Abstract
Fetuin-A (Fet-A) was one of the first hepatokines to be reportedly linked to metabolic diseases. Fet-A was also suggested to be an adipokine, but its expression in the adipose tissue remains debatable. Here we compared the expression of Fet-A between human and mice adipose tissue biopsies as well as among human subcutaneous tissue and visceral adipose tissue primary cells, and mouse 3 T3-L1 cells at various stages of differentiation. Fet-A was expressed in mice biopsies and cells but not in human biopsies and cells, except in visceral adipose tissue primary cells following differentiation. Although the marginal expression of Fet-A in human visceral adipose tissue, a major contribution of Fet-A expression in human adipose tissue to systemic Fet-A levels is discounted, but it could indicate specific local Fet-A action in the visceral adipose tissue.
Highlights
The hepatokine fetuin-A (Fet-A) is linked to obesity and type 2 diabetes, but the causality of the association was not supported by a recent Mendelian study in a global population [1]
Recent studies suggested that Fet-A is an adipokine; its expression in adipose tissue remains unclear depending on the type of cells and species investigated [5, 6]
We assessed Fet-A levels in plasma and human subcutaneous adipose tissue of obese adults with and without diabetes [6] and found that Fet-A protein levels in hSAT were significantly increased in obese adults with diabetes
Summary
The hepatokine fetuin-A (Fet-A) is linked to obesity and type 2 diabetes, but the causality of the association was not supported by a recent Mendelian study in a global population [1]. High Fet-A levels are linked to obesity, metabolic syndromes, and diabetes [4]. Recent studies suggested that Fet-A is an adipokine; its expression in adipose tissue remains unclear depending on the type of cells and species investigated [5, 6].
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