4.2 Article

Niacin promotes adipogenesis by reducing production of anti-adipogenic PGF2α through suppression of C/EBPβ-activated COX-2 expression

Journal

PROSTAGLANDINS & OTHER LIPID MEDIATORS
Volume 94, Issue 3-4, Pages 96-103

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.prostaglandins.2011.01.002

Keywords

Niacin; C/EBP beta; COX-2; PGF(2 alpha); Adipocytes

Funding

  1. Ministry of Education, Culture, Sports, Science and Technology of Japan [21570151]
  2. Japanese Biochemical Society
  3. Japan Foundation for Applied Enzymology
  4. Takeda Science Foundation
  5. Grants-in-Aid for Scientific Research [21570151] Funding Source: KAKEN

Ask authors/readers for more resources

Niacin is converted to NAD and NADP in tissues, whose products are involved in a number of cellular processes; and it is associated with the regulation of adipogenesis. In this study, we identified the molecular mechanism by which niacin promotes the adipogenesis in mouse 3T3-L1 cells. When the cells were cultured with niacin, the expression of adipogenic peroxisome proliferator-activated receptor gamma, CCAAT enhancer binding protein (C/EBP)alpha, and their target genes was enhanced concomitant with an increase in triglyceride storage. Moreover, niacin suppressed the expression of cyclooxygenase-2 and decreased the production of prostaglandin (PG) F-2 alpha in the early phase of adipogenesis, which PG suppresses the progression of adipogenesis via the PGF(2 alpha) receptor. Furthermore, niacin decreased the C/EBP beta level in the early phase of adipogenesis. These results indicate that niacin promoted adipogenesis by suppressing the production of the anti-adipogenic PGF(2 alpha) through down-regulation of C/EBP beta-activated cyclooxygenase-2 expression in adipocytes. (C) 2011 Elsevier Inc. All rights reserved.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.2
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available