| First Author | López-Soriano J | Year | 1997 |
| Journal | Mol Cell Endocrinol | Volume | 132 |
| Issue | 1-2 | Pages | 93-9 |
| PubMed ID | 9324050 | Mgi Jnum | J:42776 |
| Mgi Id | MGI:1096262 | Doi | 10.1016/s0303-7207(97)00125-1 |
| Citation | Lopez-Soriano J, et al. (1997) Lipid metabolism in tumour-bearing mice: studies with knockout mice for tumour necrosis factor receptor 1 protein. Mol Cell Endocrinol 132(1-2):93-9 |
| abstractText | The implantation of the Lewis lung carcinoma (a fast-growing mouse tumour that induces cachexia) to both wild-type and gene-deficient mice for the tumour necrosis factor (TNF) receptor type I protein (Tnfr1(0)/Tnfr1(0)), resulted in a considerable loss of carcass (26%) and white (77%) and brown adipose (37%) tissue weights in the wild-type mice, while it induced much less marked effects in the gene-deficient mice. Tumour burden also inflicted an important decrease in total lipoprotein lipase (LPL) activity in epididymal white adipose tissue (50%) in the wild-type mice while no changes were observed in the knockout mice. In addition, all tumour-bearing animals were clearly hypertriglyceridaemic (80% increase in circulating triacylglycerols in wild-type and 36% in knockout mice). It is concluded that although TNF seems to be to some extent responsible for adipose waste, LPL changes and hyperlipaemia (via receptor I), the role of other cytokines (alone or in combination with TNF) in promoting changes in lipid metabolism during cancer cachexia cannot be discarded. |
