癌症恶病质中肝糖原消耗的机制。
Mechanism of depletion of liver glycogen in cancer cachexia.
作者信息
Hirai K, Ishiko O, Tisdale M
机构信息
Department of Obstetrics and Gynecology, Osaka City University Medical School, I-Asahimachi Abeno-ku, Osaka, Japan.
出版信息
Biochem Biophys Res Commun. 1997 Dec 8;241(1):49-52. doi: 10.1006/bbrc.1997.7732.
Mice transplanted with a cachexia-inducing colonic adenocarcinoma (MAC16) show a progressive decrease in liver glycogen in direct proportion to the loss of body weight. Such tumours elaborate a lipid mobilizing factor (LMF), which produces a dose-dependent stimulation, not only of adipocyte adenylate cyclase, but also of hepatocyte adenylate cyclase in a GTP-dependent manner. These results suggest that LMF has the capacity to initiate hepatic glycogenolysis through an increase in cyclic AMP.
移植了恶病质诱导性结肠腺癌（MAC16）的小鼠，其肝脏糖原呈进行性减少，且与体重减轻成正比。此类肿瘤可产生一种脂质动员因子（LMF），该因子不仅能以GTP依赖的方式剂量依赖性刺激脂肪细胞腺苷酸环化酶，还能刺激肝细胞腺苷酸环化酶。这些结果表明，LMF有能力通过增加环磷酸腺苷来启动肝糖原分解。
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