text: G can be determined experimentally by exposing a cell culture system to saturating concentrations of T4 and measuring the T3 production. Whole body deiodination activity can be assessed by measuring production of radioactive iodine after loading the organism with marked thyroxine.
  However, both approaches are faced with draw-backs. Measuring deiodination in cell culture delivers little, if any, information on total deiodination activity. Using marked thyroxine exposes the body to thyrotoxicosis and radioactivity. Additionally, it is not possible to differentiate step-up reactions resulting in T3 production from the step-down reaction catalyzed by type 3 deiodination, which mediates production of reverse T3. Distinguishing the contribution of distinct deiodinases is possible, however, by sequential approaches using deiodinase-specific blocking agents, but this approach is cumbersome and time-consuming.
  In vivo, it may therefore be beneficial to estimate G from equilibrium levels of T4 and T3. It is obtained with
  or
  [FT4]: Serum free T4 concentration (in pmol/L)<br />
  [FT3]: Serum free T3 concentration (in pmol/L)<br />
  [TT3]: Serum total T3 concentration (in nmol/L)<br />
  : Dilution factor for T3 (reciprocal of apparent volume of distribution, 0.026 L)<br />
  : Clearance exponent for T3 (8e-6 sec) (i. e., reaction rate constant for degradation)<br />
  K: Binding constant of type-1-deiodinase (5e-7 mol/L)<br />
  K: Binding constant T3-TBG (2e9 L/mol)
  The method is based on mathematical models of thyroid homeostasis. Calculating deiodinase activity with one of these equations is an inverse problem. Therefore, certain conditions (e.g. stationarity) have to be fulfilled to deliver a reliable result.
  The product of SPINA-GD times the urinary iodine excretion can be used to assess iodine-independent factors affecting deiodinase activity, e.g. selenium deficiency.