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  • Author: Meinrad Peterlik x
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Heide S. Cross and Meinrad Peterlik

Abstract.

Embryonic chick jejunum maintained in organ-culture exhibits a characteristic stage-specific pattern of responses to calcitriol and T3. Whereas induction of luminal Na+/inorganic phosphate and Na+/D-glucose transport by calcitriol was only possible at an advanced state of differentiation prior to hatching on day 20, the sterol induced cellular calcium transport with high efficiency even in undifferentiated enterocytes in day 15 embryonic intestine. T3 had no effect at all on calcium transport, but induced Na+/inorganic phosphate transport at all stages of epithelial maturation. In contrast, Na+/D-glucose transport was effectively induced by T3 only in relatively immature intestinal epithelium. T3, at a medium concentration of 10−8 mol/l, in a permissive fashion potentiated the effects of calcitriol (10−10−10−7 mol/l) on calcium transport as well as on Na+/inorganic phosphate and Na+/D-glucose transfer. Thereby, T3 facilitated induction of transport activities by calcitriol against differentiation-related restraints. By facilitating the expression of genomic actions of calcitriol, T3 may thus play an important role in the regulation of calcium and phosphate metabolism.

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Heide S. Cross, Doris Pölzleitner and Meinrad Peterlik

Abstract. Thyroxine (T4) and triiodothyronine (T3) activate Na+-dependent inorganic phosphate (Pi) transport in organ-cultured embryonic chick small intestine. Induction of transport activity requires intact protein synthesis and can be expressed in enterocytes with varying degrees of differentiation. T3 and T4 exert their effect independent of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), which is shown to stimulate Pi uptake only in the final stage of embryonic differentiation. At this time point, a potentiating effect of 1,25(OH)2D3 and T4 on Pi transport in cultured jejunum can be demonstrated. Thyroid hormones appear to stimulate Na+ gradient-driven Pi transport without concomitantly raising (Na+-K+)-ATPase activity. T4 has no influence whatsoever on calcium uptake by cultured embryonic small intestine while 1,25(OH)2D3 is effective at all stages of embryonic development investigated (day 15–20). However, when both hormones were present in the culture medium, the effect of 1,25(OH)2D3 on calcium transport is doubled. Our results suggest that the hyperphosphataemia associated with hyperthyroidism is likely to result, at least in part, from the independent effect of thyroid hormones as well as from their potentiation of the 1,25(OH)2D3 action on Na+-dependent intestinal Pi transport. In addition, their permissive effect on 1,25(OH)2D3-induced calcium absorption provides an explanation for unaltered calcium absorption in a number of hyperthyroid patients, although reduced plasma levels of 1,25(OH)2D3 are generally observed in this condition.

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Christiane Prager, Heide S. Cross and Meinrad Peterlik

Abstract.

The possible contribution of increased D-glucose absorption from the intestine to the impairment of oral glucose tolerance in hyperthyroidism was evaluated by investigating the influence of T3 on different pathways of D-glucose transport, utilizing an organ culture system of embryonic chick small intestinal explants. T3, when present in the culture medium at a concentration between 10−10-10−8 mol/l, had no effect on uptake of α-methyl-D-glucoside, but stimulated uptake of 2-deoxy-D-glucose by the intestinal epithelium in a dose-dependent fashion. T3 thereby enhanced the maximal velocity of a saturable, cytochalasin B-sensitive but phloretin-insensitive 2-deoxy-D-glucose transport system with an apparent Km of 7 mmol/l. The combined data are consistent with the assumption that T3 can enhance D-glucose entry into the intestinal epithelium through stimulationof a low-affinity transport system at the brush-border membrane of enterocytes. Our findings provide a basis for the explanation of adaptive modulation of intestinal glucose absorption in hyperthyroidism.

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Hanna Debiec, Heide S. Cross and Meinrad Peterlik

Abstract. Jejunal brush-border membrane vesicles were harvested from 4-week old chicks whose thyroid status had been altered either by a daily injection of 20 μg T3 for 1 week or which through the preceding 4 weeks had received propylthiouracil and than had been repleted with either 20 or 80 μg T3 in divided doses within 48 h. T3 markedly stimulated D-glucose uptake in brush-border membrane vesicles in the presence of an outside/inside (100/0 mmol/l) Na+ gradient. T3 administration had no detectable influence on the Na+ permeability of the isolated vesicles. The effect of the thyroid hormone on Na+ gradient-driven D-glucose uptake was fully preserved at zero transmembrane potential difference. These findings exclude that T3 stimulates Na+-dependent D-glucose transport in the small intestine through changes of the electrochemical Na+ gradient or through alteration of the transmembrane potential difference. Tracer exchange experiments under equilibrium and voltageclamp conditions revealed a significantly shorter halftime of D-glucose uptake in brush-border membrane vesicles from T3-treated chicks. Kinetic analysis showed that T3 administration significantly increases the apparent maximal velocity of D-glucose transport in brushborder membrane vesicles, whereas the apparent Km values were virtually unaltered. From these data we conclude that T3 increases the activity of Na+-dependent D-glucose carriers in the brush-border membrane. This is interpreted as consistent with a greater rate of D-glucose absorption from the intestinal lumen under conditions of hyperthyroidism.