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Acotiamide affects antral motility, but has no effect on fundic motility, gastric emptying or symptom perception in healthy participants.
Masuy, I, Tack, J, Verbeke, K, Carbone, F
Neurogastroenterology and motility. 2019;(4):e13540
Abstract
BACKGROUND Acotiamide, a prokinetic agent was shown to be efficacious in the treatment of functional dyspepsia (FD). The exact mechanism of action is incompletely elucidated. METHODS This randomized, placebo-controlled, cross-over study aimed to examine the effect of acotiamide on gastric motility, measured as intragastric pressure, gastric emptying (GE) rate and gastrointestinal (GI) symptom perception in healthy volunteers (HVs). Participants were treated with acotiamide (100 mg tid) and placebo for 3 weeks, separated by a 1-week washout period. A daily symptom diary was collected during both treatments. At the end of each treatment period, GE rate and gastric motility were assessed with a 13 C-octanoic acid breath test and high-resolution manometry during nutrient infusion, respectively. GI symptom levels were scored during high-resolution manometry. Data were analyzed using mixed models. The study was registered as NCT03402984. KEY RESULTS Twenty HVs (10 female, 25 ± 4.1 years, 22.58 ± 2.73 kg/m2 ) participated in the study. There was no difference in GE half time between both treatments (P = 0.92). Acotiamide had no effect on fundic pressures before and after nutrient infusion (P = 0.91). However, postprandial antral pressures remained significantly lower compared to placebo (P = 0.015). There was no significant difference in hunger, satiation and GI symptoms scores assessed during IGP measurement and by the daily diary (P > 0.12 for all). CONCLUSION Acotiamide is associated with lower antral pressures after nutrient intake, whereas it has no effect on fundic pressures, GE rate and symptom perceptions in HVs. Studies in FD need to elucidate whether lower antral pressures induced by acotiamide underlie postprandial symptom improvement in FD.
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Diurnal influences of fasted and non-fasted brisk walking on gastric emptying rate, metabolic responses, and appetite in healthy males.
McIver, VJ, Mattin, LR, Evans, GH, Yau, AMW
Appetite. 2019;:104411
Abstract
Growing evidence suggests circadian rhythms, nutrition and metabolism are intimately linked. Intermittent fasting (IMF) has become an increasingly popular intervention for metabolic health and combining IMF with exercise may lead to benefits for weight management. However, little is known about the diurnal variation of fasted exercise. This study aimed to investigate the diurnal influences on gastric emptying rate (GER), metabolic responses, and appetite to fasted and non-fasted exercise. Twelve healthy males completed four 45 min walks in a randomised order. Walks were completed in the morning (AM) and evening (PM) and either fasted (FASTED) or after consumption of a standardised meal (FED). GER of a semi-solid lunch was subsequently measured for 2 h using the 13C breath test. Blood glucose concentration, substrate utilisation, and ratings of appetite were measured throughout. Energy intake was also assessed for the following 24 h. GER Tlag was slower in PM-FASTED compared to AM-FASTED, AM-FED, and PM-FED (75 ± 18 min vs. 63 ± 14 min, P = 0.001, vs. 65 ± 10 min, P = 0.028 and vs. 67 ± 16 min, P = 0.007). Blood glucose concentration was greater in the FED trials in comparison to the FASTED trials pre-lunch (P < 0.05). Fat oxidation was greater throughout exercise in both FASTED trials compared to FED, and remained higher in FASTED trials than fed trials post-exercise until 30 min post-lunch ingestion (all P < 0.05). No differences were found for appetite post-lunch (P > 0.05) or 24 h post-energy intake (P = 0.476). These findings suggest that evening fasted exercise results in delayed GER, without changes in appetite. No compensatory effects were observed for appetite, and 24 h post-energy intake for both fasted exercise trials, therefore, increased fat oxidation holds positive implications for weight management.
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Ultrasound assessment of gastric emptying time in preterm infants: A prospective observational study.
Beck, CE, Witt, L, Albrecht, L, Winstroth, AM, Lange, M, Dennhardt, N, Boethig, D, Sümpelmann, R
European journal of anaesthesiology. 2019;(6):406-410
Abstract
BACKGROUND In paediatric anaesthesia, pre-operative fasting should be short to prevent discomfort, hunger, thirst and metabolic disorders. Current European guidelines recommend pre-operative fasting times of 4 h for breast milk and 6 h for formula milk in infants, whereas some national guidelines allow both until 4 h before anaesthesia. OBJECTIVE We evaluated the gastric emptying times of preterm infants after breast milk and formula milk, hypothesising that the mean gastric emptying time would be less than 4 h. DESIGN A prospective, observational, noninterventional cohort study. SETTING Neonatal ICU of a university hospital from August to September 2017. PATIENTS Twenty-two infants with a postmenstrual mean ± SD (range) age of 35 ± 2 (32 to 40) weeks were included. Based on their prescription plan, 10 infants received breast milk and 12 received formula milk with a total volume of 50 ± 16 (24 to 70) ml. INTERVENTIONS Gastric emptying was examined by sonographic measurements of the gastric antral area (GAA) before (FT0) and hourly after breast milk or formula milk feeding (FT1 to FT3). MAIN OUTCOME MEASURES Estimated gastric emptying time after enteral feeding with breast milk and formula milk in preterm infants. RESULTS The GAA of the preterm infants initially increased and subsequently decreased after feeding. GAA correlated significantly with fasting time (r = -0.53, P < 0.0001). At FT3 [199 ± 16 (175 to 225) min], GAA was 0.57 (0.42 to 0.91) cm and showed no difference compared with FT0. Using a linear regression model, the calculated mean gastric emptying time was 218 min. CONCLUSION The study shows that the mean gastric emptying time after enteral feeding with breast milk and formula milk is less than 4 h in preterm infants. These results support our current national fasting regimen of 4 h for any milk composition in infants before anaesthesia. TRIAL REGISTRATION German registry of clinical studies (DRKS-ID: DRKS 00013893).
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Gastrointestinal hormones and regulation of gastric emptying.
Camilleri, M
Current opinion in endocrinology, diabetes, and obesity. 2019;(1):3-10
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Abstract
PURPOSE OF REVIEW This review examines the hormonal regulation of gastric emptying, a topic of increasing relevance, given the fact that medications that are analogs of some of these hormones or act as agonists at the hormonal receptors, are used in clinical practice for optimizing metabolic control in the treatment of type 2 diabetes and in obesity. RECENT FINDINGS The major effects on gastric emptying result from actions of incretins, particularly gastric inhibitory polypeptide, glucagon-like peptide-1, and peptide tyrosine-tyrosine, the duodenal and pancreatic hormones, motilin, glucagon, and amylin, and the gastric orexigenic hormones, ghrelin and motilin. All of these hormones delay gastric emptying, except for ghrelin and motilin which accelerate gastric emptying. These effects on gastric emptying parallel the effects of the hormones on satiation (by those retarding emptying) and increase appetite by those that accelerate emptying. Indeed, in addition to the effects of these hormones on hypothalamic appetite centers and glycemic control, there is evidence that some of their biological effects are mediated through actions on the stomach, particularly with the glucagon-like peptide-1 analogs or agonists used in treating obesity. SUMMARY Effects of gastrointestinal hormones on gastric emptying are increasingly recognized as important mediators of satiation and postprandial glycemic control.
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Gastrointestinal effects of extra-virgin olive oil associated with lower postprandial glycemia in type 1 diabetes.
Bozzetto, L, Alderisio, A, Clemente, G, Giorgini, M, Barone, F, Griffo, E, Costabile, G, Vetrani, C, Cipriano, P, Giacco, A, et al
Clinical nutrition (Edinburgh, Scotland). 2019;(6):2645-2651
Abstract
OBJECTIVE To explore the possible mechanisms behind the lower glycemic response observed when extra-virgin olive oil (EVOO) is added to a high-glycemic index meal in patients with type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS According to a randomized cross-over design, eleven T1D patients (6 women, 5 men) on insulin pump consumed in the metabolic ward, one week apart, three high-glycemic index meals differing only for amount and quality of fat: high-monounsaturated fat (EVOO), high-saturated fat (Butter), and low-fat (LF). Before and after the meals, blood glucose (continuous glucose monitoring), gastric emptying rate (ultrasound technique), and plasma concentrations of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide GIP (ELISA), glucagon (RIA), and lipids (colorimetric assays) were evaluated. RESULTS Blood glucose iAUC (mmol/lx360 min) was lower after the EVOO (690 ± 431) than after the Butter (1320 ± 600) and LF meals (1007 ± 990) (M ± SD, p = 0.041 by repeated measures ANOVA). Gastric antrum volume was significantly larger in the early (60-90 min) postprandial phase (106 ± 21 vs. 90 ± 16 ml, p = 0.048) and significantly smaller in the late phase (330-360 min) (46 ± 10 vs. 57 ± 22 ml, p = 0.045) after the EVOO than after Butter meal. EVOO significantly increased postprandial GLP-1 iAUC (261 ± 311) compared to Butter (189 ± 349) (pmol/Lx180 min, p = 0.009). Postprandial GIP and glucagon responses were not significantly different between EVOO and Butter. Postprandial triglyceride iAUC was significantly higher after EVOO (100 ± 53) than after Butter (65 ± 60) (mmol/l × 360 min, p = 0.048). CONCLUSIONS Changes in gastric emptying and GLP-1 secretion and reduced glucose absorption through glucose-lipid competition may contribute to lower glycemia after a high-glycemic index meal with EVOO in T1D patients. CLINICAL TRIALS NUMBER NCT02330939.
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Assessing the effect of sugar-free chewing gum use on the residual gastric volume of patients fasting for gastroscopy: A randomised controlled trial.
Best, GW, Fanning, SB, Robertson, IK, Blackford, D, Mitchell, BL
Anaesthesia and intensive care. 2019;(6):541-547
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Rapid gastric emptying in diabetes mellitus: Pathophysiology and clinical importance.
Goyal, RK, Cristofaro, V, Sullivan, MP
Journal of diabetes and its complications. 2019;(11):107414
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Abstract
Although slow gastric emptying (gastroparesis) is a well-known complication of chronic hyperglycemia in diabetes mellitus (DM), it recently has become clear that rapid gastric emptying also is a frequent and important diabetic complication. In contrast, acute hyperglycemia causes slow gastric emptying, and acute hypoglycemia causes rapid gastric emptying. Rapid gastric emptying is frequent in T2DM; however, it may also occur in T1DM, particularly in the early stages of the disease, but may persist even into late stages. Recent studies suggest that usually, the stomach restricts the emptying of nutrients to 1-4 kcals/min. This restriction is due to the action of the gastric 'braking' hormones such as GLP-1, leptin, and amylin acting via the gastric inhibitory vagal motor circuit (GIVMC). Disruption of this braking system leads to rapid gastric emptying. Acute hyperglycemia also slows gastric emptying by stimulating the GIVMC, while acute hypoglycemia causes rapid gastric emptying by stimulating the gastric excitatory vagal motor circuit (GEVMC). In contrast, chronic hyperglycemia causes rapid gastric emptying by inducing oxidative stress in the stomach wall that disrupts inhibitory neuromuscular transmission and increases the contractility of the smooth muscle, while chronic hyperglycemia may also cause slow gastric emptying via severe inflammatory stress caused by proinflammatory macrophages and reduce contractility of the smooth muscle. There is a bidirectional relationship between blood glucose and gastric emptying. Thus, rapid gastric emptying may lead to a sizeable postprandial spike, and slow gastric emptying may blunt it. Postprandial hyperglycemia is involved in the development, progression, and complications of DM. Correction of fast gastric emptying involves agents that activate GIVMC and the use of gastric 'braking' hormones or their analogs. Recognition and treatment of rapid gastric emptying may contribute to better management of postprandial hyperglycemia and prevention of some diabetic complications.
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Effects of lixisenatide on postprandial blood pressure, gastric emptying and glycaemia in healthy people and people with type 2 diabetes.
Jones, KL, Rigda, RS, Buttfield, MDM, Hatzinikolas, S, Pham, HT, Marathe, CS, Wu, T, Lange, K, Trahair, LG, Rayner, CK, et al
Diabetes, obesity & metabolism. 2019;(5):1158-1167
Abstract
AIM: To evaluate the effects of the prandial glucagon-like peptide-1 receptor agonist lixisenatide on gastric emptying and blood pressure (BP) and superior mesenteric artery (SMA) blood flow, and the glycaemic responses to a 75-g oral glucose load in healthy people and those with type 2 diabetes (T2DM). MATERIALS AND METHODS Fifteen healthy participants (nine men, six women; mean ± SEM age 67.2 ± 2.3 years) and 15 participants with T2DM (nine men, six women; mean ± SEM age 61.9 ± 2.3 years) underwent measurement of gastric emptying, BP, SMA flow and plasma glucose 180 minutes after a radiolabelled 75-g glucose drink on two separate days. All participants received lixisenatide (10 μg subcutaneously) or placebo in a randomized, double-blind, crossover fashion 30 minutes before the glucose drink. RESULTS Lixisenatide slowed gastric emptying (retention at 120 minutes, P < 0.01), attenuated the rise in SMA flow (P < 0.01) and markedly attenuated the decrease in systolic BP (area under the curve [AUC] 0-120 minutes, P < 0.001) compared to placebo in healthy participants and those with T2DM. Plasma glucose (incremental AUC 0-120 minutes) was greater in participants with T2DM (P < 0.005) than in healthy participants, and lower after lixisenatide in both groups (P < 0.001). CONCLUSIONS In healthy participants and those with T2DM, the marked slowing of gastric emptying of glucose induced by lixisenatide was associated with attenuation of the increments in glycaemia and SMA flow and decrease in systolic BP. Accordingly, lixisenatide may be useful in the management of postprandial hypotension.
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The effect of brisk walking in the fasted versus fed state on metabolic responses, gastrointestinal function, and appetite in healthy men.
McIver, VJ, Mattin, L, Evans, GH, Yau, AMW
International journal of obesity (2005). 2019;(9):1691-1700
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Abstract
OBJECTIVE To investigate the effect of brisk walking in the fasted versus fed state on gastric emptying rate (GER), metabolic responses and appetite hormone responses. SUBJECTS/METHODS Twelve healthy men completed two 45 min treadmill walks, fasted (FASTED) and followed consumption of a standardised breakfast (FED). GER of a standardised lunch was subsequently measured for 2 h using the 13C-breath test method. Blood samples were collected at baseline, post-breakfast period, pre-exercise, immediately post exercise, pre-lunch then every 30 min following lunch for 2 h. Circulating concentrations of acylated ghrelin (GHR), glucagon-like peptide-1 (GLP-1), peptide tyrosine tyrosine (PYY), pancreatic polypeptide (PP), glucose, insulin, triglycerides, non-esterified fatty acids (NEFA) and cholesterol were measured. Subjective feelings of appetite were assessed at 15 min intervals throughout. Substrate utilisation was measured every 30 min, and continuously throughout exercise by indirect calorimetry. RESULTS No differences were observed for GER T½ (FASTED 89 ± 22 vs. FED 89 ± 24 min, P = 0.868) nor Tlag (FASTED 55 ± 15 vs. FED 54 ± 14 min, P = 0.704). NEFA concentrations were higher in FASTED at pre-exercise, post exercise and 30 min post exercise (pre-lunch) (all P < 0.05) but no differences were observed for glucose, cholesterol or triglycerides. Carbohydrate oxidation was greater at all time-points during FED exercise (all P < 0.05). Minimal changes in appetite were observed post lunch ingestion with no differences in PYY or GHR observed between trials. GLP-1 concentrations were greater in FED post-breakfast and pre-exercise (P < 0.05), though no differences were observed after lunch. A greater concentration of PP was observed in FED from pre-exercise to 30 min post lunch consumption (all P < 0.05). Insulin concentrations were higher in FED pre-exercise but higher in FASTED 1.5 h post lunch (P < 0.05). CONCLUSION These findings suggest that gastrointestinal function, hunger and appetite regulatory hormones are not sensitive to low-intensity bouts of physical activity and holds positive implications for weight management practices.
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Comparative effects of proximal and distal small intestinal administration of metformin on plasma glucose and glucagon-like peptide-1, and gastric emptying after oral glucose, in type 2 diabetes.
Borg, MJ, Bound, M, Grivell, J, Sun, Z, Jones, KL, Horowitz, M, Rayner, CK, Wu, T
Diabetes, obesity & metabolism. 2019;(3):640-647
Abstract
AIMS: The gastrointestinal tract, particularly the lower gut, may be key to the anti-diabetic action of metformin. We evaluated whether administration of metformin into the distal, vs the proximal, small intestine would be more effective in lowering plasma glucose by stimulating glucagon-like pepetide-1 (GLP-1) and/or slowing gastric emptying (GE) in type 2 diabetes (T2DM). MATERIALS AND METHODS Ten diet-controlled T2DM patients were studied on three occasions. A transnasal catheter was positioned with proximal and distal infusion ports located 13 and 190 cm beyond the pylorus, respectively. Participants received infusions of (a) proximal + distal saline (control), (b) proximal metformin (1000 mg) + distal saline or (c) proximal saline + distal metformin (1000 mg) over 5 minutes, followed 60 minutes later by a glucose drink containing 50 g glucose and 150 mg 13 C-acetate. "Arterialized" venous blood and breath samples were collected over 3 hours for measurements of plasma glucose, GLP-1, insulin and glucagon, and GE, respectively. RESULTS Compared with control, both proximal and distal metformin reduced plasma glucose and augmented GLP-1 responses to oral glucose comparably (P < 0.05 each), without affecting plasma insulin or glucagon. GE was slower after proximal metformin than after control (P < 0.05) and tended to be slower after distal metformin, without any difference between proximal and distal metformin. CONCLUSIONS In diet-controlled T2DM patients, glucose-lowering via a single dose of metformin administered to the upper and lower gut was comparable and was associated with stimulation of GLP-1 and slowing of GE. These observations suggest that the site of gastrointestinal administration is not critical to the glucose-lowering capacity of metformin.