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United European Gastroenterology Journal Apr 2023
Topics: Humans; Gastric Emptying; Gastroparesis; Vomiting
PubMed: 36918964
DOI: 10.1002/ueg2.12379 -
Cleveland Clinic Journal of Medicine Jun 2024Gastroparesis is a heterogeneous motility disorder characterized by nausea, vomiting, and postprandial fullness. Its diagnosis requires objective documentation of... (Review)
Review
Gastroparesis is a heterogeneous motility disorder characterized by nausea, vomiting, and postprandial fullness. Its diagnosis requires objective documentation of delayed gastric emptying of solid food and exclusion of mechanical obstruction. Its epidemiology is unclear, and the main causes are diabetes mellitus and idiopathic disease. Cardinal symptoms often co-occur. Management involves nutritional assessment, dietary changes, drug evaluation, glycemic control (for patients with diabetes mellitus), and symptom relief. In this review, we explore challenges nongastroenterologists may encounter and how they can use current recommendations to manage patients with gastroparesis.
Topics: Gastroparesis; Humans; Gastric Emptying
PubMed: 38830702
DOI: 10.3949/ccjm.91a.23078 -
Diabetes, Obesity & Metabolism Oct 2020The effect of dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist (RA) tirzepatide on gastric emptying (GE) was...
The novel dual glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 (GLP-1) receptor agonist tirzepatide transiently delays gastric emptying similarly to selective long-acting GLP-1 receptor agonists.
The effect of dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist (RA) tirzepatide on gastric emptying (GE) was compared to that of GLP-1RAs in non-clinical and clinical studies. GE was assessed following acute and chronic treatment with tirzepatide in diet-induced obese mice versus semaglutide or long-acting GIP analogue alone. Participants [with and without type 2 diabetes (T2DM)] from a phase 1, 4-week multiple dose study received tirzepatide, dulaglutide or placebo. GE was assessed by acetaminophen absorption. In mice, tirzepatide delayed GE to a similar degree to that achieved with semaglutide; however, these acute inhibitory effects were abolished after 2 weeks of treatment. GIP analogue alone had no effect on GE or on GLP-1's effect on GE. In participants with and without T2DM, once-weekly tirzepatide (≥5 and ≥4.5 mg, respectively) delayed GE after a single dose. This effect diminished after multiple doses of tirzepatide or dulaglutide in healthy participants. In participants with T2DM treated with an escalation schedule of tirzepatide 5/5/10/10 or 5/5/10/15 mg, a residual GE delay was still observed after multiple doses. These data suggest that tirzepatide's activity on GE is comparable to that of selective GLP-1RAs.
Topics: Animals; Blood Glucose; Diabetes Mellitus, Type 2; Gastric Emptying; Gastric Inhibitory Polypeptide; Glucagon-Like Peptide 1; Glucagon-Like Peptide-1 Receptor; Glucose; Mice
PubMed: 32519795
DOI: 10.1111/dom.14110 -
The Korean Journal of Gastroenterology... Dec 2017Many disorders can cause either acute or chronic vomiting. However, in most cases, vomiting is self-limited. A correct diagnosis is possible by conducting careful... (Review)
Review
Many disorders can cause either acute or chronic vomiting. However, in most cases, vomiting is self-limited. A correct diagnosis is possible by conducting careful histories and physical examinations. In cases of severe vomiting, further testing, including laboratory studies, radiological images, endoscopic evaluation, and gastrointestinal motility tests, can also be considered. The correction of clinical consequences of vomiting should be initiated, including dehydration, electrolyte imbalances, malnutrition, and suppression of symptoms via the use empirical antiemetic treatments. Moreover, underlying disorders should be treated using dietary, pharmacological, and even surgical interventions.
Topics: Antineoplastic Agents; Feeding Behavior; Gastric Emptying; Gastritis; Gastroparesis; Humans; Metoclopramide; Vomiting
PubMed: 29277090
DOI: 10.4166/kjg.2017.70.6.283 -
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 Nuclear Medicine Technology Jun 2019
Review
Topics: Gastric Emptying; Humans; Radionuclide Imaging; Stomach
PubMed: 31167827
DOI: 10.2967/jnmt.117.227892 -
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 -
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 -
Reviews in Endocrine & Metabolic... Sep 2014Glucagon-like peptide 1 (GLP-1) is a cleavage product of the pre-proglucagon gene which is expressed in the α-cells of the pancreas, the L-cells of the intestine, and... (Review)
Review
Glucagon-like peptide 1 (GLP-1) is a cleavage product of the pre-proglucagon gene which is expressed in the α-cells of the pancreas, the L-cells of the intestine, and neurons located in the caudal brainstem and hypothalamus. GLP-1 is of relevance to appetite and weight maintenance because it has actions on the gastrointestinal tract as well as the direct regulation of appetite. It delays gastric emptying and gut motility in humans. In addition, interventricular injections of GLP-1 inhibit food intake, independent of the presence of food in the stomach or gastric emptying. Peripherally administered GLP-1 also affects the central regulation of feeding. It is therefore the synergistic actions of GLP-1 in the gut and brain, acting on both central and peripheral receptors that seem responsible for the effects of the hormone on satiety.
Topics: Appetite; Body Weight; Eating; Gastric Emptying; Glucagon-Like Peptide 1; Humans
PubMed: 24811133
DOI: 10.1007/s11154-014-9289-5 -
Gut and Liver Sep 2017Gastroparesis (Gp) is a chronic disease that presents with clinical symptoms of early satiety, bloating, nausea, vomiting, and abdominal pain. Along with these symptoms,... (Review)
Review
Gastroparesis (Gp) is a chronic disease that presents with clinical symptoms of early satiety, bloating, nausea, vomiting, and abdominal pain. Along with these symptoms, an objective finding of delayed gastric emptying, along with a documented absence of gastric outlet obstruction, are required for diagnosis. This article focuses on updates in the pathogenesis and management of Gp. Recent studies on full thickness biopsies of Gp patients have shed light on the complex interactions of the central, autonomic, and enteric nervous systems, which all play key roles in maintaining normal gut motility. The management of Gp has evolved beyond prokinetics and antiemetics with the use of gastric electrical stimulators (GES). In addition, this review aims to introduce the concept of gastroparesis-like syndrome (GLS). GLS helps groups of patients who have the cardinal symptoms of Gp but have a normal or rapid emptying test. Recent tests have shown that patients with Gp and GLS have similar pathophysiology, benefit greatly from GES placement, and likely should be treated in a similar manner.
Topics: Abdominal Pain; Chronic Disease; Disease Management; Female; Gastric Emptying; Gastroparesis; Humans; Male; Nausea; Syndrome; Vomiting
PubMed: 28535580
DOI: 10.5009/gnl16336