Zinc-α2-glycoprotein, a lipid mobilizing factor, is expressed in adipocytes and is up-regulated in mice with cancer cachexia

摘要: Zinc-alpha2-glycoprotein (ZAG), a 43-kDa protein, is overexpressed in certain human malignant tumors and acts as lipid-mobilizing factor to stimulate lipolysis adipocytes leading cachexia mice implanted with ZAG-producing tumors. Because white adipose tissue (WAT) an endocrine organ secreting wide range of protein factors, including those involved lipid metabolism, we have investigated whether ZAG produced locally by adipocytes. mRNA was detected RT-PCR the mouse WAT depots examined (epididymal, perirenal, s.c., mammary gland) interscapular brown fat. In WAT, gene expression evident mature stromal-vascular cells. Using Ab, located Western blotting immunohistochemistry. Mice bearing MAC16-tumor displayed substantial losses body weight fat mass, which accompanied major increases levels 3T3-L1 cells, before after induction differentiation, level increasing progressively differentiation peak at days 8-10. Both dexamethasone beta3 agonist, BRL 37344, increased were also (visceral s.c.). It suggested that new factor, may be modulation Overexpression tumor-bearing suggests local role for adipocyte-derived reduction adiposity cancer cachexia.