Mosapride citrate, a 5-HT&lt;sub&gt;4&lt;/sub&gt; receptor agonist, increased the plasma active and total glucagon-like peptide-1 levels in non-diabetic men

Aoki, Kazutaka; Kono, Hiroshi; Masuda, Kiyomi; Togashi, Yuichi; Terauchi, Yasuo

doi:10.1507/endocrj.ej12-0350

Cited by 12 publications

(9 citation statements)

References 28 publications

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“…Furthermore, plasma GLP-1 levels were shown to be lower in the MCD diet than in the NCD group, whereas they were normalized in the MCD plus MC group (Fig. 3D), observations which agree well with those in a previous report (4). GLP-1 secretion is decreased in NASH patients (6) and GLP-1 reportedly attenuates NASH development (38).…”

Section: Discussionsupporting

confidence: 91%

Mosapride citrate improves nonalcoholic steatohepatitis with increased fecal lactic acid bacteria and plasma glucagon-like peptide-1 level in a rodent model

Okubo

Nakatsu

Sakoda

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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T. Mosapride citrate improves nonalcoholic steatohepatitis with increased fecal lactic acid bacteria and plasma glucagon-like peptide-1 level in a rodent model. Am J Physiol Gastrointest Liver Physiol 308: G151-G158, 2015. First published November 26, 2014; doi:10.1152/ajpgi.00198.2014.-Several lines of evidence have suggested a role of gut microbiota in the etiology of nonalcoholic steatohepatitis (NASH). NASH subjects reportedly showed a prolonged orocecal transit time coexistent with small intestinal bacterial overgrowth. We considered the possibility that enhanced gastrointestinal motility would influence gut microbiota and thus investigated the effects of the gastroprokinetic agent mosapride citrate (MC) on gut microbiota and the development of NASH using a methionine-choline deficient (MCD) diet-fed rodent model. Mice were divided into three groups, given the normal chow diet (NCD), the MCD diet, or the MCD diet containing 10 mg·kg Ϫ1 ·day Ϫ1of MC (MCD plus MC) for 6 wk. NASH development was evaluated based on hepatic histochemical findings, serum parameters and various mRNA and/or protein expression levels. MC treatment suppressed MCD diet-induced NASH development, with reduced serum lipopolysaccharide and increased plasma glucagon-like peptide-1 (GLP-1) concentrations. Calculation of the relative abundance of each strain based on gut microbiota analyses indicated lactic acid bacteria specifically, such as Bifidobacterium and Lactobacillus, in feces to be decreased in the MCD, compared with the NCD group. Interestingly, the reduction in lactic acid bacteria in the MCD diet group was reversed in the MCD plus MC group. In addition, colon inflammation observed in the MCD diet group was reduced in the MCD plus MC group. Therefore, MC showed a protective effect against MCD dietinduced NASH development in our rodent model, with possible involvements of increased fecal lactic acid bacteria, protection against colon inflammation and elevated plasma GLP-1. mosapride citrate; inflammation; gut microbiota; nonalcoholic steatohepatitis; glucagon-like peptide-1

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Section: Discussionsupporting

confidence: 91%

Mosapride citrate improves nonalcoholic steatohepatitis with increased fecal lactic acid bacteria and plasma glucagon-like peptide-1 level in a rodent model

Okubo

Nakatsu

Sakoda

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Mosapride citrate is a selective agonist of the 5-hydroxytryptamine (5-HT) 4 receptor, which is typically used to treat heartburn, nausea, and vomiting associated with chronic gastritis or to prepare for a barium enema X-ray examination and it may also have an antidiabetic effect by increasing GLP-1 secretion. Aoki et al [ 92 ] examined the effect of the administration of mosapride citrate on plasma incretin levels in men with normal glucose tolerance (NGT) or impaired glucose tolerance (IGT) and showed that the AUCs of the plasma active and total GLP-1 levels were significantly higher in the M (mosapride citrate 20 mg) group than in the control (no drug) group. Ma et al [ 93 ] evaluated GLP-1 responses to intraduodenal glucose in T2DM with results showing that the small intestinal glucose load is critical in determining GLP-1 responses.…”

Section: Glp-1 Levels and Drugsmentioning

confidence: 99%

Multiple Factors Related to the Secretion of Glucagon-Like Peptide-1

Wang

Liu²,

Chen

et al. 2015

International Journal of Endocrinology

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The glucagon-like peptide-1 is secreted by intestinal L cells in response to nutrient ingestion. It regulates the secretion and sensitivity of insulin while suppressing glucagon secretion and decreasing postprandial glucose levels. It also improves beta-cell proliferation and prevents beta-cell apoptosis induced by cytotoxic agents. Additionally, glucagon-like peptide-1 delays gastric emptying and suppresses appetite. The impaired secretion of glucagon-like peptide-1 has negative influence on diabetes, hyperlipidemia, and insulin resistance related diseases. Thus, glucagon-like peptide-1-based therapies (glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors) are now well accepted in the management of type 2 diabetes. The levels of glucagon-like peptide-1 are influenced by multiple factors including a variety of nutrients. The component of a meal acts as potent stimulants of glucagon-like peptide-1 secretion. The levels of its secretion change with the intake of different nutrients. Some drugs also have influence on GLP-1 secretion. Bariatric surgery may improve metabolism through the action on GLP-1 levels. In recent years, there has been a great interest in developing effective methods to regulate glucagon-like peptide-1 secretion. This review summarizes the literature on glucagon-like peptide-1 and related factors affecting its levels.

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“…However, the mechanisms of GLP-1 upregulation by the use of these drugs remain unclear. Aoki et al [27] reported that a single administration of 20 mg of mosapride citrate 2 h before breakfast significantly reduced postprandial blood glucose and increased postprandial plasma active GLP-1. Based on the findings that the GLP-1 concentration after a meal test is reportedly increased after a sleeve gastrectomy [28] and is significantly higher in patients after gastrectomy compared with patients without gastrectomy [29]; Aoki et al [27] suggested that mosapride citrate-a gastrokinetic agentfacilitates the entry of a large amount of food into the small intestine and thus increases the plasma active GLP-1 concentration.…”

Section: Discussionmentioning

confidence: 99%

“…Aoki et al [27] reported that a single administration of 20 mg of mosapride citrate 2 h before breakfast significantly reduced postprandial blood glucose and increased postprandial plasma active GLP-1. Based on the findings that the GLP-1 concentration after a meal test is reportedly increased after a sleeve gastrectomy [28] and is significantly higher in patients after gastrectomy compared with patients without gastrectomy [29]; Aoki et al [27] suggested that mosapride citrate-a gastrokinetic agentfacilitates the entry of a large amount of food into the small intestine and thus increases the plasma active GLP-1 concentration. Because the predominant location of L cells is the distal portion of the gut [30], 20 mg of mosapride citrate-a comparatively high dosage-may lead to the transportation of nutrients to the distal portion of gut at a much earlier phase and increase secretion of GLP-1.…”

Section: Discussionmentioning

confidence: 99%

Mosapride Citrate Increases Postprandial Glucagon-Like Peptide-1, Insulin, and Gene Expression of Sweet Taste Receptors

et al. 2014

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Mosapride citrate, a 5-HT<sub>4</sub> receptor agonist, increased the plasma active and total glucagon-like peptide-1 levels in non-diabetic men

Cited by 12 publications

References 28 publications

Mosapride citrate improves nonalcoholic steatohepatitis with increased fecal lactic acid bacteria and plasma glucagon-like peptide-1 level in a rodent model

Mosapride citrate improves nonalcoholic steatohepatitis with increased fecal lactic acid bacteria and plasma glucagon-like peptide-1 level in a rodent model

Multiple Factors Related to the Secretion of Glucagon-Like Peptide-1

Mosapride Citrate Increases Postprandial Glucagon-Like Peptide-1, Insulin, and Gene Expression of Sweet Taste Receptors

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