title: Lentinan depresses 3T3-L1 fat cell formation by inhibiting PPARγ/AKT signaling pathway.
abstract: We investigated the mechanism of the effect of lentinan on 3T3-L1 fat cell formation by inhibiting the peroxisome proliferator-activated receptor gamma (PPARγ)/protein kinase B (AKT) signaling pathway. 3T3-L1 fat cells were treated with 80 mM lentinan with or without the PPARγ activator, 100 mM rosiglitazone for 24 h. Reverse transcription-polymerase chain reaction was applied to detect PPARγ and AKT mRNA expression levels. Western blotting was used to detect AKT protein expression level. Compared with the control group, 80 mM lentinan increased PPARγ mRNA expression and downregulated AKT mRNA expression. After treatment with rosiglitazone, PPARγ mRNA expression increased by 78% (P < 0.05), while AKT mRNA expression decreased by 71% (P < 0.05). Lentinan treatment decreased AKT protein expression by 33%, and AKT protein expression in the lentinan and rosiglitazone co-treatment group was reduced by 28% compared with the lentinan treatment group. We found that 80 mM lentinan increased PPARγ mRNA expression and reduced AKT mRNA. Combination treatment with rosiglitazone increased this effect. This suggests that lentinan can depress 3T3-L1 fat cell formation by inhibiting the PPARγ/AKT signaling pathway.
authors.affiliation: Department of Pediatric Surgery, The Second Hospital of Shandong University, Jinan, China.
authors.forename: D G
authors.initials: DG
authors.lastname: Li
authors.affiliation: Department of Pediatric Surgery, The Second Hospital of Shandong University, Jinan, China.
authors.forename: J L
authors.initials: JL
authors.lastname: Li
authors.affiliation: Department of Pediatric Surgery, The Second Hospital of Shandong University, Jinan, China.
authors.forename: D Q
authors.initials: DQ
authors.lastname: Sun
authors.affiliation: Department of Pediatric Surgery, The Second Hospital of Shandong University, Jinan, China.
authors.forename: X B
authors.initials: XB
authors.lastname: Sun
authors.affiliation: Department of Pediatric Surgery, The Second Hospital of Shandong University, Jinan, China.
authors.forename: X G
authors.initials: XG
authors.lastname: Sun
authors.affiliation: Department of Pediatric Surgery, The Second Hospital of Shandong University, Jinan, China.
authors.forename: Q
authors.initials: Q
authors.lastname: Liu
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects; D007912:Lentinan / Q000494:pharmacology*; D051379:Mice; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D000077154:Rosiglitazone; D015398:Signal Transduction / Q000187:drug effects* / Q000235:genetics; D045162:Thiazolidinediones / Q000494:pharmacology
chemical_list: D047495:PPAR gamma; D012333:RNA, Messenger; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D007912:Lentinan; D051057:Proto-Oncogene Proteins c-akt