Abstract
The role of glutamine synthetase (GS) during adipocyte differentiation is unclear. Here, we assess the impact of GS on the adipocytic response to a proinflammatory challenge at different differentiation stages. GS expression at the late stages of differentiation desensitized mature adipocytes to bacterial lipopolysaccharide (LPS) by increasing intracellular glutamine levels. Furthermore, LPS-activated mature adipocytes were unable to produce inflammatory mediators; LPS sensitivity was rescued following GS inhibition and the associated drop in intracellular glutamine levels. The ability of adipocytes to differentially respond to LPS during differentiation negatively correlates to GS expression and intracellular glutamine levels. Hence, modulation of intracellular glutamine levels by GS expression represents an endogenous mechanism through which mature adipocytes control the inflammatory response.
| Original language | English |
|---|---|
| Pages (from-to) | 4807-4814 |
| Number of pages | 8 |
| Journal | FEBS Letters |
| Volume | 588 |
| Issue number | 24 |
| DOIs | |
| Publication status | Published - Dec 20 2014 |
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Keywords
- Adipocyte
- Glutamine
- Glutamine synthetase
- Inflammation
- Metabolic syndrome
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Cell Biology
- Genetics
- Molecular Biology
- Structural Biology
- Medicine(all)
Cite this
Glutamine synthetase desensitizes differentiated adipocytes to proinflammatory stimuli by raising intracellular glutamine levels. / Palmieri, Erika Mariana; Spera, Iolanda; Menga, Alessio; Infantino, Vittoria; Iacobazzi, Vito; Castegna, Alessandra.
In: FEBS Letters, Vol. 588, No. 24, 20.12.2014, p. 4807-4814.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Glutamine synthetase desensitizes differentiated adipocytes to proinflammatory stimuli by raising intracellular glutamine levels
AU - Palmieri, Erika Mariana
AU - Spera, Iolanda
AU - Menga, Alessio
AU - Infantino, Vittoria
AU - Iacobazzi, Vito
AU - Castegna, Alessandra
PY - 2014/12/20
Y1 - 2014/12/20
N2 - The role of glutamine synthetase (GS) during adipocyte differentiation is unclear. Here, we assess the impact of GS on the adipocytic response to a proinflammatory challenge at different differentiation stages. GS expression at the late stages of differentiation desensitized mature adipocytes to bacterial lipopolysaccharide (LPS) by increasing intracellular glutamine levels. Furthermore, LPS-activated mature adipocytes were unable to produce inflammatory mediators; LPS sensitivity was rescued following GS inhibition and the associated drop in intracellular glutamine levels. The ability of adipocytes to differentially respond to LPS during differentiation negatively correlates to GS expression and intracellular glutamine levels. Hence, modulation of intracellular glutamine levels by GS expression represents an endogenous mechanism through which mature adipocytes control the inflammatory response.
AB - The role of glutamine synthetase (GS) during adipocyte differentiation is unclear. Here, we assess the impact of GS on the adipocytic response to a proinflammatory challenge at different differentiation stages. GS expression at the late stages of differentiation desensitized mature adipocytes to bacterial lipopolysaccharide (LPS) by increasing intracellular glutamine levels. Furthermore, LPS-activated mature adipocytes were unable to produce inflammatory mediators; LPS sensitivity was rescued following GS inhibition and the associated drop in intracellular glutamine levels. The ability of adipocytes to differentially respond to LPS during differentiation negatively correlates to GS expression and intracellular glutamine levels. Hence, modulation of intracellular glutamine levels by GS expression represents an endogenous mechanism through which mature adipocytes control the inflammatory response.
KW - Adipocyte
KW - Glutamine
KW - Glutamine synthetase
KW - Inflammation
KW - Metabolic syndrome
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UR - http://www.scopus.com/inward/citedby.url?scp=84915755954&partnerID=8YFLogxK
U2 - 10.1016/j.febslet.2014.11.015
DO - 10.1016/j.febslet.2014.11.015
M3 - Article
VL - 588
SP - 4807
EP - 4814
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 24
ER -