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Sports Medicine (Auckland, N.Z.) Mar 2017The gastrointestinal (GI) tract plays a critical role in delivering carbohydrate and fluid during prolonged exercise and can therefore be a major determinant of... (Review)
Review
The gastrointestinal (GI) tract plays a critical role in delivering carbohydrate and fluid during prolonged exercise and can therefore be a major determinant of performance. The incidence of GI problems in athletes participating in endurance events is high, indicating that GI function is not always optimal in those conditions. A substantial body of evidence suggests that the GI system is highly adaptable. Gastric emptying as well as stomach comfort can be "trained" and perceptions of fullness decreased; some studies have suggested that nutrient-specific increases in gastric emptying may occur. Evidence also shows that diet has an impact on the capacity of the intestine to absorb nutrients. Again, the adaptations that occur appear to be nutrient specific. For example, a high-carbohydrate diet will increase the density of sodium-dependent glucose-1 (SGLT1) transporters in the intestine as well as the activity of the transporter, allowing greater carbohydrate absorption and oxidation during exercise. It is also likely that, when such adaptations occur, the chances of developing GI distress are smaller. Future studies should include more human studies and focus on a number of areas, including the most effective methods to induce gut adaptations and the timeline of adaptations. To develop effective strategies, a better understanding of the exact mechanisms underlying these adaptations is important. It is clear that "nutritional training" can improve gastric emptying and absorption and likely reduce the chances and/or severity of GI problems, thereby improving endurance performance as well as providing a better experience for the athlete. The gut is an important organ for endurance athletes and should be trained for the conditions in which it will be required to function.
Topics: Athletes; Diet; Dietary Carbohydrates; Exercise; Gastric Emptying; Humans; Physical Endurance; Physical Exertion
PubMed: 28332114
DOI: 10.1007/s40279-017-0690-6 -
Gastroenterology Clinics of North... Mar 2015Gastroparesis is a chronic symptomatic disorder of the stomach characterized by delayed emptying without evidence of mechanical obstruction. Idiopathic gastroparesis... (Review)
Review
Gastroparesis is a chronic symptomatic disorder of the stomach characterized by delayed emptying without evidence of mechanical obstruction. Idiopathic gastroparesis refers to gastroparesis of unknown cause not from diabetes; not from prior gastric surgery; not related to other endocrine, neurologic, rheumatologic causes of gastroparesis; and not related to medications that can delay gastric emptying. There is overlap in the symptoms of idiopathic gastroparesis and functional dyspepsia. Patients with idiopathic gastroparesis often have a constellation of symptoms including nausea, vomiting, early satiety, postprandial fullness, and upper abdominal pain. Current treatment options of dietary management, prokinetics agents, antiemetic agents, and symptom modulators do not adequately address clinical need for idiopathic gastroparesis.
Topics: Combined Modality Therapy; Diet Therapy; Electric Stimulation Therapy; Gastric Emptying; Gastrointestinal Agents; Gastroparesis; Humans
PubMed: 25667023
DOI: 10.1016/j.gtc.2014.11.015 -
Asia Pacific Journal of Clinical... 2014Dietary fibre plays an important role in controlling postprandial glycemic and insulin response in diabetic patients. The intake of dietary fibre has been shown to delay... (Randomized Controlled Trial)
Randomized Controlled Trial
Dietary fibre plays an important role in controlling postprandial glycemic and insulin response in diabetic patients. The intake of dietary fibre has been shown to delay the gastric emptying in healthy subjects. The relationship between gastric emptying and postprandial blood glucose in diabetic patients with fibre-load liquids needs to be investigated. To investigate the impact of soluble dietary fibre (SDF) on gastric emptying, postprandial glycemic and insulin response in patients with type 2 diabetes. 30 patients with type 2 diabetes (DM) and 10 healthy subjects (HS) matched for gender and age were randomized to receive SDF-free liquid (500 mL, 500 Kcal) and isoenergetic SDF liquid (oat β-glucan 7.5 g, 500 mL, 500 Kcal) on two separate days based on a cross-over with 6-day wash-out period. Gastric emptying was monitored by ultrasonography at intervals of 30 min for 2 hours. Fasting and postprandial blood was collected at intervals of 30-60 min for 180 min to determine plasma glucose and insulin. Proximal gastric emptying was delayed by SDF-treatment both in DM (p=0.001) and HS (p=0.037). SDF resulted in less output volume in the distal stomach in DM (p<0.05). SDF decreased postprandial glucose (p=0.001) and insulin (p=0.001) in DM subjects. Postprandial glucose (r=-0.547, p=0.047) and insulin (r=-0.566, p=0.004) were negatively correlated with distal emptying of SDF in DM subjects. Distal gastric emptying was delayed significantly in DM subjects with HbA1c levels ≥6.5% (p=0.021) or with complications (p=0.011) by SDF, respectively. SDF improved postprandial glycaemia which was related to slowing of gastric emptying.
Topics: Aged; Beverages; Biomarkers; Blood Glucose; Cross-Over Studies; Diabetes Mellitus, Type 2; Dietary Fiber; Female; Gastric Emptying; Humans; Insulin; Male; Middle Aged; Postprandial Period; Prospective Studies; Stomach; Ultrasonography
PubMed: 24901089
DOI: 10.6133/apjcn.2014.23.2.01 -
Current Opinion in Endocrinology,... Feb 2019This 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... (Review)
Review
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.
Topics: Appetite; Diabetes Mellitus, Type 2; Gastric Emptying; Gastrointestinal Hormones; Humans; Obesity; Satiation
PubMed: 30418188
DOI: 10.1097/MED.0000000000000448 -
Neurogastroenterology and Motility Apr 2019There have been many recent advances in the understanding of various aspects of the physiology of gastric motility and gastric emptying. Earlier studies had discovered... (Review)
Review
There have been many recent advances in the understanding of various aspects of the physiology of gastric motility and gastric emptying. Earlier studies had discovered the remarkable ability of the stomach to regulate the timing and rate of emptying of ingested food constituents and the underlying motor activity. Recent studies have shown that two parallel neural circuits, the gastric inhibitory vagal motor circuit (GIVMC) and the gastric excitatory vagal motor circuit (GEVMC), mediate gastric inhibition and excitation and therefore the rate of gastric emptying. The GIVMC includes preganglionic cholinergic neurons in the DMV and the postganglionic inhibitory neurons in the myenteric plexus that act by releasing nitric oxide, ATP, and peptide VIP. The GEVMC includes distinct gastric excitatory preganglionic cholinergic neurons in the DMV and postganglionic excitatory cholinergic neurons in the myenteric plexus. Smooth muscle is the final target of these circuits. The role of the intramuscular interstitial cells of Cajal in neuromuscular transmission remains debatable. The two motor circuits are differentially regulated by different sets of neurons in the NTS and vagal afferents. In the digestive period, many hormones including cholecystokinin and GLP-1 inhibit gastric emptying via the GIVMC, and in the inter-digestive period, hormones ghrelin and motilin hasten gastric emptying by stimulating the GEVMC. The GIVMC and GEVMC are also connected to anorexigenic and orexigenic neural pathways, respectively. Identification of the control circuits of gastric emptying may provide better delineation of the pathophysiology of abnormal gastric emptying and its relationship to satiety signals and food intake.
Topics: Animals; Enteric Nervous System; Gastric Emptying; Gastrointestinal Motility; Ghrelin; Humans; Motilin; Neurons
PubMed: 30740834
DOI: 10.1111/nmo.13546 -
Journal of Diabetes and Its... Nov 2019Although slow gastric emptying (gastroparesis) is a well-known complication of chronic hyperglycemia in diabetes mellitus (DM), it recently has become clear that rapid... (Review)
Review
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.
Topics: Blood Glucose; Diabetes Complications; Diabetes Mellitus; Gastric Emptying; Gastroparesis; Humans; Hyperglycemia; Postprandial Period; Prognosis; Stomach Diseases
PubMed: 31439470
DOI: 10.1016/j.jdiacomp.2019.107414 -
Journal of Nuclear Medicine Technology Jun 2019
Review
Topics: Gastric Emptying; Humans; Radionuclide Imaging; Stomach
PubMed: 31167827
DOI: 10.2967/jnmt.117.227892 -
Alimentary Pharmacology & Therapeutics May 2008Gastroparesis is a chronic disorder caused by stomach pump failure and characterized by profound nausea, vomiting and epigastric pain. Most often, the cause is... (Review)
Review
BACKGROUND
Gastroparesis is a chronic disorder caused by stomach pump failure and characterized by profound nausea, vomiting and epigastric pain. Most often, the cause is unapparent and of the known associations, diabetes is the most common. Diagnosis is usually made using an isotope-labelled test meal. Treatment is incremental and includes education, dietary support, prokinetic and antiemetic agents. There are novel approaches including gastric neurostimulation.
AIM
To review current concepts of gastric motor function, aetiology, investigation and treatment of gastroparesis.
METHODS
A systematic web-based review of the literature was undertaken using a lexicon of terms associated with gastroparesis.
RESULTS
There are few controlled studies of this condition. Little is known about causation or underlying nerve, muscle or pacemaker pathology. Idiopathic gastroparesis occurs most commonly in women and gastric emptying is often abnormal in diabetes. Isotopic gastric scintigraphy remains the gold standard investigation, but alternative tests are being developed. Treatment is multimodal and includes education, and nutritional support. There are no adequately powered controlled trials to support a particular drug regimen. In intractable gastroparesis, gastric neurostimulation appears to offer benefit.
CONCLUSION
Despite a significant progress in the past decade, further controlled trials are required into the therapeutic options available for treating this intriguing condition.
Topics: Diet; Gastric Emptying; Gastrointestinal Agents; Gastroparesis; Humans; Life Style
PubMed: 18248660
DOI: 10.1111/j.1365-2036.2008.03637.x -
Frontiers in Endocrinology 2020Oral levothyroxine sodium is absorbed in the small intestine, mainly in the jejunum and the ileum being lower the absorption rate at duodenal level. The time interval... (Review)
Review
Oral levothyroxine sodium is absorbed in the small intestine, mainly in the jejunum and the ileum being lower the absorption rate at duodenal level. The time interval between the ingestion of oral thyroxine and its appearance in the plasma renders unlike a gastric absorption of the hormone. However, several evidence confirm the key role of the stomach as a prerequisite for an efficient absorption of oral levothyroxine. In the stomach, in fact, occur key steps leading to the dissolution of thyroxine from the solid form, the process bringing the active ingredient from the pharmaceutical preparation to the aqueous solution. In particular, gastric juice pH, volume, viscosity, as well as gastric emptying time seem to be the most important limiting factors. These hypotheses are confirmed by the detection of an increased need for levothyroxine in patients with infection, chronic atrophic gastritis, gastroparesis, or in simultaneous treatment with drugs interfering with gastric acidic output. The aim of the present article is to focus on the knowledge of pathophysiologic events that determine the absorptive fate of traditional (tablet) and alternative thyroxine preparations (softgel capsule and liquid solution) in patients bearing gastric disorders.
Topics: Administration, Oral; Animals; Gastric Absorption; Gastric Emptying; Gastroparesis; Helicobacter Infections; Humans; Malabsorption Syndromes; Thyroxine
PubMed: 33584549
DOI: 10.3389/fendo.2020.621616 -
The Journal of Nutrition Dec 2021When sufficient breast milk is not available, infant formula is often used as an alternative. As for digestion, gastric behavior of infant formula and breast milk have... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
When sufficient breast milk is not available, infant formula is often used as an alternative. As for digestion, gastric behavior of infant formula and breast milk have not been studied in detail.
OBJECTIVE
This study aimed to compare gastric emptying and intragastric behavior between breast milk and infant formula in vivo using MRI.
METHODS
In this randomized crossover study, 16 lactating mothers (age: 31.7 ± 2.9 y; time since giving birth: 9.3 ± 2 mo), underwent gastric MRI scans before and after consumption of 200 mL of infant formula or their own breast milk. MRI scans were performed after an overnight fast (baseline) and every 10 min up until 60 min following ingestion. Primary outcomes were gastric emptying measures and the secondary outcome was gastric layer volume over time. Differences between infant formula and breast milk in total gastric volume and layering volume were tested using linear mixed models.
RESULTS
Gastric emptying half-time was 5.1 min faster for breast milk than for infant formula (95% CI: -19.0 to 29.2) (n = 14). Within a subgroup (n = 12) with similar initial gastric volume (<20 mL difference), gastric emptying half-time was 20 min faster for breast milk (95% CI: 1.23-43.1). Top layer volume (n = 16) was 6.4 mL greater for infant formula than for breast milk (95% CI: 1.9-10.8). This effect is driven by t = 10 and t = 20 min postingestion.
CONCLUSIONS
When taking initial gastric volume into account, breast milk emptied faster than infant formula in women, which is in line with previous findings in infants. Infant formula showed a significantly larger top layer volume in the first 20 min after ingestion. MRI in adults may find application in studies assessing gastric behavior of infant formula.
Topics: Adult; Cross-Over Studies; Female; Gastric Emptying; Humans; Infant; Infant Formula; Infant, Newborn; Infant, Premature; Lactation; Milk, Human; Mothers; Pregnancy
PubMed: 34590118
DOI: 10.1093/jn/nxab295