Regulation of the pro-inflammatory cytokine osteopontin by GIP in adipocytes - A role for the transcription factor NFAT and phosphodiesterase 3B.
Omar, Bilal LU ; Banke, Elin LU ; Guiguis, Emilia ; Kesson, Lina ; Manganiello, Vincent ; Lyssenko, Valeriya LU ; Groop, Leif LU ; Gomez, Maria LU
and Degerman, Eva
LU
(2012)
In Biochemical and Biophysical Research Communications
425(4).
p.812-817
- Abstract
- The incretin - glucose-dependent insulinotropic polypeptide (GIP) - and the pro-inflammatory cytokine osteopontin are known to have important roles in the regulation of adipose tissue functions. In this work we show that GIP stimulates lipogenesis and osteopontin expression in primary adipocytes. The GIP-induced increase in osteopontin expression was inhibited by the NFAT (the transcription factor nuclear factor of activated T-cells) inhibitor A285222. Also, the NFAT kinase glycogen synthase kinase (GSK) 3 was upregulated by GIP. To test whether cAMP might be involved in GIP mediated effects on osteopontin a number of strategies were used. Thus, the β3-adrenergic receptor aganist CL316,243 stimulated osteopontin expression, an effects... (More)
- The incretin - glucose-dependent insulinotropic polypeptide (GIP) - and the pro-inflammatory cytokine osteopontin are known to have important roles in the regulation of adipose tissue functions. In this work we show that GIP stimulates lipogenesis and osteopontin expression in primary adipocytes. The GIP-induced increase in osteopontin expression was inhibited by the NFAT (the transcription factor nuclear factor of activated T-cells) inhibitor A285222. Also, the NFAT kinase glycogen synthase kinase (GSK) 3 was upregulated by GIP. To test whether cAMP might be involved in GIP mediated effects on osteopontin a number of strategies were used. Thus, the β3-adrenergic receptor aganist CL316,243 stimulated osteopontin expression, an effects which was mimicked by OPC3911, a specific inhibitor of phosphodiesterase 3. Furthermore, treatment of phosphodiesterase 3B knock-out mice with CL316,243 resulted in a dramatic upregulation of osteopontin in adipose tissue which was not the case in wild-type mice. In summary, we delineate mechanisms by which GIP stimulate osteopontin in adipocytes. Given the established link between osteopontin and insulin resistance, our data suggest that GIP by stimulating osteopontin expression, also could promote insulin resistance in adipocytes. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/3047510
- author
- Omar, Bilal
LU
; Banke, Elin
LU
; Guiguis, Emilia
; Kesson, Lina
; Manganiello, Vincent
; Lyssenko, Valeriya
LU
; Groop, Leif
LU
; Gomez, Maria
LU
and Degerman, Eva
LU
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Biochemical and Biophysical Research Communications
- volume
- 425
- issue
- 4
- pages
- 812 - 817
- publisher
- Elsevier
- external identifiers
-
- wos:000309017700020
- pmid:22892131
- scopus:84865991405
- pmid:22892131
- ISSN
- 1090-2104
- DOI
- 10.1016/j.bbrc.2012.07.157
- language
- English
- LU publication?
- yes
- id
- 9a6d1ef4-625f-4198-9fb0-d062071ed22e (old id 3047510)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/22892131?dopt=Abstract
- date added to LUP
- 2016-04-01 14:08:23
- date last changed
- 2024-01-09 23:20:11
@article{9a6d1ef4-625f-4198-9fb0-d062071ed22e,
abstract = {{The incretin - glucose-dependent insulinotropic polypeptide (GIP) - and the pro-inflammatory cytokine osteopontin are known to have important roles in the regulation of adipose tissue functions. In this work we show that GIP stimulates lipogenesis and osteopontin expression in primary adipocytes. The GIP-induced increase in osteopontin expression was inhibited by the NFAT (the transcription factor nuclear factor of activated T-cells) inhibitor A285222. Also, the NFAT kinase glycogen synthase kinase (GSK) 3 was upregulated by GIP. To test whether cAMP might be involved in GIP mediated effects on osteopontin a number of strategies were used. Thus, the β3-adrenergic receptor aganist CL316,243 stimulated osteopontin expression, an effects which was mimicked by OPC3911, a specific inhibitor of phosphodiesterase 3. Furthermore, treatment of phosphodiesterase 3B knock-out mice with CL316,243 resulted in a dramatic upregulation of osteopontin in adipose tissue which was not the case in wild-type mice. In summary, we delineate mechanisms by which GIP stimulate osteopontin in adipocytes. Given the established link between osteopontin and insulin resistance, our data suggest that GIP by stimulating osteopontin expression, also could promote insulin resistance in adipocytes.}},
author = {{Omar, Bilal and Banke, Elin and Guiguis, Emilia and Kesson, Lina and Manganiello, Vincent and Lyssenko, Valeriya and Groop, Leif and Gomez, Maria and Degerman, Eva}},
issn = {{1090-2104}},
language = {{eng}},
number = {{4}},
pages = {{812--817}},
publisher = {{Elsevier}},
series = {{Biochemical and Biophysical Research Communications}},
title = {{Regulation of the pro-inflammatory cytokine osteopontin by GIP in adipocytes - A role for the transcription factor NFAT and phosphodiesterase 3B.}},
url = {{https://lup.lub.lu.se/search/files/3811340/3222343.pdf}},
doi = {{10.1016/j.bbrc.2012.07.157}},
volume = {{425}},
year = {{2012}},
}