Lack of Modulation of Gastric Emptying by Dietary Nitrate in Healthy Volunteers

Terai, Shiho; Iijima, Katsunori; Asanuma, Kiyotaka; Ara, Nobuyuki; Uno, Kaname; Abe, Yasuhiko; Koike, Tomoyuki; Imatani, Akira; Ohara, Shuichi; Shimosegawa, Tooru

doi:10.1620/tjem.218.73

Cited by 4 publications

(3 citation statements)

References 46 publications

(58 reference statements)

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“…However, a more recent study demonstrated that NO generated luminally, at more physiological conditions, did not affect LES function . Similarly, we have demonstrated that dietary nitrate ingestion did not affect the gastric motility such as gastric emptying …”

Section: Effect Of Exogenous No Generated Luminally On the Function Osupporting

confidence: 67%

Involvement of luminal nitric oxide in the pathogenesis of the gastroesophageal reflux disease spectrum

Iijima

Shimosegawa

2014

J of Gastro and Hepatol

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Over the last 3 decades, the incidence of esophageal adenocarcinoma has dramatically increased in Western countries; a similar increase may be observed in Asian countries in the near future. Esophageal adenocarcinoma arises from a sequential gastroesophageal reflux disease (GERD) spectrum from reflux erosive esophagitis, to Barrett's esophagus, and finally to esophageal adenocarcinoma. At present, gastric acid and bile are assumed to be primarily involved in the etiology of the GERD spectrum. We reported in 2002 that, at the gastroesophageal junction in humans, abundant amounts of nitric oxide (NO) are generated luminally through the entero-salivary re-circulation of dietary nitrate. Since then, we have carried out a series of experiments to demonstrate that NO diffuses into the adjacent epithelium at cytotoxic levels. This diffusion results in disruption of the epithelial barrier function, exacerbation of inflammation, acceleration of columnar transformation in the esophagus (Barrett's esophagus) via the induction of caudal-type homeobox 2, and the shifting of carcinogenic N-nitroso compound formation from the luminal to epithelial compartment. These results suggest that, in addition to conventionally recognized causative factors, luminal NO could also be involved in the pathogenesis of the GERD spectrum. In addition, we recently showed that there is a prominent gender-related difference in NO-related cytotoxicity in the esophagus and that estrogen attenuated the esophageal tissue damage via the estrogen receptor in female rats. The role of estrogen in attenuating the esophageal tissue damage in NO-related esophageal damage could explain the well-recognized male predominance in the GERD spectrum in humans.

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Section: Effect Of Exogenous No Generated Luminally On the Function Osupporting

confidence: 67%

Involvement of luminal nitric oxide in the pathogenesis of the gastroesophageal reflux disease spectrum

Iijima

Shimosegawa

2014

J of Gastro and Hepatol

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“…Thus, before discussing mechanisms by which PPIs may affect gastric emptying, this section C breath test [33] provides an overview of the physiological basis of gastric motor-secretory functions [5,7,8,34,42].…”

Section: Basic Physiology Of Gastric Motor-secretory Functionsmentioning

confidence: 99%

Effects of Proton Pump Inhibitors on Gastric Emptying: A Systematic Review

2009

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The proton pump inhibitor (PPI) is widely used for the treatment of gastroesophageal reflux disease, peptic ulcer diseases, and functional dyspepsia. The pathogenesis of these acid-related and/or functional upper gastrointestinal disorders is potentially associated with abnormal gastric emptying. To date, variable effects of PPIs on gastric emptying have been reported. Therefore, it is relevant to gather and analyze published information on this topic. A systematic literature search has been performed, showing that the delaying effect of PPIs on gastric emptying of solid meals is consistent, whereas the effect of PPIs on the emptying of liquids is inconsistent. The underlying mechanisms whereby PPIs may affect gastric emptying have been discussed, most of which still remain hypothetic. Gastric emptying of solids involves a process of peptic hydrolysis. PPIs impair the hydrolytic digestion by inhibiting acid-dependent peptic activity, thereby delaying the solid emptying. Gastric emptying of liquids largely depends on volume and energy density of intragastric contents. PPIs variably modify the volume and the energy density by reducing gastric fluid secretion, thereby modifying the liquid emptying in an unpredictable manner. Hypergastrinemia has been considered to delay gastric emptying, but it seems of minor importance in the regulation of gastric emptying during PPI use. The delayed emptying of solids due to PPI therapy may have clinical implications in the management of gastroesophageal reflux disease, functional dyspepsia, as well as diabetes.

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“…PPIs are effective in preventing bleeding after ESD 26 and thus were orally administered to the patients in this study from the day of ESD until 8 weeks after the procedure. Some investigators have reported that PPIs do not affect the gastric emptying function 17 27 28 , whereas others have reported that these drugs negatively affect the emptying function 17 29 30 . The use of PPIs may have been responsible for the decreased gastric emptying observed in the present study.…”

Section: Discussionmentioning

confidence: 99%

Change in gastric emptying eight weeks after endoscopic submucosal dissection in patients with early gastric cancer

et al. 2016

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Background: Gastric emptying after endoscopic submucosal dissection (ESD) for early gastric cancer is not clear. The aim of this study was to evaluate changes in gastric emptying from before ESD to 8 weeks after ESD. Methods: In total, 54 patients with early gastric cancer were enrolled in this study. A breath test with carbon 13 (13C) was conducted before ESD and at 1 and 8 weeks after ESD. The Tlag and T1/2 values were analyzed at each time point. The primary outcomes were the changes in the Tlag and T1/2 values from before ESD to 1 and 8 weeks after ESD. The secondary outcomes were the factors associated with the changes in the Tlag and T1/2 values. Results: Gastric emptying was delayed at 1 and 8 weeks after ESD compared with before ESD (Tlag P = 0.002, P < 0.001; T1/2 P = 0.005, P = 0.001, respectively). The changes in the Tlag and T1/2 values from before ESD to 1 week after ESD were greater for proximal stomach lesions than for distal stomach lesions (P = 0.028, P < 0.001). Proximal stomach lesions were identified as the significant factor that influenced changes in the Tlag and T1/2 values from before ESD to 1 week after ESD in the multivariate analyses (Tlag P = 0.003, T1/2 P = 0.005). Conclusions: ESD induced delayed gastric emptying until 8 weeks after ESD. Proximal stomach lesions were also associated with decreased emptying 1 week after ESD.

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Lack of Modulation of Gastric Emptying by Dietary Nitrate in Healthy Volunteers

Cited by 4 publications

References 46 publications

Involvement of luminal nitric oxide in the pathogenesis of the gastroesophageal reflux disease spectrum

Involvement of luminal nitric oxide in the pathogenesis of the gastroesophageal reflux disease spectrum

Effects of Proton Pump Inhibitors on Gastric Emptying: A Systematic Review

Change in gastric emptying eight weeks after endoscopic submucosal dissection in patients with early gastric cancer

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