CircuLex Rat FABP4/A-FABP ELISA Kit

  • Applications
    • ELISA
  • Code # CY-8076
  • Size 96 Assays
  • Price
    $593.74
Specifications

Background

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 (1, 2). 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 (1). Mice deficient in aP2/FABP4 are protected from development of hyperinsulinemia, hyperglycemia, and insulin resistance in the context of both dietary and genetic obesity (3, 4). Adipocytes obtained from aP2/FABP4-null mice had markedly reduced efficiency of lipolysis in vivo and in vitro (5, 6) and exhibited a 2- to 3-fold decrease in fatty acid release, suggesting that FABP4 mediates efflux of fatty acids in normal physiology (7). 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 (2, 8) and have shown that aP2/FABP4 expression can be induced by peroxisome proliferatoractivated receptor gamma (PPAR gamma) agonists (8), by toll-like receptor agonists (9), oxidized LDL (10), and the differentiation of monocytes to macrophages and can be suppressed by treatment with a cholesterol-lowering statin (11). In these cells, aP2/FABP4 modulates inflammatory cytokine production and cholesterol ester accumulation (12). In apolipoprotein E-deficient mice, ablation of the aP2/FABP4 gene conferred remarkable protection against atherosclerosis, which commonly occurs in this rat strain (13, 14). 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.
  • Application:
    ELISA
  • Components:
    • Microplate
    • 10X Wash Buffer
    • Dilution Buffer
    • Rat FABP4/A-FABP Standard
    • HRP conjugated Detection Antibody
    • Substrate Reagent
    • Stop Solution
  • Description:

    The CycLex Research Product CircuLex 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. It can be used for 96 Assays.

  • Product Type:
    ELISA Kit
  • Research Area:
    Metabolism
  • Short Description:

    CircuLex Rat FABP4/A-FABP ELISA Kit.

  • Size:
    96 Assays
References
  1. Makowski L, Hotamisligil GS. J Nutr (2004) 134: 2464S–8S.
  2. Boord JB, Fazio S, Linton MF. Curr Opin Lipidol (2002) 13: 141–7.
  3. Uysal KT, Scheja L, Wiesbrock SM, Bonner-Weir S, Hotamisligil GS. Endocrinology (2000) 141: 3388–96.
  4. Hotamisligil GS, Johnson RS, Distel RJ, Ellis R, Papaioannou VE, Spiegelman BM. Science (1996) 274: 1377–9.
  5. Coe NR, Simpson MA, Bernlohr DA. J Lipid Res (1999) 40: 967–72.
  6. Scheja L, Makowski L, Uysal KT et al. Diabetes (1999) 48: 1987–94.
  7. Baar RA, Dingfelder CS, Smith LA, Bernlohr DA, Wu C, Lange AJ, et al. Biochem Biophys Res Commun (1999) 261: 456–8.
  8. Kazemi MR, McDonald CM, Shigenaga JK, Grunfeld C, Feingold KR. Arterioscler Thromb Vasc Biol (2005) 25: 1220–4.
  9. Fu Y, Luo N, Lopes-Virella MF. J Lipid Res. (2000) 41: 2017–23.
  10. Llaverias G, Noe V, Penuelas S, Vazquez-Carrera M, Sanchez RM, Laguna JC, et al. Biochem Biophys Res Commun (2004) 318: 265–74.
  11. Makowski L, Brittingham KC, Reynolds JM, Suttles J, Hotamisligil GS. J Biol Chem (2005) 280: 12888–95.
  12. Makowski L, Boord JB, Maeda K, Babaev VR, Uysal KT, Morgan MA, et al. Nat Med (2001) 7: 699–705.
  13. Boord JB, Maeda K, Makowski L, Babaev VR, Fazio S, Linton MF, et al. Circulation (2004) 110: 1492–8.
  14. M Furuhashi, G Tuncman, CZ Gorgun, L Makowski, G Atsumi, E Vaillancourt, K Kono, VR Babaev, S Fazio, MF Linton, R Sulsky, JA Robl, RA Parker, and GS Hotamisligil. Nature (2007) 447: 959-65.