Fatty Acid Oxidation Assay (ab217602)

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製品の概要

  • 製品名

    Fatty Acid Oxidation Assay
    Fatty Acid Oxidation キット 製品一覧

  • 検出方法

    Fluorescent

  • サンプルの種類

    Adherent cells, Suspension cells

  • アッセイタイプ

    Cell-based (quantitative)

  • 製品の概要

    Fatty Acid Oxidation Assay (ab217602) allows the detection of Fatty Acid Oxidation (FAO) in live cells when used in combination with our Extracellular Oxygen Consumption Assay (ab197243).


    The assay uses the 18C unsaturated fatty acid Oleate as substrate, and includes two FAO modulators, etomoxir and FCCP. Etomoxir, an inhibitor of the carnitine transporter CPT1, prevents Oleate import and thereby limits the supply of reducing equivalents to the ETC, reducing oxygen consumption in turn. The remaining ETC (electron transport chain) activity is driven by non-long chain FAO. FCCP treatment induces maximal ETC activity by dissipating the mitochondrial membrane potential, while the increased demand for reducing equivalents causes a concomitant increase in the FAO activity. If exogenous long-chain fatty acid is unavailable or import is inhibited, FAO activity will be limited.

  • 特記事項

    Learn more about the full range of assays to measure glycolysis, oxygen consumption, fatty acid oxidation and metabolic flux in live cells.

    Or review the full metabolism assay guide for other assays for metabolites, metabolic enzymes, mitochondrial function, and oxidative stress.

  • 試験プラットフォーム

    Microplate reader

製品の特性

画像

  • FAO-driven oxygen respiration in HepG2 cells.
    FAO-driven oxygen respiration in HepG2 cells.

    FAO-driven oxygen respiration in HepG2 cells treated with the CPT-1 inhibitor Etomoxir (white) and uncoupler FCCP (gray).

    Untreated cells (basal FAO) curve shows a steady increase of the Extracellular O2 Consumption Reagent signal reflecting ETC-driven oxygen consumption. Signal Control shows probe signal in the absence of cell respiration. Etomoxir treatment prevents oleate import, resulting in reduced availability of reducing equivalents and a resultant decrease in ETC activity. The remaining ETC activity (difference between Etoxomir treatment and Signal Control) is driven by metabolic activity other than long chain FAO. FCCP treatment induces maximal ETC activity by dissipating the mitochondrial membrane potential. Increased demand for reducing equivalents causes a concomitant increase in FAO as indicated by the rapid increase in Extracellular O2 Consumption Reagent signal. This strong increase in ETC activity is not observed where exogenous LCFA is unavailable or where import is inhibited.

  • FAO-driven respiration of HepG2 cells treated with etomoxir and FCCP
    FAO-driven respiration of HepG2 cells treated with etomoxir and FCCP

    The figure summarizes the balance between these parameters under “Basal” and “Maximum” (FCCP treated) conditions. The increased energy demand imposed by FCCP treatment is met by increased FAO.

プロトコール

参考文献

ab217602 has not yet been referenced specifically in any publications.

ab217602 を使用した論文を発表された方は、こちらまでお知らせください。データシートに掲載させていただきます。

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