The Effect of Thyroxine on the Movement of Calcium and Inorganic Phosphate Through the Small Intestine of the Rat

Noble, H. M.; Matty, A. J.

doi:10.1677/joe.0.0370111

Cited by 23 publications

(8 citation statements)

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“…In addition, the bath to lumen flux of 36 C and 32 P increased with thyroid hormone administration, consistent with a decrease in the paracellular permeability to these anions (39,40). However, passive phosphate and calcium transport across the small intestine was less in rats that received thyroid hormone for 7 d than in control rats, consistent with a decrease in paracellular movement of these ions with thyroid hormone treatment (38).…”

Section: Discussionmentioning

confidence: 64%

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Developmental Changes in Proximal Tubule Tight Junction Proteins

et al. 2005

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We demonstrated previously that neonatal proximal tubules have a lower passive paracellular permeability to chloride ions and higher resistance than that of adult proximal tubules. In addition, administration of thyroid hormone to neonates, before the normal maturational increase in serum thyroid hormone levels, prematurely accelerates the developmental increase in chloride permeability to adult levels. To test the hypothesis that there is a maturational change in tight junction proteins and that thyroid hormone mediates these changes, we examined the two known tight junction proteins present in proximal tubules, occludin and claudin 2. Using immunoblot and immunohistochemistry, we demonstrated that claudin 2 has a 4-fold greater abundance in neonatal proximal tubules than in adult tubules. Occludin, however, has a 4-fold greater expression in adult tubules than in neonatal tubules. Administration of thyroid hormone to neonates did not affect claudin 2 expression, occludin expression, or the transepithelial resistance in rat proximal tubule cells in vitro. In conclusion, there are postnatal maturational changes in tight junction proteins. The factors that cause these maturational changes are unknown but unlikely to be due solely to the maturational increase in thyroid hormone.The proximal tubule receives an ultrafiltrate from the glomerulus and reabsorbs two thirds of the ultrafiltrate in a nearly iso-osmotic manner. In addition to active transcellular fluid transport, the proximal tubule reabsorbs solutes via passive diffusion across the paracellular pathway. The early proximal tubule reabsorbs glucose and amino acids and preferentially reabsorbs bicarbonate over chloride ions (1,2), which leaves the luminal fluid delivered to the late proximal tubule with a higher chloride concentration and lower bicarbonate concentration than that in the peritubular plasma (1,2). Passive solute transport is dependent on the gradients that develop between lumen and peritubular capillary and permeability properties of the paracellular pathway.Approximately two thirds of the filtered chloride is reabsorbed by the adult proximal tubule (1,3 active and transcellular and half is passive and paracellular (3-5). Active NaCl transport is mediated by the parallel operation of the Na+/H+ exchanger and a Cl−/base exchanger (3,4). Passive Cl absorption is mediated by diffusion of chloride ions down its concentration gradient generated in the early proximal tubule (6,7). Thus, the permeability properties of the paracellular pathway can affect a significant amount of proximal tubule NaCl transport.Furthermore, the permeability properties of the paracellular pathway serve as a barrier to prevent the back diffusion of glucose, amino acids, phosphate, bicarbonate, and other solutes that are in higher concentration in the peritubular fluid than in the lumen of the late proximal tubule. In previous in vitro rabbit microperfusion studies, our laboratory demonstrated that unlike the adult segment, the neonatal proximal tubule was impermeab...

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Section: Discussionmentioning

confidence: 64%

“…Other studies suggested that thyroid hormone may be involved in the regulation of the permeability of the paracellular pathway (38)(39)(40). Thyroid hormone has been shown to decrease the resistance of toad bladders (40).…”

Section: Discussionmentioning

confidence: 99%

Developmental Changes in Proximal Tubule Tight Junction Proteins

et al. 2005

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“…Phosphorus absorption is enhanced secondarily to that of calcium, and all three minerals, calcium, phosphorus, and magnesium, probably follow the same transport-pathway system in the gut [2,32]. Although this is disputed by some investigators [26,50], PTH is not considered to be an absolute requirement for transport of these minerals across the intestine; to date, a direct action of PTH on mineral absorption has not been consistently demonstrated [36,42].…”

Section: Discussionmentioning

confidence: 99%

“…Specimens of urine were collected hourly and measured, and aliquots were immediately frozen and stored at -20° until 3',5'-AMP could be determined. Base line (control), interval, and total test time excretion of 3',5'-AMP were measured according to the technique of Chase et al [9] which is based upon the enzymatic conversion of the nucleotide to adenosine triphosphate and detection of the latter by means of an adenosine triphosphate- 32 Pj exchange. About 200 ml water/hr were given by mouth from 6 AM to noon.…”

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confidence: 99%

Vitamin D-Dependent Rickets: Actions of Parathyroid Hormone and 25-Hydroxycholecalciferol

Rosen

Finberg

1972

Pediatr Res

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ExtractDuring active rickets, the increase in 3',5'-adenosine monophosphate (3',5'-AMP) excretion after infusion of parathyroid hormone (PTH) can be claimed as a demonstration of PTH responsiveness, at least as far as the kidney is concerned (Table II). In patients with vitamin D-dependent rickets, following 25-HGC therapy, the basal excretion ratios of nanomoles 3',5'-AMP/milligrams creatinine fall within the normal range, and, although the basal ratios of milligrams phosphate/milligrams creatinine excretion decrease to normal (Tables III, IV, and V), a phosphaturic response to PTH is still not evident. The high basal ratios of nanomoles 3',5'-AMP/ milligrams creatinine and milligrams phosphate/milligrams creatinine suggest underlying hyperparathyroidism during a phase of this syndrome marked by hypocalcemia and hyperaminoaciduria. During 2-day PTH challenges, while rickets was active, the peak increases in serum calcium above base line were 1.92, 1.80, and 1.86 mg/100 ml. After treatment with 25-hydroxycholecalciferol (25-HCG), no further significant increases in serum calcium above base line could be elicited (Tables VI, VII, VIII). It would seem, therefore, that, while these patients were untreated, small but sufficient amounts of 25-HCC or another metabolite of vitamin D were available to permit the calcium-mobilizing action of PTH on bone. The observed hypocalcemia in vitamin D-dependent rickets, then, is most likely secondary to a defect in gastrointestinal absorption. Mineral balance studies during active rickets revealed an absorptive defect for calcium, phosphorus, and magnesium-a defect completely reversible after 25-HCC treatment. Speculation

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“…A reduction in mixing of food with digestive secretions may also contribute to decreased fat absorption. Alterations in intestinal absorptive function are still a matter of debate, as absorption may be increased for glucose [34,37] but decreased for calcium [38] . Anorectal physiology is impaired in hyperthyroidism; when compared to controls, mean anal resting and squeeze pressures are lower as is the rectal threshold of sensation [39] .…”

Section: Intestine and Colonmentioning

confidence: 99%

Consequences of dysthyroidism on the digestive tract and viscera

Daher¹,

Yazbeck²,

Jaoude³

et al. 2009

WJG

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Thyroid hormones define basal metabolism throughout the body, particularly in the intestine and viscera. Gastrointestinal manifestations of dysthyroidism are numerous and involve all portions of the tract. Thyroid hormone action on motility has been widely studied, but more complex pathophysiologic mechanisms have been indicated by some studies although these are not fully understood. Both thyroid hormone excess and deficiency can have similar digestive manifestations, such as diarrhea, although the mechanism is different in each situation. The liver is the most affected organ in both hypo-and hyperthyroidism. Specific digestive diseases may be associated with autoimmune thyroid processes, such as Hashimoto's thyroiditis and Grave's disease. Among them, celiac sprue and primary biliary cirrhosis are the most frequent although a clear common mechanism has never been proven. Overall, thyroidrelated digestive manifestations were described decades ago but studies are still needed in order to confirm old concepts or elucidate undiscovered mechanisms. All practitioners must be aware of digestive symptoms due to dysthyroidism in order to avoid misdiagnosis of rare but potentially lethal situations.

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The Effect of Thyroxine on the Movement of Calcium and Inorganic Phosphate Through the Small Intestine of the Rat

Cited by 23 publications

References 0 publications

Developmental Changes in Proximal Tubule Tight Junction Proteins

Developmental Changes in Proximal Tubule Tight Junction Proteins

Vitamin D-Dependent Rickets: Actions of Parathyroid Hormone and 25-Hydroxycholecalciferol

Consequences of dysthyroidism on the digestive tract and viscera

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