical staining.

A very stable cell line has been generated that produces monoclonal antibody to VIP designated as CURE.V55. This hybridoma was produced by fusion of spleen cells from an immunized Robertsonian mouse containing the translocated 8.12 chromosome with FOX-NY myeloma cells that are APRT deficient. VIP monoclonal antibody producing cell line #55 was selected by limiting dilutions using thymocytes as feeder layers. Ascites fluid containing high concentration of VIP monoclonal antibody was produced from pristane-primed BALB/c mice. Ascites fluid contained approximately 20 mg/ml IgG and bound 50% of 2 fmol 125I-VIP at a final dilution of 1:50,000. Binding of this IgG1 antibody was inhibited by 50% at 5 nM concentration of either VIP 1-28 or VIP 7-28. Protein-A purified IgG of this antibody, used in a concentration of 30 mg/kg per rat (IV), completely reversed the inhibitory effect of gastric corpus contractions induced by intravenous injection of VIP (10 nmol/kg) in sodium pentothal-anesthetized rats. A control anti-keyhole limpet hemocyanin monoclonal antibody did not alter the stimulatory effect of VIP on gastric corpus contractions. Immunohistochemistry showed that this VIP monoclonal antibody stains neurons, and nerve fibers in human and rat gallbladder and the sphincter of Oddi as previously described with our polyclonal antiserum.

Animals↗
PubMed1996

[New etiopathogenic, clinical and therapeutic findings in multiple endocrine neoplasia type 1].

Multiple Endocrine Neoplasia type 1 (MEN 1) syndrome comprises tumors or hyperplasia of different glands, including parathyroid, pituitary, adrenal cortex and the gastroenteropancreatic system. The vast majority of MEN 1 are found in familial clusters, although a few cases are sporadic. Hypercalcemia and/or nephrocalcinosis are the first and most common clinical manifestation in familial MEN 1 syndrome, followed by islet cell tumors (especially those secreting gastrin or insulin) and pituitary dysfunction due to either functioning or non-functioning microadenomas. Genetic studies indicate that familial MEN 1 syndrome is inherited through a dominant gene with incomplete penetrance and variable expression. The diagnosis of MEN 1 syndrome is mainly based on the careful assessment of the clinical history, symptoms physical evaluation along with the assay of serum electrolytes (i.e., calcium, phosphorus, etc.) and hormonal substances (i.e., gastrin, insulin, pancreatic polypeptide, prolactin, adrenocorticotropic hormone, etc.). In addition, several provocative tests have been used to identify endocrine tumors (particularly those of the gastroenteropancreatic system) and imaging techniques play a crucial role for the diagnostic approach in MEN 1 syndrome. Even though in the long term, the prognosis of MEN 1 syndrome is unfavourable. Recently, however, many therapeutic strategies, including both surgical and pharmacological options, have been developed to reduce the size of the neoplasm and control symptoms associated with hormone oversecretion.

Antineoplastic Agents, Hormonal↗
PubMed1996

[The innervation of the digestive tract: its morphofunctional and neurochemical aspects].

The innervation of the alimentary tract (or enteric nervous system, ENS) represents the third division of the autonomic nervous system and it appears to be unique for its intrinsic ability to mediate reflex activity even when disconnected from the central nervous system. Enteric nerve cells can be classified in subclasses according to combined classic morphological criteria (Dogiel type I, II and III) and electrophysiological properties (type S and AH). A further major feature of the ENS lies in the variety of chemical messengers expressed in its neuronal elements. These substances can act either as neurotransmitters or neuromodulators. A common finding of enteric neurons is to synthetize and store several chemical messengers, a phenomenon known as neurochemical coding. As a consequence, neurotransmission involves the release and action of more than one messenger, an event referred to as plurichemical transmission. Recently, the use of combination of methods (such as immunohistochemical, pharmacological and electrophysiological techniques) has led to the identification of specific functionally distinct categories of enteric neurons. Thus, inhibitory and excitatory motor neurons, interneurons, vasomotor and sensory neurons are now recognized to constitute the complex network of the ENS. These neuronal elements are synaptically connected to form microcircuits which play a pivotal role to control digestive functions, including motility, blood flow, secretion and absorbtion.

Animals↗
PubMed1995

Peptide immunoreactivities in the ganglionated plexuses and nerve fibers innervating the human gallbladder.

The mammalian gallbladder is innervated by a well-developed intrinsic neural network. However, little is known about the neurochemistry and organization of the innervation of this organ in humans. The aim of this study was to analyze the distribution of immunoreactivity (IR) for the neuropeptides, vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), tachykinins (TK) and calcitonin gene-related peptide (CGRP) in the human gallbladder by means of immunohistochemistry. Neuropeptide-IRs are found in neurons and processes of the two ganglionated plexuses, i.e., the innermost plexus located in the lamina propria at the base of the mucosal folds, and the outermost plexus situated within the fibro-muscular layer. In these two plexuses, VIP-, NPY- and TK-IRs are present in ganglion cells and varicose fibers, whereas CGRP-IR is confined to nerve processes. VIP-IR is present in most, if not all, neurons. NPY- and TK-IRs are also found in many neurons. The densities of the peptide-IR nerves in the mucosa are NPY and VIP > TK >> CGRP, and in the fibro-muscular layer are NPY > VIP and TK > CGRP. The vasculature is richly innervated by NPY-IR nerves, which are mostly perivascular. CGRP-, VIP- and TK-IR processes are found only occasionally around blood vessels and in a paravascular position. Double-label studies demonstrated that a large number of VIP-containing neurons expresses NPY- or TK-IR. On the other hand, all neurons positive for either NPY- or TK-IR are immunostained for VIP. In agreement with these findings, most of the NPY-IR fibers in the lamina propria and fibro-muscular layer contain VIP-IR, and numerous TK-IR fibers are positive for VIP. However, the perivascular NPY-IR processes do not contain VIP-IR, suggesting an extrinsic origin. In addition, a population of TK-IR processes contains CGRP-IR and presumably originates from extrinsic sources, since CGRP/TK-IR intrinsic neurons could not be detected in the gallbladder. Peptide-IRs have a similar distribution in the neck, body and fundus of the gallbladder. No peptide-containing endocrine/paracrine cells are observed in the epithelium. The presence of peptide-IRs in the ganglionated plexuses and the abundance of peptidergic innervation suggest that peptides exert their effects on gallbladder function by acting directly on tissue targets and influencing intrinsic ganglion cells. Furthermore, the co-localization of more than one peptide in the same neuron raises the possibility that peptides are co-released upon stimulation and might interact at the same target.

Gallbladder↗
PubMed1995

Nitric oxide modulates pepsinogen secretion induced by calcium-mediated agonist in guinea pig gastric chief cells.

BACKGROUND & AIMS: Nitric oxide, a putative cellular messenger synthesized from L-arginine, is a powerful modulator of gastric motility and secretions. The aim of this study was to investigate whether (1) guinea pig gastric chief cells express NO synthase, (2) NO modulates the pepsinogen secretion and guanosine 3',5'-cyclic monophosphate (cGMP) generation induced by calcium (Ca2+)-mediated agents, and (3) NO donors and cGMP analogues stimulate pepsinogen release. METHODS: Chief cells were prepared by sequential digestion with collagenase and Ca2+ chelation. NO generation was measured by determining the NO coproduct citrulline. RESULTS: NO synthase immunoreactivities were constitutively expressed in approximately 70% chief cells. Carbachol (10 mumol/L) caused a 4- 6-fold increase in pepsinogen release, citrulline generation, intracellular Ca2+ concentration ([Ca2+]i) and cGMP concentration. These effects were concentration dependently inhibited by NG-monomethyl-L-arginine (L-NMMA). As gastrin, cholecystokinin, thapsigargin, and Ca2+ ionophore increased NO generation, [Ca2+]i seemed to regulate NO synthase activity. [Ca2+]i chelator and calmodulin antagonist inhibited the carbachol-induced pepsinogen secretion and NO generation. Preincubating the cells with L-NMMA had no effect on carbachol-stimulated inositol triphosphate generation or [Ca2+]i or Ca(2+)-dependent adenosine triphosphatase levels. Nitrovasodilator agents and 8-bromo-cGMP stimulated pepsinogen release. CONCLUSIONS: Gastric chief cells express a Ca2+/calmodulin-dependent NO synthase. NO modulates the stimulatory effect of Ca(2+)-mediated agonists on pepsinogen release.

Animals↗
PubMed1995

Chronic oral administration of lansoprazole does not affect the hypothalamic pituitary gonadal axis in healthy young men.

OBJECTIVE: To assess the effects of chronic oral administration of standard doses of lansoprazole on the luteinizing hormone pulsatile pattern and on follicle stimulating hormone (FSH) and testosterone levels in young men. DESIGN AND METHODS: Eleven healthy volunteers were studied on three separate occasions, before and after two 3-week periods of treatment with lansoprazole (30 mg every morning) or a placebo, according to a randomized, double-blind, double-dummy, cross-over design. On each study day, blood samples were taken every 15 min for 8 h. The pulsatile pattern of luteinizing hormone, mean concentrations of FSH and total testosterone plasma levels were determined for each patient using specific radioimmunoassays. RESULTS: Lansoprazole did not significantly affect mean plasma levels, the pulsatile pattern of luteinizing hormone, or mean plasma concentrations of FSH and testosterone compared with the placebo. CONCLUSIONS: This study indicates that chronic oral administration of standard doses of lansoprazole does not affect the concentrations of gonadal hypothalamic pituitary or sex steroid hormones.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1994

Different mechanism of tachykinin NK2 receptor blockade by SR 48968 and MEN 10,627 in the guinea-pig isolated gallbladder and colon.

The mechanism of action of the tachykinin NK2 receptor antagonists, SR 48968 ((S)-N-methyl-N[4-acetylamino-4-phenyl-piperidino)-2-(3,4- dichlorophenyl)butyl]benzamide) and MEN 10,627 (cyclo[(Met-Asp-Trp-Phe-Dap-Leu) cyclo (2 beta-5 beta)]), was compared in the guinea-pig isolated gallbladder and circular muscle of proximal colon by using neurokinin A and [beta Ala8]neurokinin A-(4-10) as agonists. The experiments performed with colon were in the presence of the tachykinin NK1 receptor-selective antagonist, (+/-)-CP-96,345 ([2-(diphenylmethyl)-N-[(2-methoxyphenyl)-methyl]-1- azabicyclo[2,2,2]octan-3-amine]). SR 48968 caused an insurmountable antagonism of tachykinin NK2 receptor-mediated contraction in both preparations; its blockade was essentially irreversible, since it was not reversed by washout (up to 2 h) and was increased by prolonging the incubation from 15 to 120 min. In contrast, MEN 10,627 produced simple competitive antagonism, which was time-independent and fully reversible in both preparations. In both preparations, the simultaneous administration of SR 48968 and MEN 10,627 produced an intermediate antagonism of the responses to the agonists, as compared to the antagonism produced by each antagonist alone. The present results are discussed in the light of the reported interaction of SR 48968 with tachykinin NK2 receptors at a recognition epitope distinct from that of agonist(s).

Amino Acid Sequence↗
PubMed1994

Fos protein expression in the nucleus of the solitary tract in response to intestinal nutrients in awake rats.

Nutrients in the intestine inhibit food intake via an action on the vagal afferent pathway. The aim of the present study was to use immunochemical detection of Fos protein-like immunoreactivity (FLI) in the brainstem to trace the neuronal pathways activated by intestinal nutrients. Perfusion of the intestine of awake rats via an indwelling duodenal catheter with iso-osmotic mannitol, hydrochloric acid or casein hydrolysate had no effect on the number of FLI neurons in the nucleus of the solitary tract (NTS). Lipid emulsion (20%) and 2.7 M glucose significantly increased the number of immunopositive cells in the NTS. There was a significant increase in the number of immunopositive cells from caudal to rostral NTS. Nutrients effective at decreasing food intake (carbohydrate and fat) produced significant increases in Fos-like immunopositive cells in the NTS.

Animals↗
PubMed1994

Nitric oxide producing neurons in the monkey and human digestive system.

Nitric oxide has been proposed as an inhibitory transmitter molecule that plays a role in muscle relaxation and vasodilation in the gastrointestinal tract. The present study analyzes the distribution of nitric-oxide-producing neurons in the monkey and human digestive system by means of nicotinamide-adenine-dinucleotide-phosphate-diaphorase histochemistry. This histochemical method is reliable and convenient for the visualization of neuronal nitric-oxide synthase, the enzyme responsible for nitric-oxide generation. In the gastrointestinal tract, nitric-oxide-synthase-related diaphorase activity was present in nerve fibers running throughout the muscular layer (circular > longitudinal) and in numerous ganglion cells and processes in the myenteric plexus of monkeys and humans. Labelled ganglion cells and fibers also were observed in the submucous plexus, although they were much less numerous than those seen in the myenteric plexus. In the submucosa, a few positive fibers were seen around blood vessels. In the mucosa, stained fibers were sparse at the base of the villi and crypts, whereas they were quite abundant in the muscularis mucosae, especially in the small intestine and colon. In the gallbladder (human), labelling was found in ganglion cells and processes of the innermost and outermost ganglionated plexuses. Stained fibers also were distributed to the muscular layer and, less abundantly, to the mucosa and vasculature. Labelled fibers were more abundant in the sphincter of Oddi (human) than in the gallbladder. In the monkey and human pancreas, nicotinamide-adenine-dinucleotide-diaphorase staining was seen mainly in ganglion cells and fibers of intrapancreatic ganglia, and in processes running among acini, around ducts and in the stroma. A moderate density of stained fibers also was distributed to the vasculature, whereas the islets showed few positive processes. Finally, double label experiments performed in the pancreas showed that the vast majority of neurons producing nitric oxide are immunoreactive for vasoactive intestinal peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Use of the Fab fragment for immunoneutralization of somatostatin in the isolated perfused human pancreas.

The role of the somatostatin-secreting D cell in the islet remains controversial. The present study was undertaken to determine whether infusion of the Fab fragment of a highly sensitive somatostatin monoclonal antibody into the isolated, perfused human pancreas would influence insulin secretion. Single-pass perfusion was performed in pancreata obtained from cadaveric organ donors using a modified Krebs-media with 3.9 mM glucose. Sequential test periods separated by basal periods were performed with either somatostatin monoclonal antibody Fab fragment (SFab), somatostatin-14 (SS-14), or a combined infusion. Immunoneutralization of intraislet somatostatin with SFab resulted in a significant increase in both immunoreactive insulin (IRI) (1,122 +/- 497 pM) (p < 0.05) and immunoreactive C-peptide (IRC-P) secretion (146 +/- 53 pM) (p < 0.05). Infusion of SS-14 resulted in inhibition of both IRI secretion (-3,372 +/- 1,360 pM) (p < 0.05) and IRC-P secretion (-708 +/- 220 pM) (p < 0.05). Combined infusion of SFab and SS-14 reversed the inhibitory effect of exogenous SS-14 on IRI and IRC-P secretion. The data suggest that intraislet somatostatin has an inhibitory role in the regulation of B-cell secretion in the human islet and demonstrates that the Fab fragment of the somatostatin monoclonal antibody is an effective tool for immunoneutralization studies in the human pancreas. In addition, immunostaining of the donor pancreata demonstrated the presence of somatostatin-immunoreactive endocrine cells interspersed throughout the islet core and mantle. The demonstrated proximity of somatostatin-immunoreactive endocrine cells to B cells lends anatomic support to the concept that intraislet somatostatin influences insulin secretion in the human islet.

Adult↗
PubMed1994

Effects of acute cold pressor test on vagally stimulated gastric acid secretion and circulating levels of human pancreatic polypeptide and gastrin.

The aims of our study were 3-fold: (1) to determine the effect of an acute cold pressor test on vagally stimulated gastric acid secretion, (2) to evaluate whether adrenergic blockers are able to prevent the stress-induced alterations of vagally stimulated gastric acid secretion, and (3) to assess the effect of stress and adrenergic blockers on serum levels of vagally stimulated pancreatic polypeptide and gastrin. Twenty-eight studies were carried out on 7 healthy subjects, each one of them being evaluated on four separate occasions. Active (4 degrees C) or control (37 degrees C) cold pressor tests were applied in random order after an interval of 15 min following completion of a vagal stimulation represented by modified sham feeding. Each stressful stimulus was preceded by an intravenous bolus plus an infusion of either adrenergic blockers (propranolol and phentolamine) or placebo. Modified sham feeding significantly stimulated gastric acid secretion and circulating hormonal levels, compared to basal values. Cold pressor test significantly stimulated gastric acid secretion 30 min after the beginning of the stressful stimulus. This stress-induced secretory response was completely prevented by infusions of adrenergic blockers. No effect was induced by stressful stimuli or by adrenergic blockers on human pancreatic polypeptide and gastrin circulating levels. The present study demonstrates that the cold pressor test induces a late increase of vagally stimulated gastric acid secretion suggesting a possible role mediated by adrenergic neural pathways.

Adult↗
PubMed1994

Evaluation of two therapeutic regimens for the treatment of Helicobacter pylori infection.

In the present study we evaluated the efficacy and tolerability of two different therapeutic schedules in eradicating Helicobacter pylori. Forty-six consecutive patients (suffering from either peptic ulcer or non-ulcer dyspepsia) with helicobacter pylori infection were randomly allocated to one of the following two groups: group 1 (n = 23) 2 weeks of treatment with bismuth subcitrate tablets (120 mgx4) + amoxycillin capsules (500 mgx4) + metronidazole tablets (250 mgx4); group 2 (n = 23) 2 weeks of treatment with amoxycillin capsules (500 mgx4) + metronidazole tablets (250 mgx4). Endoscopy, histology and bacterial culture were performed at entry, and 30 and 90 days after treatment. Two group 1 patients and one group 2 patient did not complete the treatment. Successful eradication was obtained in 20/21 (95%) patients treated with triple therapy (group 1) and in 17/22 (77%) patients treated with double therapy (group 2) (p = 0.2). Side-effects occurred in 9/21 (43%) patients of group 1 and in 9/22 (41%) patients of group 2 (p = 0.9). These were all self-limiting and required no specific treatment. These data suggest that combined therapy with amoxycillin and metronidazole, with or without bismuth subcitrate, represents a safe and effective therapeutic approach for the treatment of Helicobacter pylori infection. In our series, triple therapy determined a numerically higher eradication rate than double therapy.

Adult↗
PubMed1993

Abdominal surgery induces c-fos expression in the nucleus of the solitary tract in the rat.

In a model of abdominal surgery, which consisted of cecal manipulation and induces postoperative ileus in rats, we studied c-fos protein expression in the nucleus of the solitary tract (NTS), the spinal cord and dorsal root ganglia. Abdominal surgery resulted in a significantly higher number of c-fos protein immunoreactive cells in the NTS compared with controls but not in dorsal root ganglia and resulted in only a few scattered cells in the spinal cord. Neurons expressing c-fos protein were concentrated in NTS regions where cecal afferents terminate. These findings support the hypothesis that sensory vagal pathways partly mediate abdominal surgery-induced postoperative ileus.

Abdomen↗
PubMed1993

Peripheral bombesin induces c-fos protein in the rat brain.

Bombesin injected intraperitoneally induces c-fos protein-like immunoreactivity in the medial nucleus tractus solitarius and the parvocellular part of the paraventricular nucleus of the hypothalamus in the rat brain. C-fos expression induced by bombesin is less densely represented compared with CCK. Capsaicin pretreatment did not influence c-fos-immunoreactivity induced by bombesin and significantly reduced that induced by CCK.

Animals↗
PubMed1993

Fat-induced ileal brake in humans: a dose-dependent phenomenon correlated to the plasma levels of peptide YY.

BACKGROUND: Upper gastrointestinal motility is regulated by the presence of nutrients in the distal gut. The present study evaluated whether lipid-induced ileal brake on gastric emptying (1) can be elicited by low fat concentrations; (2) is a dose-dependent phenomenon; and (3) is related to gastrointestinal peptide release. METHODS: Seven patients were studied in the defunctionalized stage of total colectomy, on three separate occasions. On each study day, patients ate a meal labeled in the solid component; 30 minutes later, one of the following solutions was randomly infused into the ileal pouch: 0.9% saline, 2% oleic acid, and 20% oleic acid. Plasma concentrations of peptide YY (PYY), enteroglucagon, neurotensin, and motilin were measured. RESULTS: Both oleic acid solutions slowed gastric emptying compared with saline (P < 0.001), the effect being dose dependent (P < 0.001). Ileal infusions did not modify neurotensin and enteroglucagon levels but induced a dose-dependent increase of PYY (P < 0.01) and a borderline decrease of motilin (P = 0.05) levels. Slower rates of gastric emptying were related to increased plasma concentrations of PYY (r = 0.615; P < 0.05). CONCLUSIONS: This study shows that (1) the ileal brake on gastric emptying can be evoked by low doses of lipids in the distal ileum; (2) the delay of gastric emptying is related to the release of PYY; and (3) both phenomena are dose dependent.

Adult↗