Glycine suppresses TNF-α-induced activation of NF-κB in differentiated 3T3-L1 adipocytes.
Glycine strongly reduces the serum levels of pro-inflammatory cytokines and increases the levels of anti-inflammatory cytokines. Recently, glycine has been shown to decrease the expression and secretion of pro-inflammatory adipokines in monosodium glutamate-induced obese (MSG/Ob) mice. It has been postulated that these effects may be explained by a reduction in nuclear factor kappa B (NF-κB) activation. NF-κB is a transcription factor, which is crucial to the inflammatory response. Hasegawa et al. (2011 and 2012) recently reported a glycine-dependent reduction in NF-κB levels. Here, we have investigated the role of glycine in the regulation of NF-κB in differentiated 3T3-L1 adipocytes. The results revealed that pretreatment with glycine interfered with the activation of NF-κB, which has been shown to be stimulated by tumor necrosis factor-alpha (TNF-α). Glycine alone stimulated NF-κB activation in an unusual way such that the inhibitor κB-β (IκB-β) degradation was more significant than that of the inhibitor κB-α (IκB-α) and led to NF-κB complexes comprised of p50 and p65 subunits; IκB-ε degradation did not affect by glycine. These findings suggest that glycine could be used as an alternative treatment for chronic inflammation, which is a hallmark of obesity and other comorbidities, and is characterized by an elevated production of pro-inflammatory cytokines.
Programa de Doctorado del Posgrado en Biología Experimental. D.C.B.S., Universidad Autónoma Metropolitana-Iztapalapa, Apdo-Postal 55-535, CP 09340, México, D.F. México. gera@xanum.uam.mx
Gerardo
G
Blancas-Flores
Francisco J
FJ
Alarcón-Aguilar
Rebeca
R
García-Macedo
Julio C
JC
Almanza-Pérez
José L
JL
Flores-Sáenz
Rubén
R
Román-Ramos
José L
JL
Ventura-Gallegos
Jesús
J
Kumate
Alejandro
A
Zentella-Dehesa
Miguel
M
Cruz
D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D005998:Glycine / Q000494:pharmacology*; D051379:Mice; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000096:biosynthesis*
D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D005998:Glycine