Authors: MacLaren, R.; Kalant, D.; Cianflone, K.

Source: Biochemistry and Cell Biology, Volume 85, Number 1, February 2007 , pp. 11-21(11)

Publisher: NRC Research Press

Abstract:

Acylation-stimulating protein (ASP) and interaction with its receptor C5L2 influences adipocyte metabolism. We examined insulin resistance and differentiation-mediated regulation of C5L2 and the mechanistic impact on both C5L2 cell-surface protein and ligand binding to the receptor. C5L2 mRNA increased 8.7-fold with differentiation in 3T3-L1 cells (p< 0.0001) by day 9. In preadipocytes, insulin and dexamethasone increased C5L2 mRNA (1 μmol/L insulin resulted in a 2.6-fold increase, p< 0.01; 10 nmol/L dexamethasone resulted in a 17.9-fold increase, p< 0.01) and C5L2 cell-surface protein (100 nmol insulin resulted in a 2.7-fold increase, p< 0.001; 10 nmol/L dexamethasone resulted in a 2.8-fold increase, p< 0.001). In adipocytes, 100nmol/L insulin increased C5L2 mRNA and ASP binding (respectively, 1.3-fold, p< 0.01; and 2.4-fold, p< 0.05). Dexamethasone decreased ligand binding (-60%, p< 0.02) without changing mRNA. Tumor necrosis factor alpha decreased C5L2 mRNA (-88% in preadipocytes and-38% in adipocytes, p< 0.001), C5L2 cell-surface protein (-53% in preadipocytes, p< 0.0001), and ASP binding (-60% and-49% in, respectively, preadipocytes and adipoctyes, p< 0.05). Conversely, 1 μmol/L and 10 nmol/L rosiglitazone increased, respectively, C5L2 mRNA (9.3-fold, p< 0.0001) and ASP binding (2.4-fold, p< 0.05). Thus, C5L2 mRNA increases with differentiation, insulin, and thiazolidinedione treatment, and decreases with tumor necrosis factor alpha, all of which results in functional changes in ASP-C5L2 response and may have implications for human metabolism.

La protéine ASP, qui stimule l'acylation, ainsi que son interaction avec le récepteur C5L2 influence le métabolisme de l'adipocyte. Nous avons examiné la régulation de l'expression de C5L2 en fonction de la résistance à l'insuline et de la différenciation, de même que l'impact mécanistique de ces derniers sur l'expression de la protéine C5L2 à la surface cellulaire et sa liaison à son ligand. L'ARNm de C5L2 a augmenté de 8.7 fois en fonction de la différenciation des cellules 3T3-L1 (p < 0.0001) au jour 9. Chez les préadipocytes, l'insuline et la dexaméthasone augmentent les niveaux d'ARNm (2.6 fois, 1 μmol/L insuline, p < 0.01; 17.9 fois, 10 nmol/L DEX, p < 0.01) et de protéine C5L2 à la surface cellulaire (2.7 fois, 100 nmol/L insuline, p < 0.001; 2.8 fois, 10 nmol/L DEX, p < 0.001). Chez les adipocytes, l'insuline a augmenté les niveaux d'ARNm de C5L2 et la liaison de l'ASP (1.3 fois, p < 0.01; et 2.4 fois, p < 0.05, 100 nmol/L). La dexaméthasone a diminué la liaison du ligand (-60%, p < 0.02) sans changer les niveaux d'ARNm. Le TNF-α a diminué les niveaux d'ARNm de C5L2 (-88% chez les préadipocytes, -38% chez les adipocytes, p < 0.001), l'expression de surface de la protéine C5L2 (-53% chez les préadipocytes, p < 0.0001), et de la liaison de l'ASP (-60% et -49%, préadipocytes/adipocytes, p < 0.05). À l'inverse, la roglitazone a augmenté la quantité d'ARNm de C5L2 (9.3 fois, 1 μmol/L, p < 0.0001) et la liaison de l'ASP (2.4 fois, 10 nmol/L, p < 0.05). Ainsi, les niveaux d'ARNm de C5L2 sont augmentés en fonction de la différenciation et des traitements à l'insuline et à une thiazolinedione, et ont diminué en présence de TNF-α, résultant en changements fonctionnels de la réponse ASP-C5L2 ce qui pourrait avoir des implications dans le statut métabolique chez l'humain.

Document Type: Research article

Publication date: 2007-02-01

More about this publication?

• Published since 1929, this bimonthly journal explores every aspect of general biochemistry and includes up-to-date coverage of experimental research into cellular and molecular biology, as well as review articles on topics of current interest and notes contributed by recognized international experts. Special issues each year are dedicated to expanding new areas of research in biochemistry and cell biology.
• Information for Authors
• Submit a Paper
• Subscribe to this Title
• Terms & Conditions
• Sample Issue
• Reprints & Permissions
• ingentaconnect is not responsible for the content or availability of external websites

Related content

• In this: publication
• By this: publisher
• In this Subject: Anatomy & Physiology ,  Biology ,  Organic Chemistry ,  Biochemistry
• By this author: MacLaren, R. ;  Kalant, D. ;  Cianflone, K.

Website © Publishing Technology. Article copyright remains with the publisher, society or author(s) as specified within the article.

• Terms and conditions
• Privacy policy
• Information for advertisers