1999 Fiscal Year Final Research Report Summary
Biological Roles of PPAR-γ and C/EBP on Adipogenesis and SCD-1 Gene Expression
Project/Area Number |
10671066
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Metabolomics
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Research Institution | Osaka University |
Principal Investigator |
KASAYAMA Soji Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (10240839)
|
Co-Investigator(Kenkyū-buntansha) |
SAITO Hiroshi Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (90301259)
|
Project Period (FY) |
1998 – 1999
|
Keywords | adipocyte / C / EBP / PPAR-γ / knockout mouse / thiazolidinedione / SCD-1 / molecular biology |
Research Abstract |
It is shown that C/EBP family proteins and PPAR-γ play important roles on adipocyte differentiation. However, the precise roles of each molecule have not been defined. To explore this issue, we transfected C/EBP-β and -δ double knockout mouse embryonic fibroblasts with adenovirus vector containing mouse PPAR-γ2 (pAdex-mPPARγ2). When the pAdex-mPPARγ2-transfected cells were stimulated with troglitazone or 15-deoxy-△ィイD112.14ィエD1-PGJ2, they became to show mature adipocyte phenotype stained with oil-red-O. Intracellular triglyceride content and SCD-1 and aP2 mRNA levels of these cells did not differ, compared with wild-type mouse embryonic fibroblasts transfected with pAdex-mPPARγ2. However, LPL and GLUT4 mRNA levels were significantly lower in these cells. Thus, forced expression of PPAR-γ2 alone can induce adipocyte differentiation in the absence of C/EBP-β and C/EBP-γ, although C/EBP-β and /or C/EBP-δ are important for the expression of some adipocyte-specific genes.
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[Publications] Motomura, T., Hashimoto, K., Koga, M., Arita, N., Hayakawa, T., Kishimoto, T. and Kasayama, S.: "Inhibition of signal transduction by a splice variant of the growth hormone-releasing hormone receptor expressed in human pituitary adenomas."Metabolism. 47. 804-808 (1998)
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「研究成果報告書概要(欧文)」より
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[Publications] Motomura, T., Kasayama, S., Takagi, M., Kurebayashi S., Matsui, H., Hirose, T., Miyashita, Y., Yamauchi-Takihara, K., Yamamoto, T., Okada, S. and Kishimoto, T.: "Increased interleukin-6 production in mouse osteoblastic MC3T3-E1 cells expressing activating mutant of the stimulatory G protein."J. Bone Miner. Res. 13. 1084-1091 (1998)
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[Publications] Yamamoto, H., Kurebayashi, S., Hirose, T., Sumitani, S., Kouhara, H., Kishimoto, T. and Kasayama, S.: "Forced expression of PPARγ2 induces adipogenesis in C/EBP-β, -δ deficient mouse embryonic fibroblasts (MEF)."Diabetes. 48 (Supple 1). A7
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[Publications] Takagi, M., Miyashita, Y., Koga, M., Ebara, S., Arita, N. and Kasayama, S.: "Estrogen deficiency is a potential cause for osteopenia in adult male patients with Noonan's syndrome."Calc. Tissue Int. 66. 200-203 (2000)
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[Publications] Kasayama, S., Otsuki, M., Takagi, M., Saito, H., Sumitani, S., Kouhara, H., Koga, M., Saitoh, Y., Ohnishi, T. and Arita, N.: "Impaired β-cell function in the presence of reduced insulin sensitivity determines glucose tolerance status in acromegalic patients."Clin. Endocrinol.. (in press). (2000)
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「研究成果報告書概要(欧文)」より