Skip Navigation LinksHome > May 2013 - Volume 16 - Issue 3 > Zinc-α2-glycoprotein as a marker of fat catabolism in humans
Current Opinion in Clinical Nutrition & Metabolic Care:
doi: 10.1097/MCO.0b013e32835f816c
TRANSLATIONAL RESEARCH IN WASTING DISEASES: Edited by Vickie E. Baracos, Didier Attaix and Claude Pichard

Zinc-α2-glycoprotein as a marker of fat catabolism in humans

Cabassi, Aderville; Tedeschi, Stefano

Collapse Box


Purpose of review: Cachexia development is a feature of cancer as well as other chronic diseases. Fat mass loss appears of greatest importance in cachexia, as it is related to poorer survival. Zinc-α2-glycoprotein (ZAG), firstly isolated in human plasma 50 years ago, has emerged as a novel adipokine, which plays an important role in mobilization and utilization of lipids. This review will focus on recent evidences of ZAG as a fat catabolic marker in cancer and other diseases complicated by cachexia.

Recent findings: ZAG is a lipolytic factor produced by certain cachexia-inducing tumuors and by adipose tissue. It increases lipolysis in white adipose tissue through cyclic-AMP pathway and stimulates uncoupling protein-1 in brown adipose tissue leading to heat generation. In cancer cachexia, ZAG release from white adipocytes is elevated and closely related to body weight loss. In cardiac cachexia, ZAG and circulating free fatty acids are closely related, suggesting a causative role in fat catabolism.

Summary: ZAG may play an important role, probably as an autocrine/paracrine modulator of adipose mass in cachexia. A better comprehension of ZAG involvement in fat wasting mechanisms will be useful in the development of new therapeutic agents.

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins


Article Tools


Article Level Metrics

Search for Similar Articles
You may search for similar articles that contain these same keywords or you may modify the keyword list to augment your search.