PHI structural requirements for potentiation of glucose-induced insulin release

C. Yanaihara; Y. Hashimoto; Y. Takeda; I. Kato; N. S. Track; K. Nokihara; H. Manaka; T. Iwanaga; T. Fujita; H. Okamoto; N. Yanaihara

doi:10.1016/0196-9781(86)90169-5

PHI structural requirements for potentiation of glucose-induced insulin release

C. Yanaihara, Y. Hashimoto, Y. Takeda, I. Kato, N. S. Track, K. Nokihara, H. Manaka, T. Iwanaga, T. Fujita, H. Okamoto, N. Yanaihara

HOSP - Surgery

Research output: Contribution to journal › Article › peer-review

8 Citations (Scopus)

Abstract

Immunoreactive PHI was detected in rat pancreas. The potentiating effect of 10^-9 M PHI upon insulin release from the isolated perfused rat pancreas was significant and most consistent when 250 mg% glucose was present in the perfusion medium. PHI(1-15) retained a substantial potentiating effect on insulin release, while PHI(14-27) was essentially inactive. Replacement of amino-terminal decapeptide portion of the PHI molecule with the corresponding part of VIP resulted in a drastic decrease of the potentiating effect of PHI on insulin release. 10^-8 M PHI(14-27) substantially diminished the potentiation by 10^-9 M PHI while PHI(1-15) was without an inhibitory effect. The present results indicate that the PHI active site for potentiation of glucose-induced insulin release resides in the amino-terminal segment of the molecule but requires the carboxyl terminal segment primarily for binding to exhibit full biological activity.

Original language	English
Pages (from-to)	83-88
Number of pages	6
Journal	Peptides
Volume	7
Issue number	SUPPL. 1
DOIs	https://doi.org/10.1016/0196-9781(86)90169-5
Publication status	Published - 1986

Keywords

Insulin release potentiation
Isolated perfused rat pancreas
PHI
PHI fragments
Structure-function relationship

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10.1016/0196-9781(86)90169-5

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title = "PHI structural requirements for potentiation of glucose-induced insulin release",

abstract = "Immunoreactive PHI was detected in rat pancreas. The potentiating effect of 10-9 M PHI upon insulin release from the isolated perfused rat pancreas was significant and most consistent when 250 mg% glucose was present in the perfusion medium. PHI(1-15) retained a substantial potentiating effect on insulin release, while PHI(14-27) was essentially inactive. Replacement of amino-terminal decapeptide portion of the PHI molecule with the corresponding part of VIP resulted in a drastic decrease of the potentiating effect of PHI on insulin release. 10-8 M PHI(14-27) substantially diminished the potentiation by 10-9 M PHI while PHI(1-15) was without an inhibitory effect. The present results indicate that the PHI active site for potentiation of glucose-induced insulin release resides in the amino-terminal segment of the molecule but requires the carboxyl terminal segment primarily for binding to exhibit full biological activity.",

keywords = "Insulin release potentiation, Isolated perfused rat pancreas, PHI, PHI fragments, Structure-function relationship",

author = "C. Yanaihara and Y. Hashimoto and Y. Takeda and I. Kato and Track, {N. S.} and K. Nokihara and H. Manaka and T. Iwanaga and T. Fujita and H. Okamoto and N. Yanaihara",

note = "Funding Information: This work was supported in part by Grants-in Aid t\)r Special Project Research No. 59227005 and 60229005 and for Special Project Research of Selected Intractable Neurological Disorders from the Ministry of Education, Science and Culture, Japan, and a grant from Naito Foundation.",

year = "1986",

doi = "10.1016/0196-9781(86)90169-5",

language = "English",

volume = "7",

pages = "83--88",

journal = "Peptides",

issn = "0196-9781",

publisher = "Elsevier Inc.",

number = "SUPPL. 1",

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TY - JOUR

T1 - PHI structural requirements for potentiation of glucose-induced insulin release

AU - Yanaihara, C.

AU - Hashimoto, Y.

AU - Takeda, Y.

AU - Kato, I.

AU - Track, N. S.

AU - Nokihara, K.

AU - Manaka, H.

AU - Iwanaga, T.

AU - Fujita, T.

AU - Okamoto, H.

AU - Yanaihara, N.

N1 - Funding Information: This work was supported in part by Grants-in Aid t\)r Special Project Research No. 59227005 and 60229005 and for Special Project Research of Selected Intractable Neurological Disorders from the Ministry of Education, Science and Culture, Japan, and a grant from Naito Foundation.

PY - 1986

Y1 - 1986

N2 - Immunoreactive PHI was detected in rat pancreas. The potentiating effect of 10-9 M PHI upon insulin release from the isolated perfused rat pancreas was significant and most consistent when 250 mg% glucose was present in the perfusion medium. PHI(1-15) retained a substantial potentiating effect on insulin release, while PHI(14-27) was essentially inactive. Replacement of amino-terminal decapeptide portion of the PHI molecule with the corresponding part of VIP resulted in a drastic decrease of the potentiating effect of PHI on insulin release. 10-8 M PHI(14-27) substantially diminished the potentiation by 10-9 M PHI while PHI(1-15) was without an inhibitory effect. The present results indicate that the PHI active site for potentiation of glucose-induced insulin release resides in the amino-terminal segment of the molecule but requires the carboxyl terminal segment primarily for binding to exhibit full biological activity.

AB - Immunoreactive PHI was detected in rat pancreas. The potentiating effect of 10-9 M PHI upon insulin release from the isolated perfused rat pancreas was significant and most consistent when 250 mg% glucose was present in the perfusion medium. PHI(1-15) retained a substantial potentiating effect on insulin release, while PHI(14-27) was essentially inactive. Replacement of amino-terminal decapeptide portion of the PHI molecule with the corresponding part of VIP resulted in a drastic decrease of the potentiating effect of PHI on insulin release. 10-8 M PHI(14-27) substantially diminished the potentiation by 10-9 M PHI while PHI(1-15) was without an inhibitory effect. The present results indicate that the PHI active site for potentiation of glucose-induced insulin release resides in the amino-terminal segment of the molecule but requires the carboxyl terminal segment primarily for binding to exhibit full biological activity.

KW - Insulin release potentiation

KW - Isolated perfused rat pancreas

KW - PHI

KW - PHI fragments

KW - Structure-function relationship

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AN - SCOPUS:0022885323

SN - 0196-9781

VL - 7

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IS - SUPPL. 1

ER -

PHI structural requirements for potentiation of glucose-induced insulin release

Abstract

Keywords

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