Relation of pyloric motility to pyloric opening and closure in healthy subjects.

Tougas, Gervais; Anvari, Mehran; Somers, Sat; Richards, Duncan; Stevenson, Giles W.

doi:10.1136/gut.33.4.466

Cited by 116 publications

(69 citation statements)

References 21 publications

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“…This observation supports the concept that the rate of gastric emptying depends more on the spatial and temporal relationship of antral and duodenal contractions than on contraction frequency at a single site. Although it was technically impossible to additionally record fundic and pyloric motility in this study, we suggest that apart from the inhibition of coordinated antroduodenal contractions, reduction of fundic tone, elevation of pyloric tone, and stimulation of isolated pyloric pressure waves which are proven obstacles to transpyloric flow would contribute to the postprandial delay of gastric emptying (32)(33)(34).…”

Section: Discussionmentioning

confidence: 88%

Gastric emptying and release of incretin hormones after glucose ingestion in humans.

Schirra¹,

Katschinski²,

Weidmann³

et al. 1996

J. Clin. Invest.

378

287

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This study investigated in eight healthy male volunteers ( a) the gastric emptying pattern of 50 and 100 grams of glucose; (b) its relation to the phase of interdigestive motility (phase I or II) existing when glucose was ingested; and (c) the interplay between gastric emptying or duodenal perfusion of glucose (1.1 and 2.2 kcal/min; identical total glucose loads as orally given) and release of glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide-1(7-36)amide (GLP-1), C-peptide, insulin, and plasma glucose. The phase of interdigestive motility existing at the time of glucose ingestion did not affect gastric emptying or any metabolic parameter. Gastric emptying of glucose displayed a power exponential pattern with a short initial lag period. Duodenal delivery of glucose was not constant but exponentially declined over time. Increasing the glucose load reduced the rate of gastric emptying by 27.5% (P Ͻ 0.05) but increased the fractional duodenal delivery of glucose. Both glucose loads induced a fed motor pattern which was terminated by an antral phase III when ‫ف‬ 95% of the meal had emptied. Plasma GLP-1 rose from basal levels of ‫ف‬ 1 pmol/liter to peaks of 3.2 Ϯ 0.6 pmol/liter with 50 grams of glucose and of 7.2 Ϯ 1.6 pmol/ liter with 100 grams of glucose. These peaks occurred 20 min after glucose intake irrespective of the load. A duodenal delivery of glucose exceeding 1.4 kcal/min was required to maintain GLP-1 release in contrast to ongoing GIP release with negligibly low emptying of glucose. Oral administration of glucose yielded higher GLP-1 and insulin releases but an equal GIP release compared with the isocaloric duodenal perfusion. We conclude that ( a) gastric emptying of glucose displays a power exponential pattern with duodenal delivery exponentially declining over time and (b) a threshold rate of gastric emptying of glucose must be exceeded to release GLP-1, whereas GIP release is not con-

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Section: Discussionmentioning

confidence: 88%

Gastric emptying and release of incretin hormones after glucose ingestion in humans.

Schirra¹,

Katschinski²,

Weidmann³

et al. 1996

J. Clin. Invest.

378

287

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“…from the stomach correlates poorly with any change in proximal gastric relaxation (29). Indeed, it is also possible that the delaying effect of C12 could be via an action on the distal stomach, possibly by suppressing the contribution that peristaltic antral contractions make to the process of gastric emptying (12 23) and/or via a pyloric or postpyloric effect to reduce efflux through the duodenum (2,32).…”

Section: Discussionmentioning

confidence: 99%

Cholecystokinin pathways modulate sensations induced by gastric distension in humans

Lal¹,

McLaughlin²,

Barlow³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Ingested fat releases CCK, causes gastric relaxation, delays gastric emptying, and limits meal size; however, the mechanistic link among these actions has not been established. Fatty acid release of CCK is chain-length sensitive; dodecanoic acid (C12) induces greater CCK release than decanoic acid (C10). The effect of C12 or C10 on tolerance to subsequent intragastric infusion of liquid was determined in healthy subjects, with and without the CCK1 receptor antagonist dexloxiglumide. Gastric wall relaxation after either fatty acid was assessed by graded volume distension and by barostat; gastric emptying was measured by gastric aspiration and by a [13 C]octanoic acid breath technique. C12 released more CCK (mean plasma CCK after vehicle, 4.7 Ϯ 0.8 pM; C10, 4.8 Ϯ 0.3 pM; C12, 8 Ϯ 1.2 pM; P Ͻ 0.05 C12 vs. C10 or vehicle) and reduced the volume of water (and of 5 and 25% glucose solutions) delivered at maximum tolerance compared with C10 or vehicle (volume of water tolerated after vehicle, 1,535 Ϯ 164 ml; C10, 1,335 Ϯ 160 ml; C12, 842 Ϯ 103 ml; P Ͻ 0.05 C12 vs. C10 or vehicle); this effect was abolished by dexloxiglumide. Intragastric volumes were always similar at the limit of tolerance, and, whereas gastric relaxation occurred to similar degrees after the fatty acids, its duration was longer after C12, which also induced a longer delay in half-gastric emptying [t 1/2(min) after vehicle, 53 Ϯ 2; C10, 67 Ϯ 3; C12, 88 Ϯ 7; P Ͻ 0.05 C12 vs. C10 or vehicle]. In conclusion, ingestion of a CCK-releasing fatty acid reduces the tolerated volume of liquid delivered into the stomach, primarily via a CCK1 receptormediated delay in gastric emptying. fatty acid; vagus; gastric emptying THE PRESENCE OF LIPID in the upper gastrointestinal tract modifies gastrointestinal function (23,24,34), and at least some of its effects are mediated by the peptide CCK (23, 24) that is released from small intestinal enteroendocrine cells by dietary free fatty acids with an acyl chain length of Ͼ11 carbon atoms (23). It has been proposed that CCK, released by dietary lipid, is one of the means whereby meal intake is limited (22), but there seems to be a paradox in the understanding of this effect, because CCK also relaxes the proximal stomach (24), a mechanism that has been proposed to increase rather than limit the amount of a meal consumed (31). Furthermore, in animals, there is evidence that CCK limits tolerance to a meal by delaying gastric emptying (26), but it is unknown whether the same is true in humans.In an attempt to clarify these uncertainties, we performed a series of studies in healthy volunteers: 1) to explore how endogenous CCK released in response to fatty acid modulates tolerance to liquids delivered into the stomach and 2) to determine the relationship between gastric emptying and gastric relaxation in modulating tolerance. We now provide evidence that endogenous CCK reduces the volume of a liquid that can be tolerated in the upper gastrointestinal tract via a CCK 1 receptor-mediated effect and that it does so primarily by del...

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“…Motor mechanisms controlling gastric emptying are antral contractility, antro-duodenal wave propagation, the pyloric tone, isolated pyloric pressure waves and the tone of the gastric fundus (Camilleri et al 1985, Houghton et al 1988, Tougas et al 1992, Heddle et al 1993. In humans, step-doses of intravenous GLP-1 were shown to inhibit isolated pyloric pressure waves and to elevate basal pyloric tone with intraduodenal lipid perfusion in a dosedependent manner, and a complete abolition of antropyloro-duodenal wave propagation in the interdigestive state was observed (Schirra et al 1996b).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of the antidiabetic action of subcutaneous glucagon-like peptide-1(7-36)amide in non-insulin dependent diabetes mellitus

Schirra

Leicht²,

Hildebrand³

et al. 1998

Journal of Endocrinology

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Twelve patients with non-insulin dependent diabetes mellitus (NIDDM) under secondary failure to sulfonylureas were studied to evaluate the effects of subcutaneous glucagon-like peptide-1(7-36)amide (GLP-1) on (a) the gastric emptying pattern of a solid meal (250 kcal) and (b) the glycemic and endocrine responses to this solid meal and an oral glucose tolerance test (OGTT, 300 kcal). 0·5 nmol/kg of GLP-1 or placebo were subcutaneously injected 20 min after meal ingestion. GLP-1 modified the pattern of gastric emptying by prolonging the time to reach maximal emptying velocity (lag period) which was followed by an acceleration in the post-lag period. The maximal emptying velocity and the emptying half-time remained unaltered. With both meals, GLP-1 diminished the postprandial glucose peak, and reduced the glycemic response during the first two postprandial hours by 54·5% (solid meal) and 32·7% (OGTT) (P<0·05). GLP-1 markedly stimulated insulin secretion with an effect lasting for 105 min (solid meal) or 150 min (OGTT). The postprandial increase of plasma glucagon was abolished by GLP-1. GLP-1 diminished the postprandial release of pancreatic polypeptide. The initial and transient delay of gastric emptying, the enhancement of postprandial insulin release, and the inhibition of postprandial glucagon release were independent determinants (P<0·002) of the postprandial glucose response after subcutaneous GLP-1. An inhibition of efferent vagal activity may contribute to the inhibitory effect of GLP-1 on gastric emptying.

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Relation of pyloric motility to pyloric opening and closure in healthy subjects.

Abstract: The relation between pyloric motor activity, opening, and closure was examined in eight healthy men. Manometry was performed with an assembly combining 13

Cited by 116 publications

References 21 publications

Gastric emptying and release of incretin hormones after glucose ingestion in humans.

Gastric emptying and release of incretin hormones after glucose ingestion in humans.

Cholecystokinin pathways modulate sensations induced by gastric distension in humans

Mechanisms of the antidiabetic action of subcutaneous glucagon-like peptide-1(7-36)amide in non-insulin dependent diabetes mellitus

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