bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nuclear triiodothyronine receptors and metabolic response in perinatally protein-deprived rats
Authors: Coleoni Aldo H. , Munaro Norma , Recúpero Alfredo R. , Cherubini Olga 
Published: December 2008

Abstract. Pregnant rats from day 14 of pregnancy and pups were fed a control diet (24% casein) or a deprived diet (8% casein) to obtain a control and a preand post-natal protein-deprived group. From 50 days of age, all groups were fed a balanced commercial stock diet for different periods. A significant reduction in body weight was observed in the perinatally protein-deprived group (PPD) after the different periods of nutritional recovery studied. Maximal binding capacity (MBC) and apparent affinity constant (Ka) of liver nuclear T3-receptors in the PPD group were similar to those in the control group. Mitochondrial α-glycerophosphate dehydrogenase (α-GPD) and cytosolic malic enzyme (ME) activity were significantly increased in the PPD group in all the periods of nutritional recovery studied, except in the 8 months old group where it was non-significant. Plasma T3 levels were higher in rats 3 and 15 days after the removal of the hypoprotein diet while it was normal after longer periods of nutritional recovery. Serum T4 was not modified in any group.
The results indicate that protein undernutrition during perinatal life may induce an activation of hepatic T3-dependent enzymes which persists even after long periods of nutritional recovery. The lack of modification at the nuclear T3-receptor level, where supposedly the first T3-signal takes place, raises the possibility of an amplification of this signal at a step beyond the receptor.
Effect of neonatal hyperthyroidism upon the regulation of TSH secretion in rats
Authors: Besa M. E. , Pascual-Leone A. M. 
Published: December 2008

Abstract. The neo-T4 syndrome was induced in rats by administration of 30 μg T4/in 5 doses starting on the first day of life. In the first experiment (A), neo-T4 and saline-control rats were divided into two populations, one of which was thyroidectomized on day 25. All rats then received 5 μg T4/100 g b.w. on days 42, 43 and 44, and were sacrificed on day 45. In the second experiment (B), neo-T4 and saline-control rats were thyroidectomized at 25 days of age and were sacrificed 10, 20 and 40 days after the operation. In both experiments, pituitary and plasma TSH and pituitary GH were determined.
T4 administration has the same effect on plasma and pituitary TSH regulation in neo-T4 and control rats, thyroidectomized or not. The increase in pituitary GH produced by T4 is smaller in the thyroidectomized neoT4 animals. The comparison between T4-induced increases of pituitary TSH in thyroidectomized neo-T4 and saline control-rats, and the corresponding decreases in non-thyroidectomized animals suggests an alteration in TSH synthesis which has previously been compared with that found in rats with lesions of the hypothalamus. However, the changes in pituitary and plasma TSH levels in neo-T4 rats at different intervals after thyroidectomy do not coincide with those described for rats with hypothalamic lesions. The possible perturbation in pituitary TSH synthesis proposed for neo-T4 rats accords with the lack of response to TRH found in adult animals treated with thyroxine, an effect which remains even when plasma T4 levels decrease.
Effects of 1,25- and 24,25-dihydroxycholecalciferol on parathyroid hormone release from human parathyroid cells in vitro
Authors: Rudberg Claes , Åkerström Göran , Johansson Henry , Ljunghall Sverker , Malmaeus Jan , Wide Leif 
Published: December 2008

Abstract. The effects of 125-dihydroxycholecalciferol (1,25-(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25-(OH)2D3) on parathyroid hormone (PTH) release from human parathyroid cells were investigated using an in vitro system of dispersed cells. The cells were obtained from 7 patients with primary hyperparathyroidism (HPT) and adenoma, 4 patients with primary HPT due to hyperplasia and 2 patients with parathyroid hyperplasia secondary to chronic renal failure.
The dispersed cells were incubated in tissue culture medium at low, normal and high external calcium concentrations for 2–16 h. There was a gradual suppression of PTH release (5–55%) when the calcium concentration in the medium was increased from 0.5 to 3.0 mM, thus indicating retained regulation of hormone release. The addition of 1,25-(OH)2D3 in concentrations of 0.1 and 1 ng/ml and of 24,25-(OH)2D3 in concentrations of 1.0 and 10 ng/ml during the incubations did not further affect the amount of PTH released by the cells. The concentrations of the different vitamin D metabolites tested closely correspond to levels observed under normal physiological conditions and during treatment with high doses of vitamin D in vivo.
Thus, the findings contradict the idea of any direct short-term regulatory effect of either 1,25-(OH)2D3 or 24,25-(OH)2D3 on the secretion of PTH from hyperfunctioning human parathyroid tissue.
Anti-oestrogenic effects of tamoxifen on mammary gland and hypophysis in female rats
Authors: Götze Stephan , Nishino Yukishige , Neumann Friedmund 
Published: December 2008

Abstract. Adult ovariectomized rats were treated for 14 days with oestradiol benzoate (E2B) 15 μg/kg/d and oestradiol benzoate 15 μg/kg/d + progesterone (PRO) 15 mg/kg/d for induction of mammary gland parenchymal stimulation.
Histological examination and whole mount preparation demonstrated that ductal growth in the mammary gland after E2B treatment was completely antagonized by tamoxifen (TAM) 0.5 mg/kg/d. Parallel DNA concentrations in the mammary gland were decreased to control levels by TAM 0.5, 5 and 15 mg/kg/d.
E2B-induced hyperprolactinaemia in the forenoon (basal secretion was equally reduced by TAM 0.5, 5 and 15 mg/kg/d). In the afternoon, when prolactin (Prl) secretion is at its maximum, TAM 0.5 mg/kg/d turned out to be ineffective to abolish Prl surge, but TAM 5 and 15 mg/kg/d reduced serum Prl concentrations in a doserelated manner.
Immunoperoxidase staining of Prl cells in the pars distalis of the hypophysis indicated that adaptive hypertrophy and signs of hypersecretion after E2B were abolished by TAM 5 mg/kg/d. Luteotrophic cells clearly showed cellular atrophy, regression and secretory inactivity.
Maximal tubulo-alveolar mammary parenchymal stimulation in rats treated with E2B-PRO was slightly inhibited by TAM 0.5 mg/kg/d. Histology showed a small disseminated parenchymal islet. DNA concentrations only were partially decreased by the anti-oestrogen though serum Prl concentrations were found to be completely decreased to control levels. Secretory activity of Prl cells was reduced by TAM 0.5 mg/kg/d.
In E2B-PRO treated rats lisuride had poor inhibitory activity on Prl levels and none on DNA concentrations in the mammary gland.
Combined treatment with TAM and lisuride significantly decreased DNA concentration in the mammary gland compared to animals which received E2B-PRO. Also Prl levels were at a minimum. Histology performed on the mammary gland showed only slight tubulo- but no tubulo-alveolar activation. Luteotrophic cells in the pituitary gland stained by the immunoperoxidase technique appeared regressive, shrunken and atrophied.
Evidence for the presence of a neutral insulinotrophic peptide in the porcine duodenum
Authors: Rey Francois , Mauron Charlotte , Bobbioni Elisabetta , Jeanrenaud Bernard , Mutt Viktor , Felber Jean-Pierre 
Published: December 2008

Abstract. A crude mixture of thermostable peptides extracted from porcine duodenum was fractionated by electrofocusing. A neutral fraction, different from the basic fractions of GIP, VIP, PHI and CCK was found to promote insulin secretion when injected in vivo to normal rats. This neutral fraction, extracted from the crude mixture by chromatography, stimulated insulin output from an isolated rat pancreas and enhanced glucoseinduced insulin release. The insulinotrophic effect of this partially purified duodeno-jejunal material disappeared following digestion with trypsin. The insulin-releasing activity was found to correspond to a compound of molecular weight higher than that of insulin (i.e. higher than 6000). No GIP-like immunoreactivity was found in this neutral fraction indicating that the active peptide(s) are not GIP related compounds.
These observations suggest that porcine duodenum contains and incretin activity different from that of the insulinotrophic factors already reported.
Importance of the adrenal cortex for development and maintenance of hypertension in spontaneously hypertensive rats
Authors: Ruch W. , Baumann J. B. , Häusler A. , Otten U. H. , Siegl H. , Girard J. 
Published: December 2008

Abstract. Adrenal regeneration following complete bilateral adrenalectomy in spontaneously hypertensive rats (SHR) was used to study the significance of glucocorticoid and mineralocorticoid hormones for the development and maintenance of hypertension.
Pre-hypertensive (5 weeks of age) and hypertensive (10 and 16 weeks of age) male SHR underwent adrenalectomy (ADN) and were kept on 0.9% NaCl. The rats were ether stressed at various intervals to assess adrenal steroid production. Following ADN of all three age groups the development or maintenance of hypertension depended on the presence of adrenal regenerates. Animals without signs of adrenal regeneration remained or became normotensive. There was a significant correlation between plasma corticosterone levels following ether stress and blood pressure.
Aldosterone and corticosterone production of regenerates and of adrenal cortex of intact SHR was studied in vitro. Under basal condition and following ACTH stimulation both tissues produced similar amounts of corticosterone, however considerably less aldosterone was secreted by regenerates. Betamethasone substitution in adrenalectomized rats caused a dramatic increase of blood pressure which was attenuated by l-propranolol. Aldosterone had no significant effect on blood pressure.
It is concluded that glucocorticoids play a permissive role in the development of hypertension presumably via alteration of sympathetic neurotransmission.
Urine TRH immunoreactivity in hypothyroid and hyperthyroid patients
Authors: Suhonen Anna-Stina , Leppäluoto Juhani , Salmi Jorma 
Published: December 2008

Abstract. Urine samples from 8 healthy subjects, from 16 patients with primary hypothyroidism and 8 patients with Graves' hyperthyroidism were pre-purified in SP-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 ± 1.4 ng/l (mean ± sem, n = 8).
In the hypothyroid patients, the urine TRH levels were 50.6 ±40 ng/l before and 71.7 ± 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 ± 3.9 ng/l before and 8.9 ± 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.
Effect of vitamin D3 on the pancreatic secretion of insulin and somatostatin
Authors: Tanaka Yoshiyuki , Seino Yoshiki , Ishida Makoto , Yamaoka Kanji , Yabuuchi Hyakuji , Ishida Hitoshi , Seino Susumu , Seino Yutaka , Imura Hiroo 
Published: December 2008

Abstract. To clarify the role of vitamin D in the regulation of the endocrine pancreas, we have studied insulin and somatostatin secretion in vitamin D deficient rats (reared on a vitamin D dificient diet), D-replete rats (reared on a vitamin D deficient diet and given 160 IU of vitamin D3 sc twice a week) and control rats (reared on laboratory chow), using the isolated perfused rat pancreas.
In the vitamin D deficient rats, the perfusate insulin induced by 16.7 mm glucose was only 35% of the secretion in the control rats. In the D-replete rats, the insulin release was restored to that of the controls. Similarly, the plasma insulin level in the vitamin D deficient rats was very low and the level in the D-replete rats was also restored to the level of the controls. The perfusate somatostatin response to glucose was not significantly different in any of the three groups. In addition, since the plasma calcium level in the vitamin D deficient rats was very low and in the D-replete rats was still lower, compared to normal rats, we suggest that vitamin D acts not only via the plasma calcium level but possibly also directly on the B cell.
Glucose-induced somatostatin secretion by the rat pancreas is not potentiated by glucose
Authors: Gerber P. P. G. , Trimble E. R. , Herberg L. , Renold A. E. 
Published: December 2008

Abstract. The effect of previous exposure to glucose on subsequent glucose-stimulated insulin and somatostatin secretion has been investigated using the isolated perfused rat pancreas. As expected, when the pancreases of non-diabetic rats were exposed to 16.7 mM glucose on two occasions, 20 min apart, insulin secretion during the second period of exposure to high glucose was greater than that during the first period. By contrast, there was no potentiation of somatostatin secretion during the second glucose stimulation with respect to that of the first. Indeed, when the basal glucose concentration was low (1.4 or 2.8 mm) somatostatin secretion during the second glucose stimulation was lower than that during the first.
Since exogenous insulin is known to inhibit glucoseinduced somatostatin secretion, it seemed possible that lack of visible potentiation of glucose-induced somatostatin secretion by glucose could have been due to partial D cell inhibition by simultaneously augmented insulin secretion during the second glucose stimulation. In an attempt to exclude such an interaction between B and D cells, somatostatin secretion was also studied in the pancreases of spontaneously diabetic, Wistar (BB) rats (these animals are insulin deficient and are maintained by daily injections of insulin). However, even though insulin secretion was not detectable from these pancreases, glucose potentiation of glucose-induced somatostatin secretion did not occur.
Although the pancreatic B and D cells are known to respond in a similar manner to many secretagogues the present results show that glucose potentiation of glucosestimulated somatostatin secretion is not found under circumstances where potentiation of insulin secretion does occur. In addition, the absence of potentiated somatostatin secretion could not be attributed to partial inhibition of the D cell by insulin.
The combination of insulin and sulphonylurea in the treatment of secondary drug failure in patients with type II diabetes
Authors: Groop Leif , Harno Kari , Tolppanen Esa-Matti 
Published: December 2008

Abstract. Thirteen patients (6 females and 7 males) who were secondary failures on oral drug therapy were randomly allocated to either 2 months of treatment with insulin + glibenclamide or insulin + placebo. Thereafter the treatment schedules of the two groups were switched over for another two months.
The combination of insulin and glibenclamide was more effective in lowering the fasting blood glucose (P = 0.026) and 24 h urine glucose (P = 0.042) than the combination of insulin and placebo. The combination therapy with insulin and glibenclamide revealed higher basal (P = 0.021) and glucagon-stimulated C-peptide concentrations (P = 0.037) than therapy with insulin and placebo. However, insulin binding to erythrocytes did not differ between the two study periods. The results indicate that the addition of glibenclamide to insulin in type II diabetics poorly controlled by oral antidiabetics alone may slightly improve diabetic control. The mechanism of this action is due at least partly to sulphonylureainduced stimulation of endogenous insulin secretion.
The effectiveness of the combination treatment during long-term therapy still remains to be proven, however.
The effects of dopaminergic blockade on serum TSH and prolactin levels in thyrotoxicosis
Authors: Swart S. , O'Malley B. P. , Vora J. , Barnett D. B. , Rosenthal F. D. 
Published: December 2008

Abstract. In the first part of this study, we have demonstrated that, in 7 patients with untreated thyrotoxicosis, a 7 day regime of the long acting dopamine antagonist metoclopramide (10 mg orally 8 hourly) produces more adequate dopaminergic blockade at pituitary level than a single oral 10 mg dose of the compound as assessed by serum prolactin responses.
Subsequently, we have employed this protracted oral metoclopramide regime to evaluate the contribution of dopaminergic tone to the abnormal TSH and prolactin responsiveness of thyrotoxicosis. Serum TSH and prolactin responses to iv TRH (200 μg) were measured in 10 untreated thyrotoxic patients before and after a 7 day period of metoclopramide 10 mg orally 8 hourly. Ten euthyroid individuals were studied in similar fashion, their serum samples being analysed for prolactin levels alone, thus providing a control group for prolactin responsiveness to TRH, before and after metoclopramide.
In the thyrotoxic patients basal TSH levels did not change as a consequence of metoclopramide therapy and the TSH response to TRH remained flat. Basal prolactin levels were similar in thyrotoxic and euthyroid individuals and the increase in prolactin, seen in both groups after metoclopramide, was smaller in the thyrotoxic group than in the euthyroid group. Prolactin responsiveness to TRH was significantly impaired in the thyrotoxic subjects as compared to euthyroid subjects. After metoclopramide there was a significant decline in prolactin responsiveness in the euthyroid group, and a similar, though insignificant, trend in the thyrotoxic patients.
We conclude that in thyrotoxicosis dopaminergic tone plays no major part in the suppression of TSH levels, nor in the impaired prolactin responsiveness to TRH.
Insulin hypoglycaemia test guided by a glucose controlled insulin infusion system
Authors: Müller-Esch Gert , Ball Peter , Heidbüchel Karen , Wood William Graham , Scriba Peter C. 
Published: December 2008

Abstract. Insulin hypoglycaemia test (IHT) for assessment of hypothalamic-pituitary-adrenocortical (HPA) function in patients with pituitary tumours is usually performed by bolus injection of insulin, a procedure which includes the risk of overdosage and/or the need of repeated administration. This study describes that a glucose controlled insulin infusion system (GCIIS) permits to perform the IHT with standardized hypoglycaemia. Ten healthy volunteers and 10 patients with pituitary tumours were studied using the GCIIS (Biostator®) on static control (Mode 1:1, BI 35, QI 10, RI 20, FI 300). Insulin administration was discontinued and the GCIIS used only for monitoring of blood glucose (BG), when BG had fallen below 40 mg/dl and initial clinical symptoms for hypoglycaemia were observed. In controls, the GCIIS guided IHT achieved a sufficient degree of hypoglycaemia (BG 27.6 ± 2.0 mg/dl; mean ± sem) and physiological responses for GH (peak 49.4 ± 6.7 ng/ml), Prl (peak 1766 ± 614 μU/ml), ACTH (peak 76.0 ± 8.7 pg/ml) and cortisol (peak 252 ± 15 ng/ml). The total amount of insulin given was 0.115 ± 0.012 U/kg. In the patients with pituitary tumours however, the required insulin dose varied markedly from 0.090 (pituitary insufficiency) to 0.340 U/kg (Cushing's syndrome). Minimum BG obtained was 32.5 ± 1.9 mg/dl. Partial impairment of hypothalamic-pituitary function and, in particular, patients requiring exogenous cortisol supplementation during stress, could be identified. In conclusion, special advantages of the GCIIS-guided IHT are:
Optimal insulin dosage with standardized hypoglycaemia due to automatic adjustment to the individual insulin sensitivity. Patients' safety by earlier recognition of due insulin discontinuation as a result of continuous blood glucose analysis.
Prl, TSH, FSH, β-hCG and oestriol responses to repetitive (triple) LRH/TRH administration in the third trimester of human pregnancy
Authors: Pérez-López F. R. , Robert J. , Teijeiro J. 
Published: December 2008

Abstract. The effects of repetitive administration of 50 μg of LRH and 100 μg of TRH in a single bolus at 0, 90 and 180 min on Prl, TSH, FSH, μ-hCG and oestriol were tested in 11 healthy pregnant women in their third trimester of pregnancy. Basal hormonal levels were in agreement with previous reports. The Prl and TSH peaks after each injection of LRH/TRH were similar for each hormone. No significant changes in serum FSH, β-hCG and oestriol were detected after repetitive administration of LRH/TRH.
Thus, the responsiveness of lactotroph and thyrotroph cells to pulsatile stimulation with LRH/TRH is not altered during the last trimester of pregnancy, and FSH, β-hCG and oestriol levels remain constant during the period of sampling.
Foetal exposure to low doses of cyproterone acetate in the rat leads to functional endocrine abnormalities despite normal sexual morphogenesis
Authors: Gómez Fulgencio , Monnier Bernard , Lemarchand-Béraud Thérèse 
Published: December 2008

Abstract. Cyproterone acetate (CPA), an anti-androgen and a gestagen, was administered to pregnant Wistar rats at very low doses (0.5 or 1.0 mg/day) between days 15 and 20 of pregnancy. No anatomical abnormalities were observed in external genitalia of their offspring, either immediately after birth or upon reaching maturity. However, when these animals were studied in adulthood, several endocrine abnormalities became apparent.
While the pituitary content of Prl decreased in the CPA-exposed offspring, the amount of LH increased. Plasma Prl was lower and FSH was higher in treated females whereas plasma LH was higher in both sexes compared to controls. Treatment induced a Prl-responsiveness to TRH in both sexes and an enhanced LH- and FSH-response to GnRH in females.
Testicular weights, LH/hCG receptors in testicular membrane preparations and testosterone response to in vivo hCG stimulation were identical in both the treated and control groups. Basal testosterone, however, was increased in the face of decreased ventral prostate weight and of decreased androgen receptors in prostate cytosol, indicating androgen resistance of the target organ.
Females displayed normal oestrous cycles, but possessed enlarged ovaries and uteri. The decrease in oestrogen receptors (ER) in uterine cytosol during oestrus and the relative increase of ER in dioestrus were consistent with enhanced oestrogenic action, presumably by increased oestrogen secretion by the hyperstimulated ovaries.