The Mechanism of Depression of Plasma Protein Bound Iodine by 2,4 Dinitrophenol¹

INTRODUCTION IT HAS previously been shown (Wolff et at., 1950; Goldberg and Chaikoff, 1951) that the administration of 2,4 dinotrophenol (DNP), a potent stimulant of oxygen consumption, results in a prompt and profound fall in the level of plasma protein bound iodine (PBI). A compensatory increase in thyroid stimulating hormone (TSH) output by the anterior pituitary, however, could not be detected. This finding was somewhat surprising in view of the low PBI levels and the “homeostatic” relationship presumed to exist between this level and the anterior pituitary beta cells, the probable source of TSH. Two fundamental problems were thus presented: 1) by what mechanism did DNP influence the level of PBI and 2) is the presumed “feed-back” relationship between the level of plasma thyroid hormone and the anterior pituitary actually operative? Since in the earlier studies it was found that with two or three daily injections of DNP neither uptake nor conversion of radioactive iodide to organic form was materially affected