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The interrelationship between hepatic nuclear T3receptors and glucose metabolism was studied in 8 diabetic rats and 8 paired control animals.Serum glucose (mean ± sem, normal vs. diabetic, 167 ± 11 vs. 470 ± 41 mg/100 ml, P< 0.001) and plasma glucagon (183 ± 8.5 vs. 370 ± 29 pg/ml, P< 0.001) were higher in diabetic animals than in controls; serum insulin was lower but not significantly (59 ± 19 vs. 24 ± 12 μU/ml). Serum T4(4.1 ± 0.53 vs. 0.8 ± 0.27 μg/100 ml, P< 0.005) and T3(77.3 ± 3.2 vs. 41.7 ± 12.1 ng/100 ml, P< 0.05) were lower in diabetic rats than in controls. Hepatic concentration of non-protein sulfhydryl-groups was also moderately (∼ 19%) lower in diabetic rats than in controls (4.62 ± 0.11 vs. 3.75 ± 0.24 μmol/g, P< 0.02).The maximal binding capacity (MBC) of the binding of [125I]T3to isolated rat liver nuclei was significantly decreased in the diabetic rats (368 ± 37 vs. 232 ± 36 fmol/mg DNA, P< 0.01; mean decrease 38%); the affinity constant Ka) was also lower but not significantly (1.60 ± 0.13 vs. 1.25 ± 0.13 109L/M, 0.05 < P< 0.1). Addition of 1 mmdithiothreitol (DTT) enhanced the Kaof nuclear binding of T3similarly in the controls and the diabetics. However, it did not restore the decreased MBC of nuclear binding of T3in diabetic rats to the level of the controls.The decrease in MBC of hepatic nuclei for T3did not correlate (P< 0.05) with the decrease in serum T3, serum T4, or hepatic non-protein sulfhydryl-groups. There was, however, a significant negative correlation of MBC of T3with serum glucose and with plasma glucagon. These data suggest a regulatory role of glucose metabolism (or glucagon) in modulation of binding of T3by hepatic nuclear T3receptors.