Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients

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

Standard

Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients. / Yabe, Daisuke; Kuroe, Akira; Watanabe, Koin; Iwasaki, Masahiro; Hamasaki, Akihiro; Hamamoto, Yoshiyuki; Harada, Norio; Yamane, Shunsuke; Lee, Soushou; Murotani, Kenta; Deacon, Carolyn F; Holst, Jens Juul; Hirano, Tsutomu; Inagaki, Nobuya; Kurose, Takeshi; Seino, Yutaka.

In: Journal of Diabetes and its Complications, Vol. 29, 2015, p. 413-421.

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

Harvard

Yabe, D, Kuroe, A, Watanabe, K, Iwasaki, M, Hamasaki, A, Hamamoto, Y, Harada, N, Yamane, S, Lee, S, Murotani, K, Deacon, CF, Holst, JJ, Hirano, T, Inagaki, N, Kurose, T & Seino, Y 2015, 'Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients', Journal of Diabetes and its Complications, vol. 29, pp. 413-421. https://doi.org/10.1016/j.jdiacomp.2014.12.010

APA

Yabe, D., Kuroe, A., Watanabe, K., Iwasaki, M., Hamasaki, A., Hamamoto, Y., Harada, N., Yamane, S., Lee, S., Murotani, K., Deacon, C. F., Holst, J. J., Hirano, T., Inagaki, N., Kurose, T., & Seino, Y. (2015). Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients. Journal of Diabetes and its Complications, 29, 413-421. https://doi.org/10.1016/j.jdiacomp.2014.12.010

Vancouver

Yabe D, Kuroe A, Watanabe K, Iwasaki M, Hamasaki A, Hamamoto Y et al. Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients. Journal of Diabetes and its Complications. 2015;29:413-421. https://doi.org/10.1016/j.jdiacomp.2014.12.010

Author

Yabe, Daisuke ; Kuroe, Akira ; Watanabe, Koin ; Iwasaki, Masahiro ; Hamasaki, Akihiro ; Hamamoto, Yoshiyuki ; Harada, Norio ; Yamane, Shunsuke ; Lee, Soushou ; Murotani, Kenta ; Deacon, Carolyn F ; Holst, Jens Juul ; Hirano, Tsutomu ; Inagaki, Nobuya ; Kurose, Takeshi ; Seino, Yutaka. / Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients. In: Journal of Diabetes and its Complications. 2015 ; Vol. 29. pp. 413-421.

Bibtex

@article{5135da5ee14443398bdf9cd7b175b76b,
title = "Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients",
abstract = "AIMS: Hypersecretion of glucagon and reduced insulin secretion both contribute to hyperglycemia in type 2 diabetes (T2DM). However, the relative contributions of impaired glucagon and insulin secretions in glucose excursions at the various stages of T2DM development remain to be determined.METHODS: The responses of glucagon and insulin as well as those of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were examined before and after ingestion of glucose or mixed meal in Japanese subjects with normal or impaired glucose tolerance (NGT and IGT) and in non-obese, untreated T2DM of short duration.RESULTS: In OGTT, T2DM showed a rise in glucagon at 0-30min, unlike NGT and IGT, along with reduced insulin. In MTT, all three groups showed a rise in glucagon at 0-30min, with that in T2DM being highest, while T2DM showed a significant reduction in insulin. Linear regression analyses revealed that glucose area under the curve (AUC)0-120 min was associated with glucagon-AUC0-30 min and insulin-AUC0-30 min in both OGTT and MTT. Total and biologically intact GIP and GLP-1 levels were similar among the three groups.CONCLUSIONS: Disordered early phase insulin and glucagon secretions but not incretin secretion are involved in hyperglycemia after ingestion of nutrients in T2DM of even a short duration.",
author = "Daisuke Yabe and Akira Kuroe and Koin Watanabe and Masahiro Iwasaki and Akihiro Hamasaki and Yoshiyuki Hamamoto and Norio Harada and Shunsuke Yamane and Soushou Lee and Kenta Murotani and Deacon, {Carolyn F} and Holst, {Jens Juul} and Tsutomu Hirano and Nobuya Inagaki and Takeshi Kurose and Yutaka Seino",
note = "Copyright {\textcopyright} 2015. Published by Elsevier Inc.",
year = "2015",
doi = "10.1016/j.jdiacomp.2014.12.010",
language = "English",
volume = "29",
pages = "413--421",
journal = "Journal of Diabetes and its Complications",
issn = "1056-8727",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients

AU - Yabe, Daisuke

AU - Kuroe, Akira

AU - Watanabe, Koin

AU - Iwasaki, Masahiro

AU - Hamasaki, Akihiro

AU - Hamamoto, Yoshiyuki

AU - Harada, Norio

AU - Yamane, Shunsuke

AU - Lee, Soushou

AU - Murotani, Kenta

AU - Deacon, Carolyn F

AU - Holst, Jens Juul

AU - Hirano, Tsutomu

AU - Inagaki, Nobuya

AU - Kurose, Takeshi

AU - Seino, Yutaka

N1 - Copyright © 2015. Published by Elsevier Inc.

PY - 2015

Y1 - 2015

N2 - AIMS: Hypersecretion of glucagon and reduced insulin secretion both contribute to hyperglycemia in type 2 diabetes (T2DM). However, the relative contributions of impaired glucagon and insulin secretions in glucose excursions at the various stages of T2DM development remain to be determined.METHODS: The responses of glucagon and insulin as well as those of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were examined before and after ingestion of glucose or mixed meal in Japanese subjects with normal or impaired glucose tolerance (NGT and IGT) and in non-obese, untreated T2DM of short duration.RESULTS: In OGTT, T2DM showed a rise in glucagon at 0-30min, unlike NGT and IGT, along with reduced insulin. In MTT, all three groups showed a rise in glucagon at 0-30min, with that in T2DM being highest, while T2DM showed a significant reduction in insulin. Linear regression analyses revealed that glucose area under the curve (AUC)0-120 min was associated with glucagon-AUC0-30 min and insulin-AUC0-30 min in both OGTT and MTT. Total and biologically intact GIP and GLP-1 levels were similar among the three groups.CONCLUSIONS: Disordered early phase insulin and glucagon secretions but not incretin secretion are involved in hyperglycemia after ingestion of nutrients in T2DM of even a short duration.

AB - AIMS: Hypersecretion of glucagon and reduced insulin secretion both contribute to hyperglycemia in type 2 diabetes (T2DM). However, the relative contributions of impaired glucagon and insulin secretions in glucose excursions at the various stages of T2DM development remain to be determined.METHODS: The responses of glucagon and insulin as well as those of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were examined before and after ingestion of glucose or mixed meal in Japanese subjects with normal or impaired glucose tolerance (NGT and IGT) and in non-obese, untreated T2DM of short duration.RESULTS: In OGTT, T2DM showed a rise in glucagon at 0-30min, unlike NGT and IGT, along with reduced insulin. In MTT, all three groups showed a rise in glucagon at 0-30min, with that in T2DM being highest, while T2DM showed a significant reduction in insulin. Linear regression analyses revealed that glucose area under the curve (AUC)0-120 min was associated with glucagon-AUC0-30 min and insulin-AUC0-30 min in both OGTT and MTT. Total and biologically intact GIP and GLP-1 levels were similar among the three groups.CONCLUSIONS: Disordered early phase insulin and glucagon secretions but not incretin secretion are involved in hyperglycemia after ingestion of nutrients in T2DM of even a short duration.

U2 - 10.1016/j.jdiacomp.2014.12.010

DO - 10.1016/j.jdiacomp.2014.12.010

M3 - Journal article

C2 - 25613093

VL - 29

SP - 413

EP - 421

JO - Journal of Diabetes and its Complications

JF - Journal of Diabetes and its Complications

SN - 1056-8727

ER -

ID: 132046701