Adiponectin, a circulating adipocyte-derived secretory
protein, reportedly plays an important role in
liver fibrosis development, although the
biological role of
adiponectin in liver fibrogenesis is still controversial.
Adiponectin is present in the serum as three oligometric complexes; namely, high-, middle-, and low-molecular weight (HMW, MMW, and LMW, respectively).
Adiponectin exerts different
biological activities in an oligomerization-dependent manner. The aim of our current study was to examine the alteration of each
isoform of
adiponectin and its receptors (AdipoR1, AdipoR2, and
T-cadherin) during the
choline-deficient L-
amino acid-defined (
CDAA) diet-induced rat
liver fibrosis development. We also elucidated the methylation status of all receptors. The serum level of total
adiponectin significantly increased during the
liver fibrosis development. Among the three
isoforms, only HMW
adiponectin was significantly up-regulated whereas MMW and LMW were not. The expression of
T-cadherin, which exclusively binds with HMW
adiponectin, was significantly augmented as well. The AdipoR2 expression was markedly decreased and showed no marked difference from that of AdipoR1. No obvious methylation change was observed in all three receptors, suggesting that another mechanism is involved in the alteration of receptor gene expression. Collectively, since the specific
ligand and receptor were augmented together, crosstalk between HMW
adiponectin and
T-cadherin may play an important role during
liver fibrosis development in rats.