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The effect of T3 replacement and glucose supplementation on erythropoietin production was investigated in fasted hypoxic rats. It was found that 48 hr of fasting significantly reduced the circulating levels of thyroid hormones and the production of renal and extrarenal erythropoietin in response to hypoxia. These effects of fasting were completely abolished when the animals had free access to 25% glucose solution as drinking water, despite their lack of protein intake. Replacement doses of T3 (0.5 micrograms/100 gm per day) restored erythropoietin production in the fasted animals but also increased the response of the fed controls. To avoid the effect of endogenous T3, the experiments were repeated in thyroidectomized rats. Erythropoietin production in athyroid rats was found to be markedly decreased, with values equivalent to those found in normal fasted animals, and were not affected by fasting or glucose supplementation. Replacement doses of T3 increased erythropoietin production in all three groups, but the fasted animals needed five times as much T3 to obtain a response similar to that observed in the fed group. Glucose supplementation enhanced the effect of T3 in the fasted animals but did not completely restore it. These results indicate that caloric deprivation is primarily responsible for the decreased erythropoietin production induced by fasting and that this effect is probably mediated by both a decreased level of T3 and a decreased responsiveness to it.