No Ghrelin Response to Oral Glucose in Diabetes Mellitus with Gastroparesis

Asai, Shiko; Katabami, Takuyuki; Obi, Naoko; Matsui, Tomoya; Kato, Hiroyuki; Obi, Ryusei; Ogawa, Yutaka; Kawata, Takehiro; Takama, Haruyuki; Ohta, Akio; Tanaka, Yasushi

doi:10.1507/endocrj.k08e-169

Cited by 13 publications

(7 citation statements)

References 35 publications

(41 reference statements)

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“…(39) In a human study, however, the fasting plasma ghrelin level was significantly lower in diabetes mellitus with diabetic gastroparesis than in healthy controls. (40) The change in the plasma ghrelin levels with sham feeding in diabetic gastroparesis patients and postsurgical gastroparesis patients were significantly lower than in normal subjects, although the plasma ghrelin levels increased in idiopathic gastroparesis. (41) Impaired regulation of the plasma ghrelin levels in diabetic gastroparesis would be caused by vagal nerve dysfunction.…”

Section: Gastric Motility Dysfunction and Ghrelinmentioning

confidence: 94%

Ghrelin and oxidative stress in gastrointestinal tract

Suzuki

Matsuzaki

Hibi

2010

J. Clin. Biochem. Nutr.

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Oxidative stress is a major cause of the gastrointestinal damage under physical or psychological stress. Ghrelin exhibits gastroprotective effects and they are supposed to be derived from antioxidant effects. In gastroduodenal mucosal injury, the plasma ghrelin levels increase in response to the demand for gastroduodenal cytoprotection. However, in the condition of Helicobacter pylori-induced gastric mucosal severe atrophy, the plasma ghrelin concentration shifted to lower levels. In diabetic gastroparesis, the regulation of ghrelin secretion is impaired with vagal nerve dysfunction. Selective ghrelin agonist is expected to represent a new class of prokinetic agent. In addition, the plasma ghrelin levels are also enhanced by systemic oxidative stress, and ghrelin exhibits antioxidant effects in many organs, such as heart, pancreas, and lung. This suggests that ghrelin would be an important player as a sensor of systemic oxidative stress.

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Section: Gastric Motility Dysfunction and Ghrelinmentioning

confidence: 94%

Ghrelin and oxidative stress in gastrointestinal tract

Suzuki

Matsuzaki

Hibi

2010

J. Clin. Biochem. Nutr.

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“…Diabetic complications were evaluated as described previously [7]. They had not been hospitalized for acute metabolic complications, but had been admitted for initial education and improvement of glycaemic control.…”

Section: Methods Subjectsmentioning

confidence: 99%

“…None of the 16 patients were taking any gastrokinetic drugs. Diabetic complications were evaluated as described previously [7].…”

Section: Methods Subjectsmentioning

confidence: 99%

Differing effects of liraglutide on gastric emptying in Japanese patients with type 2 diabetes

Nagai

Hashimoto

Oikawa

et al. 2013

Diabetes Obesity Metabolism

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This study was performed to clarify the influence of liraglutide on gastric emptying in Japanese patients with type 2 diabetes. In 16 patients, the [(13) C]-acetate breath test was performed to compare gastric emptying before and after liraglutide treatment. We found two patterns of response, with gastric emptying being delayed by liraglutide in seven patients (delayers) and not delayed in nine patients (non-delayers). The mean increase of the maximum gastric emptying time was 31 ± 4 min (p < 0.01 vs. baseline) in the delayers, while it was only 2 ± 3 min (p = 0.60 vs. baseline) in the non-delayers. The delayers showed a greater early decrease of AUC-PG from 0 to 60 min, despite no increase of the plasma insulin level compared with non-delayers. In conclusion, the effect of liraglutide treatment on gastric emptying shows heterogeneity, and patients can be classified as delayers or non-delayers.

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“…Patients with diabetic gastroparesis may have low plasma total ghrelin levels, possibly due to vagal denervation and/or chronic glucagon excess [121, 523, 524]. What is unclear is the risk/benefit ratio of systemic GHS treatment in patients with GI bleeding, autonomic neuropathy, and/or concurrent postoperative needs for narcotics, anticholinergics, and other drugs.…”

Section: Multifaceted Actionsmentioning

confidence: 99%

Integrating GHS into the Ghrelin System

Veldhuis

Bowers

2010

International Journal of Peptides

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Oligopeptide derivatives of metenkephalin were found to stimulate growth-hormone (GH) release directly by pituitary somatotrope cells in vitro in 1977. Members of this class of peptides and nonpeptidyl mimetics are referred to as GH secretagogues (GHSs). A specific guanosine triphosphatate-binding protein-associated heptahelical transmembrane receptor for GHS was cloned in 1996. An endogenous ligand for the GHS receptor, acylghrelin, was identified in 1999. Expression of ghrelin and homonymous receptor occurs in the brain, pituitary gland, stomach, endothelium/vascular smooth muscle, pancreas, placenta, intestine, heart, bone, and other tissues. Principal actions of this peptidergic system include stimulation of GH release via combined hypothalamopituitary mechanisms, orexigenesis (appetitive enhancement), insulinostasis (inhibition of insulin secretion), cardiovascular effects (decreased mean arterial pressure and vasodilation), stimulation of gastric motility and acid secretion, adipogenesis with repression of fat oxidation, and antiapoptosis (antagonism of endothelial, neuronal, and cardiomyocyte death). The array of known and proposed interactions of ghrelin with key metabolic signals makes ghrelin and its receptor prime targets for drug development.

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No Ghrelin Response to Oral Glucose in Diabetes Mellitus with Gastroparesis

Cited by 13 publications

References 35 publications

Ghrelin and oxidative stress in gastrointestinal tract

Ghrelin and oxidative stress in gastrointestinal tract

Differing effects of liraglutide on gastric emptying in Japanese patients with type 2 diabetes

Integrating GHS into the Ghrelin System

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