Pancreatic polypeptide inhibits somatostatin secretion

Wook Kim; Jennifer L. Fiori; Yu Kyong Shin; Eitan Okun; Jung Seok Kim; Peter R. Rapp; Josephine M. Egan

doi:10.1016/j.febslet.2014.07.005

Pancreatic polypeptide inhibits somatostatin secretion

Wook Kim
, Jennifer L. Fiori
, Yu Kyong Shin
, Eitan Okun
, Jung Seok Kim
, Peter R. Rapp
, Josephine M. Egan

The Mina and Everard Goodman Faculty of Life Sciences - at Bar-Ilan University

Ajou University
National Institutes of Health

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

35 Scopus citations

Abstract

Pancreatic polypeptide (PP) is a major agonist for neuropeptide Y4 receptors (NPY4R). While NPY4R has been identified in various tissues, the cells on which it is expressed and its function in those cells has not been clearly delineated. Here we report that NPY4R is present in all somatostatin-containing cells of tissues that we tested, including pancreatic islets, duodenum, hippocampus, and hypothalamus. Its agonism by PP decreases somatostatin secretion from human islets. Mouse embryonic hippocampal (mHippo E18) cells expressed NPY4Rs and their activation by PP consistently decreased somatostatin secretion. Furthermore, central injection of PP in mice induced c-Fos immunoreactivity in somatostatin-containing cells in the hippocampus compared with PBS-injected mice. In sum, our results identify PP as a pivotal modulator of somatostatin secretion.

Original language	English
Pages (from-to)	3233-3239
Number of pages	7
Journal	FEBS Letters
Volume	588
Issue number	17
Early online date	11 Jul 2014
DOIs	https://doi.org/10.1016/j.febslet.2014.07.005
State	Published - 25 Aug 2014

Bibliographical note

Funding Information:
This work was supported by the Intramural Research Program of the National Institute on Aging (NIA)/NIH. W.K was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future (NRF-2012R1A1A1041352) and the Ministry of Education (No. 2009-0093826).

Funding

This work was supported by the Intramural Research Program of the National Institute on Aging (NIA)/NIH. W.K was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future (NRF-2012R1A1A1041352) and the Ministry of Education (No. 2009-0093826).

Funders	Funder number
Ministry of Science, ICT & Future	NRF-2012R1A1A1041352
National Institutes of Health
National Institute on Aging	ZIAAG000352
Ministry of Education	2009-0093826
National Research Foundation of Korea

Keywords

NPY4 receptor
Pancreatic polypeptide
Somatostatin secretion

Access to Document

10.1016/j.febslet.2014.07.005

Cite this

@article{27b4692cc3254df3a860b8f1474640a1,

title = "Pancreatic polypeptide inhibits somatostatin secretion",

abstract = "Pancreatic polypeptide (PP) is a major agonist for neuropeptide Y4 receptors (NPY4R). While NPY4R has been identified in various tissues, the cells on which it is expressed and its function in those cells has not been clearly delineated. Here we report that NPY4R is present in all somatostatin-containing cells of tissues that we tested, including pancreatic islets, duodenum, hippocampus, and hypothalamus. Its agonism by PP decreases somatostatin secretion from human islets. Mouse embryonic hippocampal (mHippo E18) cells expressed NPY4Rs and their activation by PP consistently decreased somatostatin secretion. Furthermore, central injection of PP in mice induced c-Fos immunoreactivity in somatostatin-containing cells in the hippocampus compared with PBS-injected mice. In sum, our results identify PP as a pivotal modulator of somatostatin secretion.",

keywords = "NPY4 receptor, Pancreatic polypeptide, Somatostatin secretion",

author = "Wook Kim and Fiori, \{Jennifer L.\} and Shin, \{Yu Kyong\} and Eitan Okun and Kim, \{Jung Seok\} and Rapp, \{Peter R.\} and Egan, \{Josephine M.\}",

note = "Funding Information: This work was supported by the Intramural Research Program of the National Institute on Aging (NIA)/NIH. W.K was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT \& Future (NRF-2012R1A1A1041352) and the Ministry of Education (No. 2009-0093826).",

year = "2014",

month = aug,

day = "25",

doi = "10.1016/j.febslet.2014.07.005",

language = "אנגלית",

volume = "588",

pages = "3233--3239",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "John Wiley and Sons Inc.",

number = "17",

}

TY - JOUR

T1 - Pancreatic polypeptide inhibits somatostatin secretion

AU - Kim, Wook

AU - Fiori, Jennifer L.

AU - Shin, Yu Kyong

AU - Okun, Eitan

AU - Kim, Jung Seok

AU - Rapp, Peter R.

AU - Egan, Josephine M.

N1 - Funding Information: This work was supported by the Intramural Research Program of the National Institute on Aging (NIA)/NIH. W.K was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future (NRF-2012R1A1A1041352) and the Ministry of Education (No. 2009-0093826).

PY - 2014/8/25

Y1 - 2014/8/25

N2 - Pancreatic polypeptide (PP) is a major agonist for neuropeptide Y4 receptors (NPY4R). While NPY4R has been identified in various tissues, the cells on which it is expressed and its function in those cells has not been clearly delineated. Here we report that NPY4R is present in all somatostatin-containing cells of tissues that we tested, including pancreatic islets, duodenum, hippocampus, and hypothalamus. Its agonism by PP decreases somatostatin secretion from human islets. Mouse embryonic hippocampal (mHippo E18) cells expressed NPY4Rs and their activation by PP consistently decreased somatostatin secretion. Furthermore, central injection of PP in mice induced c-Fos immunoreactivity in somatostatin-containing cells in the hippocampus compared with PBS-injected mice. In sum, our results identify PP as a pivotal modulator of somatostatin secretion.

AB - Pancreatic polypeptide (PP) is a major agonist for neuropeptide Y4 receptors (NPY4R). While NPY4R has been identified in various tissues, the cells on which it is expressed and its function in those cells has not been clearly delineated. Here we report that NPY4R is present in all somatostatin-containing cells of tissues that we tested, including pancreatic islets, duodenum, hippocampus, and hypothalamus. Its agonism by PP decreases somatostatin secretion from human islets. Mouse embryonic hippocampal (mHippo E18) cells expressed NPY4Rs and their activation by PP consistently decreased somatostatin secretion. Furthermore, central injection of PP in mice induced c-Fos immunoreactivity in somatostatin-containing cells in the hippocampus compared with PBS-injected mice. In sum, our results identify PP as a pivotal modulator of somatostatin secretion.

KW - NPY4 receptor

KW - Pancreatic polypeptide

KW - Somatostatin secretion

UR - https://www.scopus.com/pages/publications/84906236230

U2 - 10.1016/j.febslet.2014.07.005

DO - 10.1016/j.febslet.2014.07.005

M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???

C2 - 25019573

AN - SCOPUS:84906236230

SN - 0014-5793

VL - 588

SP - 3233

EP - 3239

JO - FEBS Letters

JF - FEBS Letters

IS - 17

ER -

Pancreatic polypeptide inhibits somatostatin secretion

Abstract

Bibliographical note

Funding

Keywords

Access to Document

Other files and links

Fingerprint

Cite this