IN A previous report (Engel, Hewson and Cole, 1954) it was shown that the administration of sodium fluoroacetate (SFA) to the fasted rat resulted in the development of a striking hyperglycemia and ketonemia beginning in a few hours and most apparent in 24 hours. However, no observations were made beyond the latter time. The ketonemia and hyperglycemia were explained in terms of primary and secondary responses to the block in the tricarboxylic acid cycle caused by the SFA. Ketonemia, thus, was considered a consequence of failure of oxidation of acetate as well as of acetoacetate itself with resultant accumulation of the latter compound. The hyperglycemia was interpreted as secondary to a decrease in hexokinase activity resulting from a declining supply of high energy phosphate from the impaired Krebs cycle. In addition the possibility was considered that Krebs cycle blockade might interfere specifically with insulin synthesis by the beta cells of the islets of Langerhans and hence insulin deficiency might be a factor in the diabetes.