Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility.

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Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. / Miki, Takashi; Minami, Kohtaro; Shinozaki, Hidehiro; Matsumura, Kimio; Saraya, Atsunori; Ikeda, Hiroki; Yamada, Yuichiro; Holst, Jens Juul; Seino, Susumu.

In: Diabetes, Vol. 54, No. 4, 2005, p. 1056-63.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Miki, T, Minami, K, Shinozaki, H, Matsumura, K, Saraya, A, Ikeda, H, Yamada, Y, Holst, JJ & Seino, S 2005, 'Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility.', Diabetes, vol. 54, no. 4, pp. 1056-63.

APA

Miki, T., Minami, K., Shinozaki, H., Matsumura, K., Saraya, A., Ikeda, H., Yamada, Y., Holst, J. J., & Seino, S. (2005). Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. Diabetes, 54(4), 1056-63.

Vancouver

Miki T, Minami K, Shinozaki H, Matsumura K, Saraya A, Ikeda H et al. Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. Diabetes. 2005;54(4):1056-63.

Author

Miki, Takashi ; Minami, Kohtaro ; Shinozaki, Hidehiro ; Matsumura, Kimio ; Saraya, Atsunori ; Ikeda, Hiroki ; Yamada, Yuichiro ; Holst, Jens Juul ; Seino, Susumu. / Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. In: Diabetes. 2005 ; Vol. 54, No. 4. pp. 1056-63.

Bibtex

@article{472dcc20ab5011ddb5e9000ea68e967b,
title = "Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility.",
abstract = "Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. We also found that GLP-1 inhibited gut motility whereas GIP did not. Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently.",
author = "Takashi Miki and Kohtaro Minami and Hidehiro Shinozaki and Kimio Matsumura and Atsunori Saraya and Hiroki Ikeda and Yuichiro Yamada and Holst, {Jens Juul} and Susumu Seino",
note = "Keywords: Animals; Arginine; Blood Glucose; Food; Gastric Inhibitory Polypeptide; Gastrointestinal Motility; Glucagon; Glucagon-Like Peptide 1; Insulin; Islets of Langerhans; Mice; Mice, Knockout; Pancreas; Peptide Fragments; Potassium Channels; Potassium Channels, Inwardly Rectifying; Protein Precursors; Time Factors",
year = "2005",
language = "English",
volume = "54",
pages = "1056--63",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association",
number = "4",

}

RIS

TY - JOUR

T1 - Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility.

AU - Miki, Takashi

AU - Minami, Kohtaro

AU - Shinozaki, Hidehiro

AU - Matsumura, Kimio

AU - Saraya, Atsunori

AU - Ikeda, Hiroki

AU - Yamada, Yuichiro

AU - Holst, Jens Juul

AU - Seino, Susumu

N1 - Keywords: Animals; Arginine; Blood Glucose; Food; Gastric Inhibitory Polypeptide; Gastrointestinal Motility; Glucagon; Glucagon-Like Peptide 1; Insulin; Islets of Langerhans; Mice; Mice, Knockout; Pancreas; Peptide Fragments; Potassium Channels; Potassium Channels, Inwardly Rectifying; Protein Precursors; Time Factors

PY - 2005

Y1 - 2005

N2 - Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. We also found that GLP-1 inhibited gut motility whereas GIP did not. Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently.

AB - Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. We also found that GLP-1 inhibited gut motility whereas GIP did not. Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently.

M3 - Journal article

C2 - 15793244

VL - 54

SP - 1056

EP - 1063

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - 4

ER -

ID: 8418067