The Rat FABP4/AFABP ELISA Kit is used for the quantitative measurement of rat FABP4/AFABP in serum, plasma, tissue culture medium and other biological media.
Intra-assay (Within-Run, n=16), CV=2.5-4.0 %
Inter-assay (Run-to-Run, n=5), CV=1.38-4.45 %
Twenty-four assays were evaluated and the minimum detectable dose (MDD) of rat FABP4/A-FABP. The MDD (defined as such a concentration of rat FABP4/A-FABP giving absorbance higher than mean absorbance of blank* plus three standard deviations of the absorbance of blank: A blank + 3*SD blank) is better than 92.5 pg/ml of sample.
Adipocyte-specific fatty acid-binding protein (AFABP), also designated aP2 and FABP4, belongs to the fatty acid-binding protein super family whose members have relative molecular masses of ~15, 000, and it is exclusively expressed in differentiated adipocytes. FABP4 is a predominant cytosolic protein of mature adipocytes, accounting for ~6 % of total cellular proteins. This protein may be an important regulator of systemic insulin sensitivity and lipid and glucose metabolism. Mice deficient in aP2/FABP4 are protected from development of hyperinsulinemia, hyperglycemia, and insulin resistance in the context of both dietary and genetic obesity. Adipocytes obtained from aP2/FABP4-null mice had markedly reduced efficiency of lipolysis in vivo and in vitro and exhibited a 2- to 3-fold decrease in fatty acid release, suggesting that FABP4 mediates efflux of fatty acids in normal physiology. Although the physiological consequences of aP2/FABP4 deficiency have been predominantly linked to changes in adipocytes, it has reported that the presence of aP2/FABP4 in macrophages and have shown that aP2/FABP4 expression can be induced by peroxisome proliferatoractivated receptor gamma (PPAR gamma) agonists, by toll-like receptor agonists, oxidized LDL, and the differentiation of monocytes to macrophages and can be suppressed by treatment with a cholesterol-lowering statin. In these cells, aP2/FABP4 modulates inflammatory cytokine production and cholesterol ester accumulation. In apolipoprotein E-deficient mice, ablation of the aP2/FABP4 gene conferred remarkable protection against atherosclerosis, which commonly occurs in this rat strain. Taken together, these animal studies demonstrate that aP2/FABP4, by integrating metabolic and inflammatory pathways, provides a key link between various components of metabolic syndrome. Moreover, Masato Furuhashi, M. et al. (2007) reported that an orally active small-molecule inhibitor of aP2/FABP4 is an effective therapeutic agent against severe atherosclerosis and type 2 diabetes in mouse models.