Glycine increases mRNA adiponectin and diminishes pro-inflammatory adipokines expression in 3T3-L1 cells.
Obesity and type 2 diabetes course with chronic low-grade inflammation, where adiponectin is down-regulated and pro-inflammatory markers, like interleukin (IL)-6, tumor necrosis factor alpha (TNF-alpha), and C-reactive protein (CRP), are up-regulated. A treatment option to improve the micro- and macro-complications in type 2 diabetes is the use of glycine, which has been demonstrated previously to increase the expression of anti-inflammatory cytokine IL-10 in monocytes and down-regulate the expression of TNF-alpha in monocytes and Kupffer cells. Recently, our group demonstrated that glycine decreases the pro-inflammatory plasmatic cytokines in type 2 diabetes. The aim of this study was to test the effect of glycine on adipokines expression in 3T3-L1 cells. Cells were grown and differentiated in the presence of 10 mM glycine. After 2 days of confluence, cells were differentiated to adipocytes in the same medium supplemented with insulin, dexamethasone, and 3-isobutyl-1-methylxanthine. The RNA was extracted at days 0 and 8 of differentiation (fibroblasts and mature adipocyte phenotypes, respectively). The expression of PPAR-gamma (peroxisome proliferator-activated receptor-gamma), adiponectin, resistin, IL-6 and TNF-alpha were analyzed by real-time PCR. We demonstrated that when 3T3-L1 cells were treated with glycine, IL-6, resistin and TNF-alpha mRNA expression was decreased, but surprisingly adiponectin and PPAR-gamma were up-regulated. In all cases the values were statistically significant (P<0.05) between glycine treatment and controls. These results show that glycine improves the pro-inflammatory profile and up-regulates adiponectin gene expression. Therefore, glycine could be useful as a modulator of the pro-inflammatory state observed in obesity and type 2 diabetes.
Garcia-Macedo
Rebeca
R
Unidad de Investigacion Medica en Bioquimica, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico, D.F., Mexico. gamareb@yahoo.es
Sanchez-Muñoz
Fausto
F
Almanza-Perez
Julio Cesar
JC
Duran-Reyes
Genoveva
G
Alarcon-Aguilar
Francisco
F
Cruz
Miguel
M
D016475:3T3 Cells; D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D054392:Adipokines / Q000096:biosynthesis*; D052242:Adiponectin / Q000096:biosynthesis*; D000818:Animals; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D005998:Glycine / Q000494:pharmacology*; D015850:Interleukin-6 / Q000096:biosynthesis; D051379:Mice; D047495:PPAR gamma / Q000096:biosynthesis; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis*; D052243:Resistin / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D015854:Up-Regulation / Q000187:drug effects
D054392:Adipokines; D052242:Adiponectin; D015850:Interleukin-6; D047495:PPAR gamma; D012333:RNA, Messenger; D052243:Resistin; D014409:Tumor Necrosis Factor-alpha; D012313:RNA; D005998:Glycine