| First Author | Granowitz EV | Year | 1997 |
| Journal | Biochem Biophys Res Commun | Volume | 240 |
| Issue | 2 | Pages | 382-5 |
| PubMed ID | 9388486 | Mgi Jnum | J:44348 |
| Mgi Id | MGI:1099924 | Doi | 10.1006/bbrc.1997.7663 |
| Citation | Granowitz EV (1997) Transforming growth factor-beta enhances and pro-inflammatory cytokines inhibit ob gene expression in 3T3-L1 adipocytes. Biochem Biophys Res Commun 240(2):382-5 |
| abstractText | Leptin is a protein which is encoded by the obese (ob) gene. It is synthesized by adipocytes and binds to receptors in the hypothalamus, thereby suppressing appetite and increasing the metabolic rate. When mouse 3T3-L1 cells are induced to differentiate into adipocytes, they begin to constitutively express low levels of ob mRNA. Using reverse transcription and a semi-quantitative polymerase chain reaction, the experiments described herein demonstrate that the anti-inflammatory cytokine transforming growth factor-beta increases steady state ob mRNA. Conversely, treatment of 3T3-L1 adipocytes with the pro-inflammatory cytokines interleukin-1 beta, interleukin-6, interleukin-11, and tumor necrosis factor-alpha results in a decrease in ob transcripts. When considered in the context of animal studies showing that interleukin-1 and tumor necrosis factor-alpha induce leptin and ob mRNA, these results suggest that pro-inflammatory cytokines induce ob gene transcription in vivo via secondary mediators such as transforming growth factor-beta. |
