Influence of the Thyroid Gland on Absorption in the Digestive Tract

Althausen, T. L.; Stockholm, M.

doi:10.1152/ajplegacy.1938.123.3.577

Cited by 98 publications

(21 citation statements)

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“…The diet used was a modified Remington diet; because rats kept on this diet for prolonged periods showed biological half-lives of thyroidal I.31 of well under 24 hours, rats were fed this diet for only 12 to 16 days prior to the release studies. Each animal served as its own control and the pooled values of each group were plotted semilogarithmically to obtain half-lives of thyroidal 18 * Thyrotropin stimulation (10 U per day) for one day only, whereas given on three successive days to the other patients.…”

Section: Methodsmentioning

confidence: 99%

“…In addition to the similarities noted above, both salicylate and thyroxine accelerate intestinal absorption of glucose (18,19), and all three agents can deplete the liver of glycogen (20)(21)(22) and uncouple oxidative phosphorylation (23,24). However, the differences of these two phenols from thyroxine are well known, covering a range of effects from an inability to act as substitution therapy in myxedema (25,26), to a failure to induce metamorphosis in the tadpole (27), to an inability to inhibit isolated dehydrogenases in vitro (28).…”

Section: Commentsmentioning

confidence: 99%

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Salicylates and Thyroid Function. II. The Effect on the Thyroid-Pituitary Interrelation

Wolff¹,

Austen²

1958

J. Clin. Invest.

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In the preceding paper (1) it was pointed out that the administration of sodium salicylate to man induces a number of changes suggestive of thyrotoxicosis. There is an elevated basal metabolic rate (BMR), negative nitrogen balance, a fall in the cholesterol level of the hypothyroid subject, and an accelerated fractional disappearance rate of labeled thyroxine from the circulation. Paradoxically, salicylate-induced hypermetabolism is not accompanied by certain of the clinical characteristics of hyperthyroidism and is associated with depressed thyroid function as measured by thyroidal radioiodine uptake and clearance, or the serum protein bound iodine (PBI) concentration. The salicylate level in the serum of such patients is not high enough to interfere with in vitro iodine metabolism in rat thyroid slices, and in acute experiments in rats no depression of the iodide concentrating mechanism can be demonstrated at blood salicylate levels comparable to those attained in the above patients (1). Similar findings had previously been recorded in rats and in man treated with 2,4-dinitrophenol (2-4). It was subsequently shown (5) that this thyroid depression produced by 2,4-dinitrophenol probably resulted from inhibition at a pituitary or higher level.The absence of a direct or immediate effect of salicylates on thyroid tissue, despite marked thyroid depression upon more prolonged exposure to the drug, suggested that this effect may also result from a decrease in thyroid stimulation by thyrotropin (TSH). It is the purpose of this report to suggest a locus of salicylate action and to present some observations on the nature of the inhibitory effect. MATERIALS AND METHODSThree euthyroid patients were studied to evaluate the effect of salicylates on the rate of release of radioiodine from the thyroid gland. The technique was similar to that described by Goldsmith, Stanbury, and Brownell (6). Each patient, while fasting, was given approximately 125 microcuries of radioiodine, and 48 hours later was started on 1-methyl-2-mercaptoimidazole, 30 mg. every six hours, to block the reaccumulation of radioiodine. Counts over the thyroid region were measured each morning with a wide angle scintillation counter. Body background was taken as the thigh count, and the logarithm of the counts remaining in the thyroid after correction for body background and physical decay was plotted against time to determine half-life and rate of release of thyroidal I'.

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Section: Methodsmentioning

confidence: 99%

Section: Commentsmentioning

confidence: 99%

Salicylates and Thyroid Function. II. The Effect on the Thyroid-Pituitary Interrelation

Wolff¹,

Austen²

1958

J. Clin. Invest.

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“…Moreover, studies with intravenous glucose tolerance tests have revealed an increased glucose utilization in hyperthyroidism and a decreased utilization in hypothyroidism [12,21]; therefore, the abnormalities in oral glucose tolerance tests in hyperthyroidism cited above are probably the expression of the increased rate of glucose absorption from the gut [1]. Increased glucose utilization has also been observed in hyperthyroid rats and in their adipose tissue in vitro [26,23,13]; it has also been postulated for human adipose tissue in hyperthyroidism [6].…”

Section: Insulinspiegel Beimentioning

confidence: 99%

Insulin levels in thyrotoxicosis and primary myxoedema: Response to intravenous glucose and glucagon

et al. 1970

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Summary. Glucose disappearance, insulin-like activity (ILA) and serum immunoreaetive insulin (Ii%I) were studied after intravenous injection of glucose or glueagon in patients suffering from thyrotoxieosis or primary myxoedema. A group of normal subjects was also investigated. Glucose disappearance rate appeared to be normal in hyperthyroid, and markedly reduced in hypothyroid subjects. Fasting ILA levels were significantly higher than normal in myxoedema, and lower than normal in thyrotoxicosis. On the other hand, fasting I1:r levels were higher than normal in myxoedema but normal in thyrotoxieosis. After glucose administration I LA in myxoedema remained at higher values than in thyrotoxieosis at any time of the study; in myxoedema, peak ILA levels were reached later than in thyrotoxieosis ; peak I1%1 levels of similar magnitude were reached slightly earlier than normal in thyrotoxicosis, and later in myxoedema; in the latter condition, elevated IgI levels were observed for a longer period than in either euthyroidism or hyperthyroidism. During this test the insulingogenic index showed only slight changes in normal and in thyrotoxie subjects, whereas it increased significantly up to 60 rain in myxoedema. The data indicate that the reduced glucose utilization in hypothyroidism is not due to insulin deficiency, but rather to insulin resistance. It also seems possible that thyroid function influences the time of maximal insulin response to intravenous glucose administration. After glueagon injection, the increase in blood glucose was lower and shorter than normal in thyrotoxieosis; it was initially somewhat slower, but later higher and more sustained than normM, in myxoedema. The smaller increment in blood glucose in the former condition is probably eormeeted with reduced glycogen stores. ILA response was very high and well sustained in myxoedema, whereas it was moderate and shortlasting in thyrotoxieosis. Ii%I response was higher than normal in hypothyroid subjects, and lower than normal in thyrotoxie subjects. No difference in the time required for maximal response was observed among the three groups.

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“…of this solution (containing 0-3 mg thyroxine) was injected intraperitoneally daily for 12-16 days. This dose was approximately the same as that used by Althausen & Stockholm (1938) in their studies on hyperthyroidism and intestinal absorption (i.e. 0-1 mg/100 g body wt.…”

Section: R J Levin and D H Smythmentioning

confidence: 99%