title: Catechin and quercetin attenuate adipose inflammation in fructose-fed rats and 3T3-L1 adipocytes.
abstract: METHODS
  This study evaluated the capacity of dietary catechin (C), quercetin (Q), and the combination of both (CQ), to attenuate adipose inflammation triggered by high fructose (HFr) consumption in rats and by tumor necrosis factor alpha (TNF-α) in 3T3-L1 adipocytes.
  
  
  RESULTS
  In rats, HFr consumption for 6 wk caused dyslipidemia, insulin resistance, reduced plasma adiponectin, adiposity, and adipose tissue inflammation. Dietary supplementation with 20 mg/kg/day of C, Q, and CQ improved all these parameters. In 3T3-L1 adipocytes, C and Q attenuated TNF-α-induced elevated protein carbonyls, increased proinflammatory cytokine expression (MCP-1, resistin), and decreased adiponectin. The protective effects of C and Q on adipose inflammation are in part associated with their capacity to (i) decrease the activation of the mitogen-activated kinases (MAPKs) JNK and p38; and (ii) prevent the downregulation of PPAR-γ. In summary, C and Q, and to a larger extent the combination of both, attenuated adipose proinflammatory signaling cascades and regulated the balance of molecules that improve (adiponectin) or impair (TNF-α, MCP-1, resistin) insulin sensitivity.
  
  
  CONCLUSIONS
  Together, these findings suggest that dietary Q and C may have potential benefits in mitigating MetS-associated adipose inflammation, oxidative stress, and insulin resistance.
authors.affiliation: Area de Fisiología Patológica, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, e Instituto de Medicina y Biología Experimental de Cuyo (IMBECU-CONICET), Mendoza, Argentina.
authors.forename: Marcela A
authors.initials: MA
authors.lastname: Vazquez Prieto
authors.forename: Ahmed
authors.initials: A
authors.lastname: Bettaieb
authors.forename: Cecilia
authors.initials: C
authors.lastname: Rodriguez Lanzi
authors.forename: Verónica C
authors.initials: VC
authors.lastname: Soto
authors.forename: Diahann J
authors.initials: DJ
authors.lastname: Perdicaro
authors.forename: Claudio R
authors.initials: CR
authors.lastname: Galmarini
authors.forename: Fawaz G
authors.initials: FG
authors.lastname: Haj
authors.forename: Roberto M
authors.initials: RM
authors.lastname: Miatello
authors.forename: Patricia I
authors.initials: PI
authors.lastname: Oteiza
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects*; D052242:Adiponectin / Q000235:genetics / Q000378:metabolism; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D002392:Catechin / Q000494:pharmacology*; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D015536:Down-Regulation; D005632:Fructose / Q000009:adverse effects*; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy*; D007333:Insulin Resistance; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D051379:Mice; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D050050:Protein Carbonylation / Q000187:drug effects; D011794:Quercetin / Q000494:pharmacology*; D051381:Rats; D052243:Resistin / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism
chemical_list: D052242:Adiponectin; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D047495:PPAR gamma; D052243:Resistin; C499623:Retn protein, mouse; D014409:Tumor Necrosis Factor-alpha; D005632:Fructose; D002392:Catechin; D011794:Quercetin; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases
keywords: Adipokines; Adipose tissue inflammation; Flavonoids; High fructose diet; Metabolic syndrome