Insulin secretion is inhibited by subtype five somatostatin receptor in the mouse

S. P. Fagan, A. Azizzadeh, S. Moldovan, M. K. Ray, T. E. Adrian, X. Ding, D. H. Coy, F. C. Brunicardi, Dana Andersen

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Background. Recently five somatostatin receptor subtypes (SSTRs) were cloned, allowing the development of highly specific agonists to these SSTRs. Previous studies have shown a species specificity phenomenon with respect to the inhibition of insulin secretion by these selective agonists. This study was undertaken to determine which SSTR (2 or 5) is responsible for the inhibitory effect of somatostatin on glucose-stimulated mouse insulin secretion. Methods. Intact mouse islets (n = 10) were stimulated with D- glucose in the presence or absence of receptor-specific somatostatin agonists. Results. D-glucose (16. 7 mmol/L) augmented insulin secretion by 158% above that seen with 3. 9 mmol/L D-glucose in the presence of DC 32-92 (SSTR5) selective agonist, D-glucose (16. 7 mmol/L) augmented insulin secretion by 64% above that seen with 3. 9 mmol/L D-glucose. The presence of SSTR 5 selective agonist resulted in a significant (P

Original languageEnglish (US)
Pages (from-to)254-259
Number of pages6
JournalSurgery
Volume124
Issue number2
DOIs
StatePublished - 1998
Externally publishedYes

Fingerprint

Somatostatin Receptors
Insulin
Glucose
Species Specificity
Somatostatin

ASJC Scopus subject areas

  • Surgery

Cite this

Fagan, S. P., Azizzadeh, A., Moldovan, S., Ray, M. K., Adrian, T. E., Ding, X., ... Andersen, D. (1998). Insulin secretion is inhibited by subtype five somatostatin receptor in the mouse. Surgery, 124(2), 254-259. https://doi.org/10.1016/S0039-6060(98)70128-X

Insulin secretion is inhibited by subtype five somatostatin receptor in the mouse. / Fagan, S. P.; Azizzadeh, A.; Moldovan, S.; Ray, M. K.; Adrian, T. E.; Ding, X.; Coy, D. H.; Brunicardi, F. C.; Andersen, Dana.

In: Surgery, Vol. 124, No. 2, 1998, p. 254-259.

Research output: Contribution to journalArticle

Fagan, SP, Azizzadeh, A, Moldovan, S, Ray, MK, Adrian, TE, Ding, X, Coy, DH, Brunicardi, FC & Andersen, D 1998, 'Insulin secretion is inhibited by subtype five somatostatin receptor in the mouse', Surgery, vol. 124, no. 2, pp. 254-259. https://doi.org/10.1016/S0039-6060(98)70128-X
Fagan SP, Azizzadeh A, Moldovan S, Ray MK, Adrian TE, Ding X et al. Insulin secretion is inhibited by subtype five somatostatin receptor in the mouse. Surgery. 1998;124(2):254-259. https://doi.org/10.1016/S0039-6060(98)70128-X
Fagan, S. P. ; Azizzadeh, A. ; Moldovan, S. ; Ray, M. K. ; Adrian, T. E. ; Ding, X. ; Coy, D. H. ; Brunicardi, F. C. ; Andersen, Dana. / Insulin secretion is inhibited by subtype five somatostatin receptor in the mouse. In: Surgery. 1998 ; Vol. 124, No. 2. pp. 254-259.
@article{b8408255857d46ce92cecff518ed1836,
title = "Insulin secretion is inhibited by subtype five somatostatin receptor in the mouse",
abstract = "Background. Recently five somatostatin receptor subtypes (SSTRs) were cloned, allowing the development of highly specific agonists to these SSTRs. Previous studies have shown a species specificity phenomenon with respect to the inhibition of insulin secretion by these selective agonists. This study was undertaken to determine which SSTR (2 or 5) is responsible for the inhibitory effect of somatostatin on glucose-stimulated mouse insulin secretion. Methods. Intact mouse islets (n = 10) were stimulated with D- glucose in the presence or absence of receptor-specific somatostatin agonists. Results. D-glucose (16. 7 mmol/L) augmented insulin secretion by 158{\%} above that seen with 3. 9 mmol/L D-glucose in the presence of DC 32-92 (SSTR5) selective agonist, D-glucose (16. 7 mmol/L) augmented insulin secretion by 64{\%} above that seen with 3. 9 mmol/L D-glucose. The presence of SSTR 5 selective agonist resulted in a significant (P",
author = "Fagan, {S. P.} and A. Azizzadeh and S. Moldovan and Ray, {M. K.} and Adrian, {T. E.} and X. Ding and Coy, {D. H.} and Brunicardi, {F. C.} and Dana Andersen",
year = "1998",
doi = "10.1016/S0039-6060(98)70128-X",
language = "English (US)",
volume = "124",
pages = "254--259",
journal = "Surgery (United States)",
issn = "0039-6060",
publisher = "Mosby Inc.",
number = "2",

}

TY - JOUR

T1 - Insulin secretion is inhibited by subtype five somatostatin receptor in the mouse

AU - Fagan, S. P.

AU - Azizzadeh, A.

AU - Moldovan, S.

AU - Ray, M. K.

AU - Adrian, T. E.

AU - Ding, X.

AU - Coy, D. H.

AU - Brunicardi, F. C.

AU - Andersen, Dana

PY - 1998

Y1 - 1998

N2 - Background. Recently five somatostatin receptor subtypes (SSTRs) were cloned, allowing the development of highly specific agonists to these SSTRs. Previous studies have shown a species specificity phenomenon with respect to the inhibition of insulin secretion by these selective agonists. This study was undertaken to determine which SSTR (2 or 5) is responsible for the inhibitory effect of somatostatin on glucose-stimulated mouse insulin secretion. Methods. Intact mouse islets (n = 10) were stimulated with D- glucose in the presence or absence of receptor-specific somatostatin agonists. Results. D-glucose (16. 7 mmol/L) augmented insulin secretion by 158% above that seen with 3. 9 mmol/L D-glucose in the presence of DC 32-92 (SSTR5) selective agonist, D-glucose (16. 7 mmol/L) augmented insulin secretion by 64% above that seen with 3. 9 mmol/L D-glucose. The presence of SSTR 5 selective agonist resulted in a significant (P

AB - Background. Recently five somatostatin receptor subtypes (SSTRs) were cloned, allowing the development of highly specific agonists to these SSTRs. Previous studies have shown a species specificity phenomenon with respect to the inhibition of insulin secretion by these selective agonists. This study was undertaken to determine which SSTR (2 or 5) is responsible for the inhibitory effect of somatostatin on glucose-stimulated mouse insulin secretion. Methods. Intact mouse islets (n = 10) were stimulated with D- glucose in the presence or absence of receptor-specific somatostatin agonists. Results. D-glucose (16. 7 mmol/L) augmented insulin secretion by 158% above that seen with 3. 9 mmol/L D-glucose in the presence of DC 32-92 (SSTR5) selective agonist, D-glucose (16. 7 mmol/L) augmented insulin secretion by 64% above that seen with 3. 9 mmol/L D-glucose. The presence of SSTR 5 selective agonist resulted in a significant (P

UR - http://www.scopus.com/inward/record.url?scp=0031858353&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031858353&partnerID=8YFLogxK

U2 - 10.1016/S0039-6060(98)70128-X

DO - 10.1016/S0039-6060(98)70128-X

M3 - Article

C2 - 9706146

AN - SCOPUS:0031858353

VL - 124

SP - 254

EP - 259

JO - Surgery (United States)

JF - Surgery (United States)

SN - 0039-6060

IS - 2

ER -