Atsuto Nagoshi

Monosodium l-glutamate added to a high-energy, high-protein liquid diet promotes gastric emptying

BACKGROUND Free glutamate activates taste receptors on nerves in the oral cavity to elicit a unique taste known as umami. Recently, umami taste receptors were also found in the gastric mucosa. Although reports suggest that mucosal receptors may respond to free glutamate to modulate gastric function, no evidence of any effect on gastric emptying has been documented. OBJECTIVE We hypothesized that glutamate may act as a modulator of gastric function. We studied the effects of L-glutamate enrichment of a protein-rich liquid meal, and similar enrichment of an equicaloric carbohydrate meal or noncaloric water, on gastric emptying. DESIGN Ten healthy men were enrolled. Nine of the 10 subjects included in the study ingested all test meals with and without monosodium L-glutamate (MSG), and the remaining subject ingested only the protein-rich meals with and without MSG. All experimental and control liquid meals included [1-(13)C]sodium acetate as a tracer. After a test meal or water was ingested, (13)C breath tests were performed to estimate gastric emptying. RESULTS MSG enrichment not only resulted in a significant decrease in the mathematically simulated half-excretion (emptying) time of a protein-rich meal, but also increased the area under the curve (%dose/h) significantly. In contrast, MSG had no significant effect on the gastric emptying of a carbohydrate meal or a noncaloric water meal. CONCLUSIONS Enrichment with MSG facilitated gastric emptying of a protein-rich meal exclusively, which suggests that free glutamate is important for protein digestion and may be helpful in the management of delayed gastric emptying.

High-viscosity liquid meal accelerates gastric emptying.

Abstract  Adding pectin to an elemental formula increases its viscosity through gelatinization, thus presumably preventing gastro‐oesophageal reflux and aspiration pneumonia. We investigated the influence of the viscosity of an elemental formula on gastric emptying. Eleven healthy volunteers underwent three tests at intervals of >1 week. After fasting for >8 h, each subject received a test meal (enteral nutrition solution, enteral solution plus pectin, or water). Then gastric emptying (continuous 13C breath test), gastro‐oesophageal intraluminal pressures, oesophageal pH, and blood levels of glucose, insulin and gastrin were all measured simultaneously. The gastric emptying coefficient was significantly increased by adding pectin to enteral nutrition (3.01 ± 0.10 vs 2.78 ± 0.10, mean ± SE, P < 0.05). The antral motility index was also significantly higher with pectin than without at 45–60 min and 60–75 min after the test meal (526 ± 237 vs 6.5 ± 4.6 mmHg s−1 and 448 ± 173 vs 2.3 ± 2.3 mmHg s−1 respectively; P < 0.05). Plasma glucose was significantly higher with pectin than without it at 60 min after ingestion (141.5 ± 6.03 vs 125.8 ± 4.69 μm mL−1, P < 0.05). In healthy individuals, pectin increased the viscosity of enteral nutrition and accelerated gastric emptying.

Monosodium glutamate stimulates secretion of glucagon‐like peptide‐1 and reduces postprandial glucose after a lipid‐containing meal

Monosodium l‐glutamate (MSG) is known to influence the endocrine system and gastrointestinal (GI) motility. The mechanism of postprandial glycemic control by food in the GI tract is mostly unknown and of great interest.

Increase of weakly acidic gas esophagopharyngeal reflux (EPR) and swallowing‐induced acidic/weakly acidic EPR in patients with chronic cough responding to proton pump inhibitors

Background  Gastro‐esophageal reflux disease (GERD)‐related chronic cough (CC) may have multifactorial causes. To clarify the characteristics of esophagopharyngeal reflux (EPR) events in CC patients whose cough was apparently influenced by gastro‐esophageal reflux (GER), we studied patients with CC clearly responding to full‐dose proton pump inhibitor (PPI) therapy (CC patients).

Assessment of Airway Inflammation by Exhaled Breath Condensate and Impedance Due to Gastroesophageal Reflux Disease (GERD)

Avoiding oxidative stress in the airways is important for the treatment of respiratory disease associated with gastroesophageal reflux disease (GERD). It is often difficult to decide whether GERD is causing airway inflammation or whether an airway disease is complicated by GERD. Measurement of exhaled breath condensate (EBC) is performed by cooling and collecting the airway lining fluid contained in exhaled air. A decrease of pH and an increase of the 8-isoprostane concentration in EBC have been observed in patients with mild to moderate asthma accompanied by GERD. There are still problems to be overcome before EBC can be used clinically, but pH and 8-isoprostane may be promising objective markers of airway inflammation due to GERD. The disease concept and diagnosis of GERD are constantly advancing, including the development of impedance methods. It is expected that treatment will be based on the latest diagnostic knowledge of GERD associated with respiratory disease and on monitoring of airway inflammation.

A Review of the Management of Gastric Acid-Related Diseases: Focus on Rabeprazole

Current treatment guidelines for acid-related diseases (ARDs) recommend first-line treatment with a proton pump inhibitor (PPI) to reduce gastric acid production. PPIs are indicated in the management of gastroesophageal reflux disease (reflux esophagitis, nonerosive reflux disease), peptic ulcer (gastric and duodenal ulcer, non-steroidal anti-inflammatory drug (NSAID)-associated ulcer, bleeding ulcer), functional dyspepsia, and in association with Helicobacter pylori eradication therapy when needed. Currently, PPIs (omeprazole, lansoprazole, pantoprazole, rabeprazole and esomeprazole) are widely used for the treatment of ARDs. All 5 PPIs are effective. However, there are differences in PPI pharmacokinetic and pharmacodynamic profiles that might influence their clinical utility. Rabeprazole is a useful option for the treatment of acid-related diseases due to its rapid onset of acid inhibition and few drug interactions.