Greenberg A S, Nordan R P, McIntosh J, Calvo J C, Scow R O, Jablons D
Laboratory of Cellular and Developmental Biology, National Institute of Diabetes, Digestive and Kidney Disease, NIH, Bethesda, Maryland 20892.
Cancer Res. 1992 Aug 1;52(15):4113-6.
To investigate whether interleukin 6 (IL-6) might be a potential mediator of the depleted fat reserves observed in malignancy-associated cachexia, we measured lipoprotein lipase (LPL) activity in adipose tissue of mice after administration of IL-6 or tumor necrosis factor and in cultured adipocytes after addition of these cytokines. Injection of IL-6 i.p. reduced adipose tissue LPL activity by 53% within 4.5 to 5.5 h. Injection of tumor necrosis factor elevated serum IL-6 levels and reduced adipose tissue LPL activity by 70%. Both human and murine IL-6 reduced heparin-releasable LPL activity in 3T3-L1 adipocytes in a dose-dependent manner; half-maximal inhibition of LPL activity was achieved with 5000 hybridoma growth factor units/ml. Thus, IL-6 reduces adipose LPL activity and may contribute to the loss of body fat stores associated with some cases of cancer cachexia. Since tumor necrosis factor increases circulating IL-6, some of its effects may be mediated or potentiated by IL-6.
为了研究白细胞介素6（IL-6）是否可能是恶性肿瘤相关性恶病质中脂肪储备减少的潜在介质，我们在给予IL-6或肿瘤坏死因子后，测量了小鼠脂肪组织中的脂蛋白脂肪酶（LPL）活性，并在添加这些细胞因子后测量了培养脂肪细胞中的LPL活性。腹腔注射IL-6在4.5至5.5小时内使脂肪组织LPL活性降低了53%。注射肿瘤坏死因子可提高血清IL-6水平，并使脂肪组织LPL活性降低70%。人源和鼠源IL-6均以剂量依赖性方式降低3T3-L1脂肪细胞中肝素可释放的LPL活性；5000杂交瘤生长因子单位/毫升可实现LPL活性的半数最大抑制。因此，IL-6降低脂肪组织LPL活性，并可能导致某些癌症恶病质病例中体脂储备的减少。由于肿瘤坏死因子会增加循环中的IL-6，其某些作用可能由IL-6介导或增强。
