bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relations between diurnal variations in serum osteocalcin, cortisol, parathyroid hormone, and ionized calcium in normal individuals
Authors: Nielsen Henning Kaspersen , Laurberg Peter , Brixen Kim , Mosekilde Leif 
Published: June 2009

Abstract.
Serum osteocalcin varies in a diurnal rhythm, with peak values during the night and minimum levels before noon, but the factors controlling this rhythm are unknown. In this study, we evaluated the temporal relations between the osteocalcin rhythm and variations in serum concentrations of cortisol, intact parathyroid hormone (PTH(1-84)), and ionized calcium (Ca2+) in 15 normal volunteers, aged 22-46 years. Serum cortisol varied in a typical way preceding inverse changes in serum osteocalcin by about 4 h (r=0.78, p<0.0001). Changes in serum osteocalcin following the early morning increase in serum cortisol were statistically indistinguishable from the changes seen after oral administration of 2.5 or 10 mg of prednisone. Serum PTH (1-84) showed a diurnal rhythm (p<0.01) with peak values (4.06±0.42 pmol/l) at 20.30 h and nadir (2.81±0.10 pmol/l) around 10.30 h, preceding changes in serum osteocalcin in the same direction by 5 h (r=0.55, p<0.02). Prednisone at a dose of 10 mg did not change the time course significantly. Serum Ca2+ varied in an almost bi-phasic pattern (p<0.01) with maximal mean levels around 16.30 and 09.30 h and minimal levels around 05.30 and 14.30 h. Serum Ca2+ correlated inversely with PTH (1-84) (r=0.53, p<0.01), and serum osteocalcin was inversely related to Ca2+ at concurrent time points (r=0.59, p<0.005). Prednisone caused a 2-3 h lasting increase in serum Ca2+ 3-5 h after ingestion (p<0.001). In conclusion, our results suggest that cortisol is strongly associated to the diurnal rhythm in serum osteocalcin. The biological relevance of the reported relation between serum osteocalcin and PTH (1-84) and serum Ca2+ is uncertain.
Why no simple relationship between thyroid peroxidase activity-inhibiting immunoglobulins and thyroid function in autoimmune thyroid disease?
Authors: Okamoto Yasuyuki , Hamada Noboru , Fujisawa Toshimichi , Noh Jaeduk , Yamakawa Junichi , Ohno Mariko , Ito Kunihiko , Morii Hirotoshi 
Published: June 2009

Abstract.
We have reported that some anti-thyroid peroxidase antibodies inhibit the activity of thyroid peroxidase in vitro. These thyroid peroxidase activity-inhibiting immunoglobulins seem to inhibit thyroid function in some patients, but the relationship between thyroid peroxidase activity-inhibiting immunoglobulins and thyroid function is not simple. We designed this study to explore this lack of a simple relationship. We stained immunoglobulin G deposits by immunofluorescence staining or the peroxidase-antiperoxidase method, and stained endogenous thyroid peroxidase activity by enzyme histochemistry in thyroid sections. When cryostat thyroid sections were incubated with thyroid peroxidase activity-inhibiting immunoglobulins, immunoglobulin G deposits were seen as lines of stain on the apical border and as intracellular staining, and endogenous thyroid peroxidase activity was inhibited. In paraffin-embedded thyroid sections from 5 Hashimoto's patients and 6 Graves' patients, immunoglobulin G deposits were not found on the apical border of the follicular epithelium. In frozen thyroid sections from 22 Graves' patients, no clear deposits of immunoglobulin G on this apical border were seen. In organ-cultured thyroid slices incubated with thyroid peroxidase activity-inhibiting immunoglobulins, endogenous thyroid peroxidase activity was not inhibited. In conclusion, thyroid peroxidase activity-inhibiting immunoglobulins may reach its antigen only with difficulty. This is one of the reasons why no simple relationship is observed between thyroid peroxidase activity-inhibiting immunoglobulins and thyroid function.
Inhibitory effects of ionophore A23187 on the release of thyroid hormone and colloid reabsorption in mouse thyroid glands
Authors: Mori-Tanaka Misuzu , Tajima Koji , Miyagawa Jun-ichiro , Oda Yasuo , Matsui Ikuko , Kitajima Koichi , Hanafusa Toshiaki , Tarui Seiichiro , Mashita Kazuhiko 
Published: June 2009

Abstract.
The effect of the ionophore A23187 on a. the release of thyroid hormone from perifused mouse thyroid glands and b. the morphological changes in follicular epithelial cells was evaluated. A23187 at a concentration of 5 μmol/l significantly inhibited both the TSH- and the forskolin-stimulated release of T3 and T4. In the presence of 3-isobutyl-1-methylxanthine or (4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone) RO 20-1724, A23187 did not affect the forskolin-stimulated release of cAMP, but did inhibit the release of T3 and T4 stimulated by forskolin. Light and electron microscopic evaluation of the follicular epithelial cells of mouse thyroid tissues following 1-h stimulation with forskolin showed numerous pseudopods engulfing luminal colloid of various size and the presence of reabsorbed colloid droplets in the apical cytoplasm. Quantitative electron microscopic analysis revealed that the addition of the ionophore A23187 reduced the number of reabsorbed colloid droplets to one eighth in follicular epithelial cells. These observations suggest that the increase in intracellular Ca2+ induced by the ionophore A23187 inhibits the TSH-stimulated thyroid hormone release independently of the cAMP level, and that the suppression of thyroid hormone release may be due to an inhibition of colloid reabsorption.
Thyroid function and autoimmune manifestations in insulin-dependent diabetes mellitus during and after pregnancy
Authors: Bech Karine , Høier-Madsen Mimi , Feldt-Rasmussen Ulla , Jensen Bente Møller , Mølsted-Pedersen Lars , Kühl Claus 
Published: June 2009

Abstract.
Insulin-dependent diabetes is associated with other autoimmune diseases and subclinical hypothyroidism has been reported in pregnant diabetic women. We studied the thyroid function of 85 women with diabetes during pregnancy and after delivery, as well as various autoantibodies. During pregnancy, thyroid microsomal antibodies were present in 17/85, antibodies against thyroid peroxidase in 16/85, thyroglobulin antibodies in 2/85, parietal cell antibodies in 23/85, adrenal antibodies in 4/77, rheumatoid factor in 15/85, and thyroid-stimulating antibodies in 43/85. Presence of antibodies was not combined with thyroid dysfunction, but TSH and HbA1c was increased (p<0.005) in women with thyroid antibodies. The gestational age of the infants was lower (p<0.01) in women with positive thyroid-stimulating antibody titre, whereas the ponderal index was only lower in those with peroxidase antibodies (p<0.05). After delivery, microsomal and peroxidase antibodies were positive in 10 (17.5%) of 57 patients followed. Six women developed postpartum thyroiditis (10.5%), of whom 5 were positive for both microsomal and peroxidase antibodies; two of those showing a hyperthyroid phase also had positive thyroid-stimulating antibody titre. We conclude that autoantibodies occur with increased incidence in pregnant diabetic women. Thyroid antibodies are related to a slightly reduced thyroid capacity and involve a high risk of postpartum thyroiditis. Further, thyroid antibodies seem to influence the nutritional status of the infant.
The effect of acute hyperglycemia on the plasma C-peptide response to intravenous glucagon or to a mixed meal in insulin-dependent diabetes mellitus
Authors: Gjessing H. J. , Reinholdt B. , Faber O. K. , Pedersen O. 
Published: June 2009

Abstract.
The dose-response relationships between prestimulatory blood glucose concentration and the plasma C-peptide responses to stimulation with 1 mg of glucagon iv or a standard mixed meal were studied in 8 C-peptide positive patients with insulin-dependent diabetes mellitus. Hyperglycemia was maintained for 90 min before stimulation using a hyperglycemic clamp technique. Each test was performed at the steady state blood glucose levels ~5, ~12, and ~20 mmol/l. The glucose potentiation of the incremental plasma C-peptide area under the curve at the two levels of hyperglycemia in percent of the area at normoglycemia (median and range) was 343% (53-1053) (p<0.05) and 341% (267-1027) (p<0.05) after glucagon and 140% (76-227) (NS) and 251% (95-1700) (p<0.05) after the meal. The corresponding relative glucose potentiation of plasma C-peptide 6 min after stimulation with glucagon was 124% (100-427) (p<0.02) and 144% (100-209) (p<0.05). There was no significant difference in the degree of glucose potentiation at ~12 or ~20 mmol/l. Furthermore, there was no significant difference in the degree of glucose potentiation of the different estimated values of B-cell function. In conclusion, the plasma C-peptide responses to iv glucagon or to a standard test meal were markedly potentiated by acute hyperglycemia in insulin-dependent diabetes mellitus. No further potentiation was, however, obtained when the prestimulatory blood glucose concentration was raised above 12 mmol/l. These findings contrast those reported in non-insulin-dependent diabetes, where endogenous insulin secretion is potentiated further when the blood glucose concentration is raised to ~20 mmol/l.
Longitudinal bone growth in vitro: effects of insulin-like growth factor I and growth hormone
Authors: Scheven Ben A. A. , Hamilton Nicola J. 
Published: June 2009

Abstract.
Longitudinal growth was studied using an in vitro model system of intact rat long bones. Metatarsal bones from 18- and 19-day-old rat fetuses, entirely (18 days) or mainly (19 days) composed of chondrocytes, showed a steady rate of growth and radiolabelled thymidine incorporation for at least 7 days in serum-free media. Addition of recombinant human insulin-like growth factor-I to the culture media resulted in a direct stimulation of the longitudinal growth. Recombinant human growth hormone was also able to stimulate bone growth, although this was generally accomplished after a time lag of more than 2 days. A monoclonal antibody to IGF-I abolished both the IGF-I and GH-stimulated growth. However, the antibody had no effect on the growth of the bone explants in control, serum-free medium. Unlike the fetal long bones, bones from 2-day-old neonatal rats were arrested in their growth after 1-2 days in vitro. The neonatal bones responded to IGF-I and GH in a similar fashion as the fetal bones. Thus in this study in vitro evidence of a direct effect of GH on long bone growth via stimulating local production of IGF by the growth plate chondrocytes is presented. Furthermore, endogenous growth factors, others than IGFs, appear to play a crucial role in the regulation of fetal long bone growth.
Inhibition of growth hormone secretion by activin A in human growth hormone-secreting tumour cells
Authors: Kitaoka Masafumi , Takano Kohji , Tanaka Yuji , Kojima Itaru , Teramoto Akira , Ogata Etsuro 
Published: June 2009

Abstract.
Effect of activin A on growth hormone secretion was studied in primary culture of 8 human GH-secreting adenomas, which were responsive to TRH in vivo. When studied in vitro, basal GH secretion was reduced in all cases when cells were pre-incubated for 48 h with activin A at a concentration of 5×10−9 mol/l or greater. Pretreatment of GH-secreting cells with 1× 10−9 mol/l activin A did not affect either basal secretion or cellular content of GH. These tumour cells also responded to TRH in vitro and the GH response to TRH was completely blocked in cells pretreated with activin A. Activin A slightly reduced the increase in cytoplasmic free calcium concentration induced by TRH. Furthermore, pretreatment of the cells with activin A attenuated GH secretion induced by A23187 or 12-O-tetradecanoyl phorbol-4-acetate, agents which bypass receptor-mediated generation of second messengers. These results indicate that activin A inhibits GH secretion by directly acting on human GH-secreting cells and that activin A inhibits the action of TRH by acting on multiple steps in the messenger system.
The effect of human growth hormone therapy on GH binding protein in GH-deficient children
Authors: Hochberg Zeev , Barkey Ronnie J. , Even Lea , Peleg Israela , Youdim Moussa B. H. , Amit Tamar 
Published: June 2009

Abstract.
Previous studies have described the close similarity of the GH binding protein to the liver membrane GH receptor. Since GH regulates its own liver receptors, we examined the effects of short- and long-term hGH therapy on GH binding protein in children with GH deficiency. Six GH-deficient children received their first hGH dose ever, and the pharmacodynamics of serum GH was followed for 12 h, along with measurements of GH binding protein activity. Over the first 6 h, serum GH and GH binding protein activity exhibited a parallel increase, followed by gradual decrease. At 8 h, some of the patients exhibited an apparent second peak in GH binding protein, despite the continuous decrease in serum hGH. During the period of hGH treatment, serum GH binding protein increased progressively over a period of 6 months. In a second uncontrolled group of 7 GH-deficient patients who had been treated with hGH for 30-36 months, GH binding protein activity was also significantly higher than pretreatment values. We suggest that the short-term pharmacodynamic changes probably represent the endogenous turnover of the GH receptor, whereas the elevated GH binding protein activity on hGH treatment may reflect up-regulation of the GH receptor.
Increased urinary free cortisol and decreased serum corticosteroid-binding globulin in polycystic ovary syndrome
Authors: Invitti Cecilia , Giraldi Francesca Pecori , Dubini Antonella , De Martin Martina , Cavagnini Francesco 
Published: June 2009

Abstract.
The adrenal participation in the pathogenesis of polycystic ovary syndrome is still under debate. In order to reappraise androgen and glucocorticoid secretion in this disease, we measured serum androstenedione, dehydroepiandrosterone-sulphate, total and free testosterone, sex hormone-binding globulin, LH, FSH, PRL, cortisol, corticosteroid-binding globulin, and urinary free cortisol in 45 women with polycystic ovary syndrome and 27 controls, subdivided in obese and normal-weight subjects. Androstenedione, total and free testosterone were significantly increased, whereas sex hormone-binding globulin tended to be reduced in patients with polycystic ovary syndrome compared with controls, reaching a significant difference between obese patients and matched controls. Free testosterone and sex hormone-binding globulin were significantly increased and reduced, respectively, in obese compared with normal-weight patients. Urinary free cortisol and serum corticosteroid-binding globulin were significantly increased (p<0.001) and decreased (p<0.005), respectively. Urinary free cortisol exceeded the upper limit of the normal range in 50% of our patients. No appreciable differences were found in PRL and cortisol levels. Besides confirming a hyperandrogenic state, our findings point to an overactivity of the hypothalamic-pituitary-adrenal axis with subsequent diminution of corticosteroid-binding globulin in polycystic ovary syndrome. They also indicate that urinary free cortisol is not a reliable index in differentiating polycystic ovary syndrome from Cushing's disease.
Biosynthetic growth hormone changes the collagen and elastin contents and biomechanical properties of the rat aorta
Authors: Brüel Annemarie , Oxlund Hans 
Published: June 2009

Abstract
The biomechanical and biochemical properties of aortas from female rats treated with biosynthetic human GH (b-hGH) for 80 days were investigated. b-hGH was administered at a dose of 5 mg·kg−1·d−1. Treatment with b-hGH increased the body weight by 75% and the diameter of the aorta by 14% compared with the control group. The concentration of collagen and the relative amount of collagen type I were increased, and the concentration of elastin was decreased. Aortas from the b-hGH-treated group showed increased extensibility in the regions corresponding to physiological load values (i.e. 100-200 mmHg), and increased stiffness in regions with higher load values. The increased extensibility at low load values corresponds well with the loss of elastin, and the increased stiffness at higher load values with the increase of collagen and relative increase of collagen type I. These alterations induced by the growth hormone treatment might influence the elasticity and recoiling properties of the aorta.
Thyroid hormone as a biological amplifier of differentiated trophoblast function in early pregnancy
Authors: Maruo Takeshi , Matsuo Hiroya , Mochizuki Matsuto 
Published: June 2009

Abstract.
Direct effects of T3 or T4 on the trophoblast function were investigated in vitro using an organ culture system of human placental tissues. Explants of trophoblastic tissues obtained from normal early and term placentas were cultured with or without graded doses of T3 or T4 for 5 days in a serum-free condition. Addition of T3 (10−8 mol/l) resulted in the maximum increase in daily secretion of progesterone, estradiol-17β as well as hCGα, hCGβ, hCG and hPL by cultured early placental tissues. Increases in progesterone and estradiol-17β secretion caused by the addition of T3 were further augmented in response to concomitant addition of pregnenolone and testosterone, respectively, suggesting that T3 (10−8 mol/l) enhances 3β-hydroxysteroid dehydrogenase and aromatase activity in the placenta. These stimulatory effects of T3 (10−8 mol/l) on the trophoblast endocrine function were also found with the use of T4 (10−7 mol/l). Addition of higher or lower concentrations of T3 or T4 gave attenuated effects. These results suggest that the optimal concentration of thyroid hormone is needed for it to exert its maximally stimulatory action on trophoblast endocrine function. Unlike early placental tissues, cultured term placental tissues did not respond to the addition of T3 or T4 with increased endocrine activity. Thus, the frequent occurrence of spontaneous abortion in early pregnancy during the state of hypothyroidism or hyperthyroidism may represent a direct consequence of inadequate thyroid hormone availability at the level of placental trophoblasts, followed by diminished expression of trophoblast endocrine function.
Effects of decreasing exogenous GnRH pulse frequency on FSH and inhibin secretion in men with idiopathic hypogonadotropic hypogonadism
Authors: Wu Frederick CW , Wallace Euan M , Howe David C , Kacser Elaine M , Sellar Robin E 
Published: June 2009

Abstract.
The potential importance of GnRH pulse frequency modulation and steroid or inhibin negative feedback in the selective control of pituitary FSH secretion was investigated in 5 adult men with idiopathic hypogonadotropic hypogonadism in whom plasma testosterone has been previously normalized by pulsatile GnRH therapy. The effects of decreasing frequency of pulsatile iv GnRH administration from 2- to 4-hourly for 7 days were examined at constant GnRH bolus dose or constant daily dose and also with interrupted gonadal steroid feedback using a combination of an anti-androgen (flutamide 250 mg t.i.d.) and an aromatase inhibitor (aminogluthetimide 125 mg b.d.) orally for a further 7 days. Slowing GnRH pulse frequency from 2- to 4-hourly did not alter mean plasma FSH at constant bolus dose or constant total daily doses of GnRH. In two subjects with subnormal but not in another two with normal testicular volumes, FSH rise was observed when the 4-hourly GnRH pulse frequency was combined with the interruption of steroid feedback. These results are not compatible with a major role for GnRH pulse frequency modulation in the regulation of pituitary FSH secretion in the presence of normal gonadal steroid feedback. Irrespective of FSH concentrations, plasma inhibin immunoactivity did not change significantly with the alteration in GnRH pulse frequency. The role of inhibin in the control of FSH therefore remains undefined in men.
Impaired conversion of cortisol to cortisone in chronic renal insufficiency - a cause of hypertension or an epiphenomenon?
Authors: Vierhapper H. , Derfler K. , Nowotny P. , Hollenstein U. , Waldhäusl W. 
Published: June 2009

Abstract.
To study the possible impairment of 11 β-hydroxysteroid-dehydrogenase in patients with chronic renal insufficiency, urinary excretion rates of the four main glucocorticoid-metabolites, tetrahydrocortisol, tetrahydrocortisone, allotetrahydrocortisol and allotetrahydrocortisone were determined by capillary gas chromatography in 22 patients with chronic renal insufficiency with (N=15) and without (N=7) hypertension, but without hemodialysis treatment. Whereas the sum of all 41 steroid metabolites determined by capillary gas chromatography was reduced (p<0.001) in patients with chronic renal insufficiency as compared with 22 healthy individuals, the relative contribution of the four glucocorticoid metabolites to total steroid excretion was similar in patients with renal insufficiency (22±12%) and in healthy subjects (20±5%). However, the excreted amount of tetrahydrocortisol exceeded that of tetrahydrocortisone in all but 3 (normotensive) patients with chronic renal insufficiency, but only in one healthy subject resulting, in patients with chronic renal insufficiency, in a ratio of tetrahydrocortisone vs tetrahydrocortisone of 0.7±0.4 (hypertensive patients 0.5±0.2; normotensive patients 1.1±0.4; controls 1.9±0.9, p<0.001 vs patients with chronic renal insufficiency). This ratio of tetrahydrocortisone/tetrahydrocortisol showed a correlation with serum concentrations of creatinine (p<0.001). These results provide indirect proof of an impaired conversion of cortisol to cortisone in moderate renal insufficiency and may suggest a relationship with the hypertension frequently seen in this group of patients.
Differential effects of insulin-like growth factors I and II on growth, differentiation and glucoregulation in differentiating chondrocyte cells in culture
Authors: Bhaumick Banani , Bala R. Marvin 
Published: June 2009

Abstract.
Insulin-like growth factors I and II have been shown differentially to affect the growth and carbohydrate metabolism of differentiating cartilage developed from mouse embryonic limb buds in organ culture. To gain insight into the relative importance of IGF-I and II actions in different stages of development of cartilage we have established a primary culture of differentiating chondrocytes from mouse embryonic limb buds. Trypsin digested limb bud cells from 9-11 day old mouse embryos differentiated into chondrocytes by 5-7 days in culture. At all stages of differentiation, distinct receptors of IGF-I and II were observed. IGF-I stimulated growth and sulphate incorporation of the non-differentiated and differentiated chondrocytes. IGF-II stimulated growth of the non-differentiated cells and had no effect on growth or sulphate incorporation by the differentiated cells. IGF-II, however, stimulated the glucose uptake by the cells at all stages of differentiation. These data confirm our previous suggestion that IGF-I in cartilage is the regulator of growth and differentiation, while IGF-II may be an important regulator of glucose metabolism in the tissue.