Effects of thyroxine and cold exposure on hypothalamic TRH levels in rats with various pituitary-thyroid states.

Utsumi, M.; Makimura, Hiroyuki; Tateiwa, M; Sakoda, M; Baba, Shigeaki

doi:10.1507/endocrj1954.24.537

Cited by 10 publications

(3 citation statements)

References 13 publications

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“…Protein in supernatants of sonicated islets was measured by the method of Lowry et al (1951). TRH was determined by the double antibody radioimmunoassay (Utsumi et al 1975(Utsumi et al , 1977 using syn¬ thetic TRH (Takeda Chemical Industries, Osaka, Japan) as a standard. Our anti-TRH serum was specific to alterations in pGlu-and Pro-His-moieties, but crossreacted with Thr-His-Pro-NH2.…”

Section: Methodsmentioning

confidence: 99%

Protection by nicotinamide against streptozotocin-induced reduction in pancreatic TRH

Kazumi¹,

Utsumi²,

Hirose³

et al. 1982

Acta Endocrinologica

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The concentration of thyrotrophin-releasing hormone (TRH) immunoreactivity was determined in pancreatic islets and acini in the rat. In addition, timecourse changes in TRH in response to an iv injection of streptozotocin (65 mg/kg body weight) with or without nicotinamide (500 mg/kg body weight) were examined in the whole pancreas. Furthermore, pancreatic TRH was measured in diabetic rats treated with insulin for 3 weeks.The TRH concentration in rat islets was 42-fold higher than in exocrine glands, indicating that the majority of pancreatic TRH is of islet origin. The mean concentration of pancreatic TRH decreased to 60 and 65% of the respective control values at 4 and 7 h after administration of streptozotocin, respectively. At 24 h, it fell to 10% of control values without significant changes in TRH levels in the hypothalamus and gastrointestinal tract. In contrast, no significant change in pancreatic TRH was noted in rats given combined treatment with streptozotocin and nicotinamide. The injection of streptozotocin alone resulted in severe hypoglycaemia at 7 h and hyperglycaemia at 24 h, whereas neither resulted from the combined treatment. Insulin therapy had no influence on the decreased TRH concentrations in the diabetic pancreas.These results suggest that TRH may be localized to the B cells of pancreatic islets, and that the marked reduction in TRH in diabetic pancreases is not a metabolic consequence of insulin deficiency. Thyrotrophin-releasing hormone (TRH) immuno¬ reactivity and biological activity has been shown to be present throughout the gastrointestinal tract and pancreas in rats (Morley et al. 1977), with the largest amount occurring in the islets of Langer¬ hans (Martino et al. 1978). On the other hand, streptozotocin exerts a diabetogenic action through the selective destruction of B cells of pancreatic islets (Junod et al. 1967;Kazumi et al. 1979Kazumi et al. , 1980b, which is prevented by combined treatment with nicotinamide (Junod et al. 1969;Kazumi et al. 1979;Stauffacher et al. 1970). Recently, Martino et al. (1978) reported that marked decreases in TRH in whole pancreas and in isolated islets were found in rats 7-10 days after induction of streptozotocin diabetes. Therefore, the present study was de¬ signed to investigate acute effects of a diabetogenic dose of streptozotocin alone or streptozotocin with nicotinamide on the concentration of TRH immu¬ noreactivity in rat pancreas. In addition, effects of insulin replacement therapy on pancreatic TRH were examined in diabetic rats. Materials and MethodsMale Wistar rats, weighing 210-290 g and fed rat chow ad libitum, were used throughout the study. They were fasted for 16 h prior to the injection of streptozotocin (Upjohn, Kalamazoo, Michigan). After the injection, ani¬ mals which were to be killed after 4 and 7 h remained fasting until that time, while the others were allowed 1 To whom requests for reprints should be addressed.

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Section: Methodsmentioning

confidence: 99%

Protection by nicotinamide against streptozotocin-induced reduction in pancreatic TRH

Kazumi¹,

Utsumi²,

Hirose³

et al. 1982

Acta Endocrinologica

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“…Since it has not been previously feasible to measure TRH levels in plasma or urine, the knowledge of the feedback mechanism between the secretion of TRH and thyroid hormones is insufficient. The results of the effects of thyroid hormone treatments on the hypothalamic TRH contents in experimental ani¬ mals, for example, are highly controversial (Bassiri & Utiger 1974;Montoya et al 1975;Kardon et al 1977;Utsumi et al 1977). It is also possible that the amounts of TRH secreted are so small that they cannot be detected after dilution into peripheral circulation.…”

Section: Discussionmentioning

confidence: 99%

Urine TRH immunoreactivity in hypothyroid and hyperthyroid patients

Suhonen

Leppäluoto

Salmi

1984

Acta Endocrinologica

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Urine samples from 8 healthy subjects, from 16 patients with primary hypothyroidism and 8 patients with Graves' hyperthyroidism were pre-purified in SP\ x=r eq-\ Sephadex-C-25 cation-exchange-chromatography, subjected to reverse phase high-pressure liquid chromatography (HPLC) with 0.01 M ammonium acetate pH 4 as a polar and propanol as a non-polar solvent with a 1%/min gradient and assayed in our TRH radioimmunoassay. Urine TRH-immunoreactivity levels were measured before and after 3 months of treatment with thyroxine or methimazole. The urine TRH-levels in healthy subjects were 5.5 \m=+-\1.4 ng/l (mean \m=+-\SEM, n = 8). In the hypothyroid patients, the urine TRH levels were 50.6 \m=+-\40 ng/l before and 71.7 \ m=+-\ 45.3 ng/l after 3 months of treatment with thyroxine. These values did not significantly differ from those in healthy subjects. The large variations were due to highly elevated values in 3 patients. In 2 hypothyroid patients with initially high urine TRH values, 67 and 657 ng/l, urine TRH was measured 5 and 18 months later and was found to have decreased to 5 and 11 ng/l. In the hyperthyroid patients, urine TRH levels were 10.3 \ m=+-\ 3.9 ng/l before and 8.9 \ m=+-\ 3.3 ng/l after the treatment with methimazole and did not differ significantly from the levels in healthy subjects. After 3 months of treatment, the hyper-and the hypothyroid patients were euthyroid. Our results show, that, except in 2 hypothyroid patients, there does not appear to be any relationship between urine TRH levels and serum TSH or thyroid hormone levels in hypothyroid and hyperthyroid patients.

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“…Extracts were serially diluted with the buffer used in each RIA. TRH (Kazumi et al 1982;Utsumi, Makimura, Tateiwa, Sakoda and Baba 1977) and IRI (Morgan and Lazarow 1963) were determined by double antibody RIAs using synthetic TRH and rat insulin as a Fig. 1 Distribution of TRH immunoreactivity in acetic acid extracts of two pancreatic islet cell tumors chromatographed on a Sephadex G10 column (1.5 x 45 cm) which was equilibrated and eluted with phosphate-buffered saline, pH 7.6.…”

Section: Methodsmentioning

confidence: 99%

Thyrotropin-Releasing Hormone and Insulin in Chemically Induced Pancreatic Islet Cell Tumors in Rats

Kazumi¹,

Hirose²,

Ishihara³

et al. 1986

Horm Metab Res

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Thyrotropin-releasing hormone (TRH) and insulin were measured by radioimmunoassay in acetic-acid extracts of 19 pancreatic islet cell tumors induced by streptozotocin and nicotinamide in rats. In addition, gel filtration properties of TRH-immunoreactivity and immunoreactive insulin (IRI) were examined in 5 and 14 tumors, respectively. TRH was demonstrated in 10 of 19 tumors, with a mean of 166 +/- 47 (SEM) pg/mg wet weight, whereas the concentration was less than 3 pg/mg wet weight in the other tumors. In contrast, all tumors contained IRI, with a mean of 11.0 +/- 1.6 micrograms/mg wet weight. Ten tumors in which TRH was demonstrated contained more IRI than those in which TRH was not detected (13.1 +/- 1.8 vs 6.5 +/- 1.7 micrograms/mg wet weight, P less than 0.02). After gel filtration, all TRH immunoreactivity was eluted at the same place as synthetic TRH in the 5 tumors. In addition, gel filtration elutes showed essentially the same pattern of IRI in the 14 tumors, with 3 peaks. The predominant IRI peak comigrated with marker insulin (95.7 +/- 0.8%), another prominent peak occurred coincident with proinsulin standard (3.3 +/- 0.5%), a third peak was present in the void volume (0.28 +/- 0.04%). These distributions of IRI were similar to those in extracts of normal pancreases. The present studies demonstrate TRH immunoreactivity in pancreatic islet cell tumors induced by streptozotocin and nicotinamide in rats. Chemically induced insulinomas can serve as a model for insulin storage which is analogous to islet B cells.

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Effects of thyroxine and cold exposure on hypothalamic TRH levels in rats with various pituitary-thyroid states.

Cited by 10 publications

References 13 publications

Protection by nicotinamide against streptozotocin-induced reduction in pancreatic TRH

Protection by nicotinamide against streptozotocin-induced reduction in pancreatic TRH

Urine TRH immunoreactivity in hypothyroid and hyperthyroid patients

Thyrotropin-Releasing Hormone and Insulin in Chemically Induced Pancreatic Islet Cell Tumors in Rats

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