The effect of mosapride (5HT-4 receptor agonist) on insulin sensitivity and GLUT4 translocation

J. S. Nam, J. Y. Nam, J. S. Yoo, M. Cho, J. S. Park, C. W. Ahn, B. S. Cha, Eunjig Lee, Sungkil Lim, K. R. Kim, H. C. Lee

Research output: Contribution to journalArticle

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Abstract

Aims: We investigated the effect of mosapride, 5HT-4 (5-hydroxytryptamine) agonist, on blood glucose level and insulin sensitivity in subjects with impaired glucose tolerance (IGT) and conducted an in vitro study to evaluate the action mechanism. Methods: Thirty IGT patients were randomly assigned to receive either mosapride or placebo for 2 weeks. Biochemical profiles and insulin sensitivity index from euglycemic hyperinsulinemic clamp test were assessed before and after treatment. In cultured myotubes from human skeletal muscle cells, insulin- and mosapride-induced GLUT4 translocation and tyrosine phosphorylation of IRS-1 were determined. Results: After 2 weeks of treatment with mosapride, glucose disposal rates were significantly increased up to those of control (mosapride 5.47 ± 1.72 vs 7.06 ± 2.13, P = 0.004, placebo 5.42 ± 1.85 vs 5.23 ± 1.53 mg kg-1 min-1). Fasting plasma glucose (FPG) and insulin levels were decreased. Mosapride increased the contents of GLUT4 in plasma membrane representing the increased recruitment of glucose transporters from intracellular pool. While insulin treatment on human skeletal muscle cell resulted in an increased tyrosine phosphorylation of IRS-1, mosapride did not have any effect. Conclusions: Mosapride is effective in decreasing FPG without stimulating insulin secretion in IGT subjects, possibly by inducing GLUT4 translocation in skeletal muscles.

Original languageEnglish
Pages (from-to)329-334
Number of pages6
JournalDiabetes Research and Clinical Practice
Volume87
Issue number3
DOIs
Publication statusPublished - 2010 Mar 1

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Insulin Resistance
Glucose Intolerance
Insulin
Skeletal Muscle
Glucose
Muscle Cells
Tyrosine
Fasting
Placebos
Phosphorylation
Serotonin Receptor Agonists
Glucose Clamp Technique
Facilitative Glucose Transport Proteins
mosapride
Skeletal Muscle Fibers
Blood Glucose
Therapeutics
Cell Membrane

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Nam, J. S. ; Nam, J. Y. ; Yoo, J. S. ; Cho, M. ; Park, J. S. ; Ahn, C. W. ; Cha, B. S. ; Lee, Eunjig ; Lim, Sungkil ; Kim, K. R. ; Lee, H. C. / The effect of mosapride (5HT-4 receptor agonist) on insulin sensitivity and GLUT4 translocation. In: Diabetes Research and Clinical Practice. 2010 ; Vol. 87, No. 3. pp. 329-334.
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abstract = "Aims: We investigated the effect of mosapride, 5HT-4 (5-hydroxytryptamine) agonist, on blood glucose level and insulin sensitivity in subjects with impaired glucose tolerance (IGT) and conducted an in vitro study to evaluate the action mechanism. Methods: Thirty IGT patients were randomly assigned to receive either mosapride or placebo for 2 weeks. Biochemical profiles and insulin sensitivity index from euglycemic hyperinsulinemic clamp test were assessed before and after treatment. In cultured myotubes from human skeletal muscle cells, insulin- and mosapride-induced GLUT4 translocation and tyrosine phosphorylation of IRS-1 were determined. Results: After 2 weeks of treatment with mosapride, glucose disposal rates were significantly increased up to those of control (mosapride 5.47 ± 1.72 vs 7.06 ± 2.13, P = 0.004, placebo 5.42 ± 1.85 vs 5.23 ± 1.53 mg kg-1 min-1). Fasting plasma glucose (FPG) and insulin levels were decreased. Mosapride increased the contents of GLUT4 in plasma membrane representing the increased recruitment of glucose transporters from intracellular pool. While insulin treatment on human skeletal muscle cell resulted in an increased tyrosine phosphorylation of IRS-1, mosapride did not have any effect. Conclusions: Mosapride is effective in decreasing FPG without stimulating insulin secretion in IGT subjects, possibly by inducing GLUT4 translocation in skeletal muscles.",
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The effect of mosapride (5HT-4 receptor agonist) on insulin sensitivity and GLUT4 translocation. / Nam, J. S.; Nam, J. Y.; Yoo, J. S.; Cho, M.; Park, J. S.; Ahn, C. W.; Cha, B. S.; Lee, Eunjig; Lim, Sungkil; Kim, K. R.; Lee, H. C.

In: Diabetes Research and Clinical Practice, Vol. 87, No. 3, 01.03.2010, p. 329-334.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The effect of mosapride (5HT-4 receptor agonist) on insulin sensitivity and GLUT4 translocation

AU - Nam, J. S.

AU - Nam, J. Y.

AU - Yoo, J. S.

AU - Cho, M.

AU - Park, J. S.

AU - Ahn, C. W.

AU - Cha, B. S.

AU - Lee, Eunjig

AU - Lim, Sungkil

AU - Kim, K. R.

AU - Lee, H. C.

PY - 2010/3/1

Y1 - 2010/3/1

N2 - Aims: We investigated the effect of mosapride, 5HT-4 (5-hydroxytryptamine) agonist, on blood glucose level and insulin sensitivity in subjects with impaired glucose tolerance (IGT) and conducted an in vitro study to evaluate the action mechanism. Methods: Thirty IGT patients were randomly assigned to receive either mosapride or placebo for 2 weeks. Biochemical profiles and insulin sensitivity index from euglycemic hyperinsulinemic clamp test were assessed before and after treatment. In cultured myotubes from human skeletal muscle cells, insulin- and mosapride-induced GLUT4 translocation and tyrosine phosphorylation of IRS-1 were determined. Results: After 2 weeks of treatment with mosapride, glucose disposal rates were significantly increased up to those of control (mosapride 5.47 ± 1.72 vs 7.06 ± 2.13, P = 0.004, placebo 5.42 ± 1.85 vs 5.23 ± 1.53 mg kg-1 min-1). Fasting plasma glucose (FPG) and insulin levels were decreased. Mosapride increased the contents of GLUT4 in plasma membrane representing the increased recruitment of glucose transporters from intracellular pool. While insulin treatment on human skeletal muscle cell resulted in an increased tyrosine phosphorylation of IRS-1, mosapride did not have any effect. Conclusions: Mosapride is effective in decreasing FPG without stimulating insulin secretion in IGT subjects, possibly by inducing GLUT4 translocation in skeletal muscles.

AB - Aims: We investigated the effect of mosapride, 5HT-4 (5-hydroxytryptamine) agonist, on blood glucose level and insulin sensitivity in subjects with impaired glucose tolerance (IGT) and conducted an in vitro study to evaluate the action mechanism. Methods: Thirty IGT patients were randomly assigned to receive either mosapride or placebo for 2 weeks. Biochemical profiles and insulin sensitivity index from euglycemic hyperinsulinemic clamp test were assessed before and after treatment. In cultured myotubes from human skeletal muscle cells, insulin- and mosapride-induced GLUT4 translocation and tyrosine phosphorylation of IRS-1 were determined. Results: After 2 weeks of treatment with mosapride, glucose disposal rates were significantly increased up to those of control (mosapride 5.47 ± 1.72 vs 7.06 ± 2.13, P = 0.004, placebo 5.42 ± 1.85 vs 5.23 ± 1.53 mg kg-1 min-1). Fasting plasma glucose (FPG) and insulin levels were decreased. Mosapride increased the contents of GLUT4 in plasma membrane representing the increased recruitment of glucose transporters from intracellular pool. While insulin treatment on human skeletal muscle cell resulted in an increased tyrosine phosphorylation of IRS-1, mosapride did not have any effect. Conclusions: Mosapride is effective in decreasing FPG without stimulating insulin secretion in IGT subjects, possibly by inducing GLUT4 translocation in skeletal muscles.

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