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Zinc-alpha2-glycoprotein in cachexia and obesity.

Michael J Tisdale¹

¹Nutritional Biomedicine, School of Life and Health Sciences, Aston University, Birmingham, B4 7ET, UK. m.j.tisdale@aston.ac.uk

Current Opinion in Supportive and Palliative Care

|October 14, 2009

Summary

Zinc-alpha2-glycoprotein (ZAG) influences adipose mass by promoting lipid breakdown in cachexia and heat generation in brown fat. Low ZAG levels are linked to obesity, while high levels are seen in cachexia.

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Area of Science:

Endocrinology
Metabolism
Adipose Tissue Biology

Background:

Adipose mass regulation is critical for managing cachexia and obesity.
Zinc-alpha2-glycoprotein (ZAG) is a novel adipokine involved in lipid mobilization and utilization.

Purpose of the Study:

To review the role of ZAG in the regulation of adipose mass.
To explore ZAG's function in both cachexia and obesity.

Main Methods:

Literature review focusing on ZAG's role in lipolysis and energy expenditure.
Analysis of ZAG expression in cachexia and obesity models.
Examination of ZAG's effects on white and brown adipose tissue.

Main Results:

ZAG increases lipolysis in white adipose tissue via the cyclic AMP pathway.
ZAG stimulates uncoupling protein-1 expression in brown adipose tissue, promoting thermogenesis.
ZAG null mice exhibit increased body weight, particularly on high-fat diets, and resistant adipocytes.

Conclusions:

ZAG plays a significant role in regulating adipose mass.
ZAG's distinct expression patterns in cachexia and obesity highlight its dual function.
Targeting ZAG may offer therapeutic potential for obesity and cachexia.