Leptin inhibits apolipoprotein M transcription and secretion in human hepatoma cell line, HepG2 cells.
Författare
Summary, in English
Apolipoprotein M (apoM) is a novel apolipoprotein presented mostly in high-density lipoprotein (HDL) in human plasma. Previously we have reported that both leptin and leptin receptor are essential for apoM expression in vivo. The expression of apoM is lower in the leptin deficient (ob/ob) mouse and leptin receptor deficient (db/db) mouse than in the normal mouse. In the present study, however, we demonstrated that supra-physiological concentrations of recombinant leptin significantly inhibited apoM transcription and secretion in the human hepatoma cell line, HepG2 cells. Both Northern blotting and real-time RT-PCR were applied into the analyses of apoM mRNA levels, and compatible data were obtained. The inhibitory effect of leptin on apoM mRNA levels in HepG2 cells is dose dependent, i.e. 100 ng/mL of leptin decreased apoM mRNA levels by 30%, and 500 ng/mL of leptin decreased apoM mRNA levels about 50%. Even at a physiological concentration of leptin (10 ng/mL), apoM expression was decreased, and in parallel, the secretion of apoM into the medium was also decreased. Furthermore, we examined apoAI, apoB and apoE by Northern blotting analyses. The results demonstrated that leptin does not significantly influence the expressions of apoAI, apoB and apoE in HepC2 cells, suggesting that leptin has a specific regulatory effect on hepatic apoM transcription and secretion in vitro. The mechanism on the contradictory effects of leptin on apoM expression in vivo and in vitro needs further investigation.
Avdelning/ar
Publiceringsår
2005
Språk
Engelska
Sidor
198-202
Publikation/Tidskrift/Serie
Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids
Volym
1734
Issue
2
Fulltext
Dokumenttyp
Artikel i tidskrift
Förlag
Elsevier
Ämne
- Medicinal Chemistry
- Pharmacology and Toxicology
Nyckelord
- HepG2 cell line
- lipoprotein
- apolipoprotein M
- leptin
Status
Published
ISBN/ISSN/Övrigt
- ISSN: 1388-1981