SUMMARY1. Thyroxine (T4) and triiodothyronine (T3) injected into adult rats causes first an increase and then a decrease in lactase activity measured subsequently in intestinal homogenates of rat jejunum. These changes are not associated with any alteration in intestinal structure or enterocyte migration rate.2. Quantitative cytochemistry shows T4 stimulation and inhibition of lactase activity to take place in upper villus and crypt cells respectively (0-and C-enterocytes). T3 injected into thyroidectomized rats produces identical stimulatory effects on lactase development to T4 injected into control animals.3. Radioactive T3 is distributed in all cell types following intraperitoneal injection into thyroidectomized rats. Highest amounts of recovered T3 are found in C-rather than 0-enterocytes. Quantitative autoradiography shows intracellular T3 to be located in nuclear and cytoplasmic compartments following intraperitoneal injection. Simultaneous injection of non-radioactive hormone displaces 50-750o of radioactive T3.4. These results are discussed in relation to what is already known concerning the ability of thyroid hormones to affect intestinal development. The future need to study the physiological effects of T3 at the cellular level in the intestine is also emphasized.
10-M) and low (KD 1-9 + 0 8 x 10-7 M) affinity binding sites in these cells.5. Previous injection of non-radioactive T3 into thyroidectomized rats, at a time chosen to ensure negligible levels of circulating T3 at the time of the experiment, caused a 3-fold reduction in the maximal binding capacity of the low-affinity site (83 compared with 28 pmol/mg protein). Neither the affinity nor the number of high-affinity binding sites for T3 were significantly affected by this treatment.6. These results are compared with those obtained using other types of cell responsive to T3. The possible physiological importance of these findings is discussed.
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