Academic literature on the topic 'Antropyloroduodenal motility'

The presence of nutrients in the small intestine slows gastric emptying and suppresses appetite and food intake; these effects are partly mediated by the release of gut hormones, including CCK. We investigated the hypothesis that the modulation of antropyloroduodenal motility, suppression of appetite, and stimulation of CCK and glucagon-like peptide-1 secretion by intraduodenal fat are dependent on triglyceride hydrolysis by lipase. Sixteen healthy, young, lean men were studied twice in double-blind, randomized, crossover fashion. Ratings for appetite-related sensations, antropyloroduodenal motility, and plasma CCK and glucagon-like peptide-1 concentrations were measured during a 120-min duodenal infusion of a triglyceride emulsion (2.8 kcal/min) on one day with, on the other day without, 120 mg tetrahydrolipstatin, a potent lipase inhibitor. Immediately after the duodenal fat infusion, food intake at a buffet lunch was quantified. Lipase inhibition with tetrahydrolipstatin was associated with reductions in tonic and phasic pyloric pressures, increased numbers of isolated antral and duodenal pressure waves, and stimulation of antropyloroduodenal pressure-wave sequences (all P < 0.05). Scores for prospective consumption and food intake at lunch were greater, and nausea scores were slightly less, and the rises in plasma CCK and glucagon-like peptide-1 were abolished (all P < 0.05). In conclusion, lipase inhibition attenuates the effects of duodenal fat on antropyloroduodenal motility, appetite, and CCK and glucagon-like peptide-1 secretion.

Both load and duration of small intestinal lipid infusion affect antropyloroduodenal motility and CCK and peptide YY (PYY) release at loads comparable to and higher than the normal gastric emptying rate. We determined 1) the effects of intraduodenal lipid loads well below the mean rate of gastric emptying on, and 2) the relationships between antropyloroduodenal motility, CCK, PYY, appetite, and energy intake. Sixteen healthy males were studied on four occasions in double-blind, randomized fashion. Antropyloroduodenal motility, plasma CCK and PYY, and appetite perceptions were measured during 50-min IL (Intralipid) infusions at: 0.25 (IL0.25), 1.5 (IL1.5), and 4 (IL4) kcal/min or saline (control), after which energy intake at a buffet meal was quantified. IL0.25 stimulated isolated pyloric pressure waves (PWs) and CCK release, albeit transiently, and suppressed antral PWs, PW sequences, and hunger ( P < 0.05) but had no effect on basal pyloric pressure or PYY when compared with control. Loads ≥ 1.5 kcal/min were required for the stimulation of basal pyloric pressures and PYY and suppression of duodenal PWs ( P < 0.05). All of these effects were related to the lipid load ( R > 0.5 or < −0.5, P < 0.05). Only IL4 reduced energy intake (in kcal: control, 1,289 ± 62; IL0.25, 1,282 ± 44; IL1.5, 1,235 ± 71; and IL4, 1,139 ± 65 compared with control and IL0.25, P < 0.05). In conclusion, in healthy males the effects of intraduodenal lipid on antropyloroduodenal motility, plasma CCK and PYY, appetite, and energy intake are load dependent, and the threshold loads required to elicit responses vary for these parameters.

Gastric emptying (GE) of glucose is regulated closely, not only as a result of inhibitory feedback arising from the small intestine, but also because of the resulting hyperglycemia. Fructose is used widely in the diabetic diet and is known to empty from the stomach slightly faster than glucose but substantially slower than water. The aims of this study were to determine whether intravenous (iv) fructose affects GE and antropyloroduodenal motility and how any effects compare to those induced by iv glucose. Six healthy males (age: 26.7 ± 3.8 yr) underwent concurrent measurements of GE of a solid meal (100 g ground beef labeled with 20 MBq99mTc-sulfur colloid) and antropyloroduodenal motility on three separate days in randomized order during iv infusion of either fructose (0.5 g/kg), glucose (0.5 g/kg), or isotonic saline for 20 min. GE (scintigraphy), antropyloroduodenal motility (manometry), and blood glucose (glucometer) were measured for 120 min. There was a rise in blood glucose ( P < 0.001) after iv glucose (peak 16.4 ± 0.6 mmol/l) but not after fructose or saline. Intravenous glucose and fructose both slowed GE substantially ( P < 0.005 for both), without any significant difference between them. Between t = 0 and 30 min, the number of antral pressure waves was less after both glucose and fructose ( P < 0.002 for both) than saline, and there were more isolated pyloric pressure waves during iv glucose ( P = 0.003) compared with fructose and saline ( P = NS for both) infusions. In conclusion, iv fructose slows GE and modulates gastric motility in healthy subjects, and the magnitude of slowing of GE is comparable to that induced by iv glucose.

There is evidence that gastrointestinal function adapts in response to a high-fat (HF) diet. This study investigated the hypothesis that an HF diet modifies the acute effects of duodenal lipid on appetite, antropyloroduodenal pressures, plasma CCK and plasma glucagon-like peptide-1 (GLP-1) levels in humans. Twelve healthy men were studied twice in randomized, crossover fashion. The effects of a 90-min duodenal lipid infusion (6.3 kJ/min) on the above parameters were assessed immediately following 14-day periods on either an HF or a low-fat (LF) diet. After the HF diet, pyloric tonic and phasic pressures were attenuated, and the number of antropyloroduodenal pressure-wave sequences was increased when compared with the LF diet. Plasma CCK and GLP-1 levels did not differ between the two diets. Hunger was greater during the lipid infusion following the HF diet, but there was no difference in food intake. Therefore, exposure to an HF diet for 14 days attenuates the effects of duodenal lipid on antropyloroduodenal pressures and hunger without affecting food intake or plasma hormone levels.

Enterally administered lipid modulates antropyloroduodenal motility, gut hormone release, appetite, and energy intake. We hypothesized that these effects would be dependent on both the load, and duration, of small intestinal exposure to lipid. Eleven healthy men were studied on four occasions in a double-blind, randomized, fashion. Antropyloroduodenal motility, plasma CCK and peptide YY (PYY) concentrations, and appetite perceptions were measured during intraduodenal infusion of lipid (Intralipid) at 1) 1.33 kcal/min for 50 min, 2) 4 kcal/min for 50 min, and 3) 1.33 kcal/min for 150 min, or 4) saline for 150 min. Immediately after the infusions, energy intake was quantified. Pressure wave sequences (PWSs) were suppressed, and basal pyloric pressure, isolated pyloric pressure waves (IPPWs), plasma CCK and PYY stimulated (all P < 0.05), during the first 50 min of lipid infusion, in a load-dependent fashion. The effect of the 4 kcal/min infusion was sustained so that the suppression of antral pressure waves (PWs) and PWSs and increase in PYY remained evident after cessation of the infusion (all P < 0.05). The prolonged lipid infusion (1.33 kcal/min for 150 min) suppressed antral PWs, stimulated CCK and PYY and basal pyloric pressure (all P < 0.05), and tended to stimulate IPPWs when compared with saline throughout the entire infusion period. There was no significant effect of any of the lipid infusions on appetite or energy intake, although nausea was slightly higher ( P < 0.05) with the 4 kcal/min infusion. In conclusion, both the load, and duration, of small intestinal lipid influence antropyloroduodenal motility and patterns of CCK and PYY release.

There is little information about the effects of cisapride on human antropyloroduodenal motility, despite its documented efficacy for increasing the rate of gastric emptying in patients with gastroparesis. Cisapride has been reported to have little effect on gastric emptying in normal subjects. Antral, pyloric, and duodenal pressures were recorded simultaneously with gastric emptying in 20 healthy volunteers. Thirty minutes after the solid component of the meal had started to empty from the stomach, each subject received either 10 mg cisapride i.v. (11 subjects) or intravenous saline (9 subjects). Intravenous saline had no effect on either motility or gastric emptying. In contrast, cisapride administration was associated with a dual effect on motility, with initial suppression of antral pressure waves (P < 0.05) followed by stimulation of associated antropyloroduodenal pressure waves (P < 0.01). Gastric emptying slowed in the first 30 min after cisapride (P < 0.05), and this was followed by more rapid gastric emptying (P < 0.01). The amount of the meal emptied in the 60 min after cisapride correlated with the number of associated antroduodenal pressure waves (r = 0.75, P < 0.001) but not with the number of antral waves (r = 0.42, NS). These results indicate that cisapride in a dose of 10 mg i.v. has dual effects on gastric emptying and gastric motility. The stimulation of associated antral pressure waves is a plausible mechanism for the efficacy of cisapride in the treatment of gastroparesis.

Gastric emptying is a major determinant of glycemia, gastrointestinal hormone release, and appetite. We determined the effects of different intraduodenal glucose loads on glycemia, insulinemia, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and cholecystokinin (CCK), antropyloroduodenal motility, and energy intake in healthy subjects. Blood glucose, plasma hormone, and antropyloroduodenal motor responses to 120-min intraduodenal infusions of glucose at 1) 1 (“G1”), 2) 2 (“G2”), and 3) 4 (“G4”) kcal/min or of 4) saline (“control”) were measured in 10 healthy males in double-blind, randomized fashion. Immediately after each infusion, energy intake at a buffet meal was quantified. Blood glucose rose in response to all glucose infusions ( P < 0.05 vs. control), with the effect of G4 and G2 being greater than that of G1 ( P < 0.05) but with no difference between G2 and G4. The rises in insulin, GLP-1, GIP, and CCK were related to the glucose load ( r > 0.82, P < 0.05). All glucose infusions suppressed antral ( P < 0.05), but only G4 decreased duodenal, pressure waves ( P < 0.01), resulted in a sustained stimulation of basal pyloric pressure ( P < 0.01), and decreased energy intake ( P < 0.05). In conclusion, variations in duodenal glucose loads have differential effects on blood glucose, plasma insulin, GLP-1, GIP and CCK, antropyloroduodenal motility, and energy intake in healthy subjects. These observations have implications for strategies to minimize postprandial glycemic excursions in type 2 diabetes.

Bibliography: leaves 258-294.
xv, 294 leaves : ill. (1 col.) ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
Examines the organisation and control of the antropyloroduodenal motor unit in both healthy human volunteers and patients with gastroparesis.
Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1992

The research presented within this thesis has focussed on the complex and interrelated postprandial gastrointestinal mechanisms involved in the regulation of appetite and energy intake. The three broad areas that have been investigated include: (i) the effect of gastrointestinal hormones on gastric motility, gastrointestinal hormone release/suppression, appetite and energy intake in healthy lean subjects, (ii) the effect of oral macronutrients on appetite and energy intake in both lean and obese subjects and (iii) the effects of acute energy restriction on gastrointestinal motility, gastrointestinal hormone release, appetite and energy intake in obese subjects. Following meal ingestion, the presence of nutrients in the small intestine stimulate small intestinal receptors that trigger a number of gastrointestinal mechanisms within ~ 15 minutes; these include the modulation of gastric emptying and gastrointestinal motility and the release, or suppression, of gastrointestinal hormones i.e. cholecystokinin (CCK), peptide-YY (PYY), glucagon-like peptide-1 (GLP-1) and ghrelin. Hence, it is conceivable that interactions occur between one or more of these stimuli. The study in Chapter 5 assessed possible interactions between intravenous CCK (1.8 pmol/kg/min) and GLP-1 (0.9 pmol/kg/min) that may modulate ghrelin and PYY release. At the doses evaluated, exogenous CCK-8 and GLP-1 had discrepant effects on the secretion of ghrelin and PYY; CCK-8 markedly suppressed ghrelin whereas GLP-1 had no effect, and the stimulation of PYY by CCK-8 was attenuated markedly by GLP-1. Of the gastrointestinal hormones modulated following nutrient ingestion, CCK and its role in appetite regulation has been studied the most comprehensively. A recent study from our laboratory using exogenous CCK-8 suggested that the ability of CCK to suppress appetite and energy intake were mediated, at least in part, by its actions on the gastrointestinal tract. However, the plasma CCK concentrations resulting from this study were moderately supraphysiological and infusion of CCK-8 was associated with an increase, albeit modest, in nausea. The effects of increasing doses of CCK-8 on gastrointestinal motility, gut hormone release and the relationships between these effects with those on hunger and energy intake had not hitherto been assessed in humans. In Chapter 6, exogenous CCK-8 stimulated pressures in the pylorus, increased plasma PYY concentrations and suppressed desire-to-eat and energy intake in a dose-dependent manner, while all CCK-8 doses equally suppressed ghrelin. There were relationships between plasma CCK with basal pyloric pressure and isolated pyloric pressure waves, and energy intake with isolated pyloric pressure waves. The prevalence of obesity is rapidly increasing, the cause of which is related, in part, to the readily available supply of high-fat, energy-dense foods. Recent data indicate that there are more than 250 million obese people worldwide, representing ~ 7 % of the adult population. There is evidence that gastrointestinal function in obesity is modified, which may be the result of the eating habits of obese individuals, and in turn, may also contribute to the maintenance of obesity by causing insufficient suppression of energy intake. However, much of the literature relating to gastrointestinal function in the obese is inconclusive and controversial. A better understanding of any adaptations that occur in obesity is important, particularly in regards to treatment approaches for weight loss. Protein is considered to be the most satiating macronutrient and studies have demonstrated that consumption of dietary protein reduces appetite and ad libitum energy intake when compared with either carbohydrate or fat. One option in the dietary management of obesity has been to replace some carbohydrate in the diet with protein, which has been demonstrated to facilitate loss of fat and blunt loss of lean mass. However, there are discrepancies in the ranking of macronutrients and not all studies demonstrate that protein is more satiating than carbohydrates or fat. Furthermore, studies that have demonstrated effects of high-protein preloads on appetite and energy intake have often used preloads consisting of ~ 60 % protein. Thus, it is plausible that the observed effects may have been due to excessive amounts of protein in the test meal; such meals would be less palatable, which may also lead to reduced energy intake. Since there may be differences in the regulation of gastrointestinal motor function, gastrointestinal hormone release, appetite and energy intake between lean and obese individuals, it is likely that ingestion of individual macronutrients may also have different effects on these parameters, which might have implications for the dietary treatment of obesity. The study in Chapter 7 evaluated the effects of high-protein, high-fat and high-carbohydrate test meals, and increasing amounts of protein in a test meal, on appetite and energy intake in lean and obese subjects. In addition, the study compared these responses between lean and obese subjects. In lean, but not obese, subjects, hunger was less, and fullness increased, following ingestion of the HF and HP meals. In addition, energy intake was reduced in lean subjects following the HF and HP meals when compared with the HC meal, while in obese subjects, the HP and AP meals reduced energy intake when compared with the HF and HC meals, and HC meal, respectively. When these responses were compared, the percentage change in energy intake between the HF and AP test meals was significantly different between lean and obese, suggesting that obese subjects may be less sensitive to the satiating effects of fat. The studies presented in the subsequent two chapters (Chapters 8 and 9) investigated the contribution of factors that may influence the effects of oral macronutrients on gastrointestinal function, appetite and energy intake. While young, lean males are the subject group most capable of adjusting their energy intake in response to caloric manipulation, it has been observed that significant inter-individual variation occurs within this group. Therefore, it was important to evaluate whether there was a day-to-day variability in gastrointestinal function, including gastric emptying and gastrointestinal hormone secretion, and if so, how these variations influenced temporal changes in appetite and energy intake. The study in Chapter 8 demonstrated that, in a laboratory setting, appetite perceptions and energy intake in response to a nutrient preload in healthy lean men were highly reproducible, and that this consistency in energy intake was associated with reproducible patterns of gastric emptying and insulin and CCK secretion. A major reason that females are used less frequently than males in research studies assessing gastrointestinal function, appetite and energy intake is the perceived confounding effect of the menstrual cycle on these parameters. There is evidence that fluctuations in hormone levels over the menstrual cycle affect energy intake, such that hunger and energy intake are less during the follicular phase and increased during the luteal phase. How this modulation of appetite and energy intake would be related to changes in gastrointestinal function, i.e. gastric emptying and gastrointestinal hormone release, remained unclear. The study described in Chapter 9 demonstrated that gastric emptying was slower, and glycaemia, plasma GLP-1 and insulin responses, hunger and energy intake were less, during the follicular when compared with the luteal phase. Moreover, energy intake and the glucose, plasma GLP-1 and insulin responses were related to gastric emptying. In addition, these parameters were reproducible when assessed twice within the follicular phase of the menstrual cycle. There is evidence that both previous patterns of macronutrient intake and fasting affect gastrointestinal function. In the context of obesity, both are of relevance. For example, in humans after a high-fat diet for 2 weeks, gastric emptying and mouth-to-caecum transit in response to a high-fat test meal were faster. In contrast, fasting has the opposite effect and a 4-day fast slowed gastric emptying of a glucose drink in both lean and obese subjects, suggesting that a reduction in nutrient exposure may increase the sensitivity of gastrointestinal responses to nutrients in the obese. The study in Chapter 10 demonstrated that following a four-day very-low calorie diet (VLCD) there was a significant increase in basal pyloric pressure and the number and amplitude of isolated pyloric pressure waves, and a decrease in the number of antral and duodenal pressure waves and pressure wave sequences, during a 120 minute intraduodenal lipid infusion. In addition, following the four-day VLCD, hunger and prospective consumption scores were lower, and energy intake was reduced, indicating that gastrointestinal function, appetite and energy intake in the obese can be modified over a short period of time. The studies reported in this thesis provide new information relating to the regulation of appetite and energy intake by gastrointestinal motor function and hormone release and/or suppression, in healthy lean and obese subjects. These observations will contribute to advances in basic appetite physiology and have clinical implications for further development of dietary interventions for successful treatment of obesity.
Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2009