Gastric hypermotility and antropyloric dysfunction in gastric ulcer patients

Liebermann-Meffert, D; Allgöwer, M.

doi:10.1002/bjs.1800690105

Cited by 9 publications

(5 citation statements)

References 24 publications

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“…Supramaximal vagal stimulation can induce peptic ulcer, 25 possibly through the enhancement of acid secretion 25 or GI motility. 26 Recently, Simonian et al 27 reported that vagal efferent pathway could mediate ghrelin release and supramaximal activation of vagal efferent nerve may also encounter the elevated levels of plasma ghrelin. Isomoto et al 21 reported that enhancement of plasma ghrelin concentration was more marked in patients with acute gastritis than that in patients with peptic ulcer disease.…”

Section: Discussionmentioning

confidence: 99%

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Increased levels of plasma ghrelin in peptic ulcer disease

Suzuki

Masaoka²,

Nomoto

et al. 2006

Aliment Pharmacol Ther

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SUMMARY BackgroundGhrelin is a novel appetite-promoting peptide secreted primarily from the A-like cells in the gastric fundic mucosa. As gastric inflammation caused by Helicobacter pylori infection extends, the number of ghrelinproducing A-like cells is diminished and gastric ghrelin content decreases significantly. We previously reported that plasma levels of ghrelin, which correlated well with the serum levels of pepsinogen (PG) I and PG I/II ratio, decreased as gastric mucosal atrophy increased in non-ulcerogenic conditions and that plasma ghrelin level increased in rats with cysteamine-induced duodenal ulcer.

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Section: Discussionmentioning

confidence: 99%

“…10,11 Polyclonal rabbit antibodies were raised against the C-terminal [13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28] (Gln13-Arg28) fragments of rat ghrelin. 10 The anti-ghrelin antisera did not recognize other enteric peptides.…”

Section: Plasma Ghrelin Assaymentioning

confidence: 99%

Increased levels of plasma ghrelin in peptic ulcer disease

Suzuki

Masaoka²,

Nomoto

et al. 2006

Aliment Pharmacol Ther

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“…Supramaximal vagal stimulation can induce peptic ulcer, 25 possibly through the enhancement of acid secretion 25 or GI motility 26 . Recently, Simonian et al 27 reported that vagal efferent pathway could mediate ghrelin release and supramaximal activation of vagal efferent nerve may also encounter the elevated levels of plasma ghrelin.…”

Section: Discussionmentioning

confidence: 99%

Increased levels of plasma ghrelin in peptic ulcer disease

Suzuki

Masaoka²,

Nomoto

et al. 2006

Ali Pharm Thera Symp Ser

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Summary Background Ghrelin is a novel appetite‐promoting peptide secreted primarily from the A‐like cells in the gastric fundic mucosa. As gastric inflammation caused by Helicobacter pylori infection extends, the number of ghrelin‐producing A‐like cells is diminished and gastric ghrelin content decreases significantly. We previously reported that plasma levels of ghrelin, which correlated well with the serum levels of pepsinogen (PG) I and PG I/II ratio, decreased as gastric mucosal atrophy increased in non‐ulcerogenic conditions and that plasma ghrelin level increased in rats with cysteamine‐induced duodenal ulcer. Aim To investigate the plasma levels of ghrelin in patients with peptic ulcer disease. Patients and Methods Two hundred and eighty‐six patients with epigastric symptoms, who underwent upper gastrointestinal endoscopy, were enrolled. Blood samples were collected after a 12‐h fast before endoscopy. Patients were divided into four groups, namely chronic gastritis with high PG (n = 197), chronic gastritis with low PG (n = 58), duodenal ulcer (n = 14) and gastric ulcer (n = 17) and plasma concentrations of total and active ghrelin as well as serum concentrations of PG I and PG II were measured by radioimmunoassay. Six patients with duodenal ulcer and seven with gastric ulcer were also examined after ulcer healing. Results Plasma ghrelin levels were significantly higher in patients with duodenal ulcer or gastric ulcer than in those without ulcers. Elevated plasma total ghrelin levels did not significantly change after the healing of ulcers. Conclusions Plasma ghrelin levels were significantly higher in patients with peptic ulcer than in those with gastritis without ulcer. This finding suggests a possible relationship between mucosal injury susceptibility and elevated fasting plasma ghrelin.

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“…Our previous experiments have clearly shown that gastric ulcers strongly affected the enteric nervous system in the stomach wall [ 15 , 16 , 17 , 18 ] and these complex changes differed in several respects from other gastrointestinal pathologies. Importantly, ulcers in the distal part of the stomach (pyloric antrum) affect the gastric emptying [ 19 , 20 ] leading to maldigestion, malabsorption, and malnutrition. These specific symptoms were even referred to as “pyloric syndrome complex” [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Cocaine and Amphetamine Regulated Transcript (CART) Expression Changes in the Stomach Wall Affected by Experimentally Induced Gastric Ulcerations

Załęcki

Plywacz

Antushevich

et al. 2021

IJMS

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Cocaine- and amphetamine-regulated transcript (CART) is a peptide suggested to play a role in gastrointestinal tract tissue reaction to pathology. Gastric ulceration is a common disorder affecting huge number of people, and additionally, it contributes to the loss of pig livestock production. Importantly, ulceration as a focal disruption affecting deeper layers of the stomach wall differs from other gastrointestinal pathologies and should be studied individually. The pig’s gastrointestinal tract, due to its many similarities to the human counterpart, provides a valuable experimental model for studying digestive system pathologies. To date, the role of CART in gastric ulceration and the expression of the gene encoding CART in porcine gastrointestinal tube are completely unknown. Therefore, we aimed to verify the changes in the CART expression by Q-PCR (gene encoding CART in the tissue) and double immunofluorescence staining combined with confocal microscopy (CART immunofluorescence in enteric nervous system) in the porcine stomach tissues adjacent to gastric ulcerations. Surprisingly, we found that gastric ulcer caused a significant decrease in the expression of CART-encoding gene and huge reduction in the percentage of CART-immunofluorescent myenteric perikarya and neuronal fibers located within the circular muscle layer. Our results indicate a unique CART-dependent gastric response to ulcer disease.

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Gastric hypermotility and antropyloric dysfunction in gastric ulcer patients

Cited by 9 publications

References 24 publications

Increased levels of plasma ghrelin in peptic ulcer disease

Increased levels of plasma ghrelin in peptic ulcer disease

Increased levels of plasma ghrelin in peptic ulcer disease

Cocaine and Amphetamine Regulated Transcript (CART) Expression Changes in the Stomach Wall Affected by Experimentally Induced Gastric Ulcerations

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