Even though a HF diet itself did not reduce Mfn and UCP levels in liver tissues, the CoPP-mediated increase was effectively reduced in mice concomitantly treated with the HO-inhibitor, SnMP, corroborating our recent report showing that impaired HO-expression and activity decrease mitochondrial function in adipose tissues of obese mice and 3T3-L1-derived adipocytes, contributing to increased mitochondrial derived superoxide formation [12, 46]. This evidence concerns the gene UCP1 and hydrops fetalis.