title: Tectorigenin regulates adipogenic differentiation and adipocytokines secretion via PPARγ and IKK/NF-κB signaling.
abstract: BACKGROUND
  Obesity is associated with a number of diseases with metabolic abnormalities such as type 2 diabetes (T2D).
  
  
  OBJECTIVE
  We investigate the effects of tectorigenin on 3T3-L1 preadipocyte differentiation and adipocytokines secretion.
  
  
  METHODS
  The effects of tectorigenin on adipocyte differentiation were studied using Oil Red O staining. Effects of tectorigenin on adipogenesis-related genes expression and adipocytokines secretion were measured by the real-time quantitative RT-PCR and ELISA method, respectively. Reporter gene assays were performed to determine the PPARγ and NF-κB transactivation. We also used [(3)H]-2-deoxy-d-glucose to study the glucose uptake, and the IKK/NF-κB signaling pathway was assessed by western blot analysis. HFD/STZ rats were used to evaluate the therapeutic efficacies of tectorigenin.
  
  
  RESULTS
  Tectorigenin 10, 25, 50, and 75 μM inhibited 3T3-L1 adipogenesis and related genes transcription. TNF-α-induced changes of IL-6, MCP-1, as well as adiponectin in 3T3-L1 were markedly reversed by tectorigenin at 75 μM. Further investigation using reporter gene revealed that tectorigenin was a partial PPARγ agonist with an IC50 value of 13.3 μM. Tectorigenin improved basal and insulin-stimulated glucose uptake in mature 3T3-L1 adipocytes. Moreover, tectorigenin antagonized TNF-α-induced NF-κB transactivation and p65 nuclear translocation. Although tectorigenin (50 and 100 mg/kg) displayed the ability to promote insulin sensitivity and improve glucose metabolism in HFD/STZ rats, it did not cause significant side effects such as body weight gain, fluid retention, or cardiac hypertrophy.
  
  
  CONCLUSIONS
  These results suggest that tectorigenin may ameliorate hyperglycemia by blocking preadipocyte differentiation and adipocytokines secretion in which PPARγ and NF-κB signaling pathways were involved.
authors: Clinical Pharmacy Laboratory, Huashan Hospital, Fudan University , Shanghai , China .
authors: Qun-Yi
authors: QY
authors: Li
authors: Li
authors: L
authors: Chen
authors: Ming-Ming
authors: MM
authors: Yan
authors: Xiao-Jin
authors: XJ
authors: Shi
authors: Ming-Kang
authors: MK
authors: Zhong
mesh_terms: D041721:3T3-L1 Cells; D050156:Adipogenesis / Q000187:drug effects / Q000502:physiology*; D054392:Adipokines / Q000378:metabolism*; D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D007529:Isoflavones / Q000494:pharmacology*; D008297:Male; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D047495:PPAR gamma / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology
chemical_list: D054392:Adipokines; D007529:Isoflavones; D016328:NF-kappa B; D047495:PPAR gamma; C120039:tectorigenin
keywords: Adipogenesis; adipocyte; inflammation; peroxisome proliferator-activated receptor γ; type 2 diabetes