Open AccessLactoferrin gene knockdown leads to similar effects to iron chelation in human adipocytes
Author(s) -
MorenoNavarrete José María,
Ortega Francisco,
Moreno Maria,
Serrano Marta,
Ricart Wifredo,
FernándezReal José Manuel
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12234
Subject(s) - adipogenesis , adipocyte , lactoferrin , adipose tissue , gene knockdown , endocrinology , medicine , deferoxamine , white adipose tissue , endogeny , biology , chemistry , biochemistry , gene
In human and mice adipose tissue, lactoferrin ( LTF ) has been found to be associated with increased adipogenesis and decreased inflammatory markers. Here, we aimed to investigate the effects of LTF knockdown (KD) in human adipocyte differentiation. In addition, the effects of exogenous LTF administration and iron chelation [using deferoxamine ( DFO , 10 μM)] were tested. In both subcutaneous and visceral pre‐adipocytes, LTF KD led to decrease significantly adipogenic, lipogenic and insulin signalling‐related gene expression and a significant increase in the gene expression of inflammatory mediators. Human lactoferrin (hLf, 1 μM) administration led to recover adipocyte differentiation in LTF KD pre‐adipocytes. Interestingly, iron chelation triggered similar effects to LTF KD , decreasing significantly adipogenic gene expressions. Of note, DFO (10 μM) and hLf (1 and 10 μM) co‐administration led to a dose‐dependent recovery of adipocyte differentiation. These new data reveal that endogenous LTF biosynthesis during human adipocyte differentiation is essential to achieve this process, possibly, modulating adipocyte iron homoeostasis. hLf administration might be a useful therapeutic target in obesity‐associated adipose tissue dysfunction.