Tumor necrosis factor (TNF)-α acts directly on adipocytes to increase production of the lipostatic factor, leptin. However, which TNF receptor (TNFR) mediates this response is not known. To answer this question, leptin was measured in plasma of wild-type (WT), p55, and p75 TNFR knockout (KO) mice injected intraperitoneally with murine TNF-α and in supernatants from cultured WT, p55, and p75 TNFR KO adipocytes incubated with TNF-α. Leptin also was measured in supernatants from C3H/HeOuJ mouse adipocytes cultured with blocking antibodies to each TNFR and TNF-α as well as in supernatants from adipocytes incubated with either human or murine TNF-α, which activate either one or both TNFR, respectively. The results using all four strategies show that the induction of leptin production by TNF-α requires activation of the p55 TNFR and that although activation of the p75 TNFR alone cannot cause leptin production, its presence affects the capability of TNF-α to induce leptin production through the p55 TNFR. These results provide new information on the interplay between cells of the immune system and adipocytes.
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||2 47-2|
|State||Published - Feb 2000|
- Ob gene
- Tumor necrosis factor receptor