Effects of growth hormone on bone modeling and remodeling in intact middle-aged female rats

Bone ◽  
2009 ◽  
Vol 44 ◽  
pp. S433
Author(s):  
J.K. Yeh⁎ ◽  
J.F. Aloia
1987 ◽  
Vol 46 (2) ◽  
pp. 137-142 ◽  
Author(s):  
Sumio Takahashi ◽  
Paul E. Gottschall ◽  
Kathleen L. Quigley ◽  
Rodolfo G. Goya ◽  
Joseph Meites

2017 ◽  
Author(s):  
Branka Šošić-Jurjević ◽  
Snežana Janković ◽  
Dieter Lutjohann ◽  
Ivana Jarić ◽  
Marko Miler ◽  
...  
Keyword(s):  

Author(s):  
Sajad Jeddi ◽  
Saeedeh Khalifi ◽  
Mahboubeh Ghanbari ◽  
Asghar Ghasemi

Background and objective: The effects of hypothyroidism during pregnancy and lactation on carbohydrate metabolism have been mostly studied in male animals. The aim of this study is therefore to investigate effect of fetal and neonatal hypothyroidism (FH and NH) on the glucose tolerance in middle-aged female rat offspring. Methods: Pregnant female rats were divided into three groups: Rats in the control group consumed tap water, while those in the FH and NH groups consumed 250 mg/L of 6-propyl-2-thiouracil (PTU) in their drinking water during gestation or lactation periods, respectively. After weaning, the female offspring were separated and divided into 3 groups (n=8/group): Control, FH, and NH. Body weight was recorded monthly and intravenous glucose tolerance test (IVGTT) was performed at month 12. Results: Compared to controls, female rats in the FH group had significantly higher plasma glucose levels than controls throughout the IVGTT except at min 60. Values at min 5 of the FH and control group were 196.1±1.9 and 155.3±5.9 mg/dL, respectively (P<0.05). In the NH group, plasma glucose levels were significantly higher only at min 5 (185.7±14.1 vs. 155.3±5.9 mg/dL, P<0.05). Conclusion: Hypothyroidism during fetal or neonatal periods caused glucose intolerance in middle-aged female offspring rats.


1982 ◽  
Vol 100 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Oddvar Naess ◽  
Egil Haug ◽  
Arne Attramadal ◽  
Kaare M. Gautvik

Abstract. Progesterone and corticosterone have a similar effect on the production of growth hormone (GH) and prolactin (Prl) by pituitary tumour cells (GH3 cells) in culture. Previously we have shown that progesterone has a high affinity for the glucocorticoid receptors in these cells. Progesterone may therefore exert its effects through binding to the glucocorticoid receptor. The aim of the present study was to investigate if the GH3 tumour cells and an oestrogen induced pituitary tumour, which also produce GH and Prl, possess specific receptors for progesterone. Both the GH3 tumours and the oestrogen induced pituitary tumour were in fact found to possess cytoplasmatic receptor molecules for progesterone by using the potent progestin R5020 as a marker. Isoelectric focusing revealed one binding component (pH 5.9), which was of protein nature. The binding was of high affinity (Kd 2 × 10−9 mol/l). In the oestrogen induced tumour, the maximal binding was 70 fmol/mg cytosol protein. In female rats with GH3 tumours the binding was 55 fmol/mg cytosol protein. Priming of the animals with 1 mg oestradiol-valerate increased the binding to 116 fmol/mg cytosol protein, whereas very little binding was found in GH3 tumours from rats castrated 7 days before sacrifice. The receptors in the oestrogen induced pituitary tumour and the GH3 tumours exhibited high affinity for R5020 and progesterone, whereas corticosterone had no significant affinity for the receptors. Using exchange assay, it was demonstrated that the cytoplasmic progestin receptors could be translocated to the nucleus after administration of progesterone to the animals. Thus, the presence of specific progesterone receptors, different from the glucocorticoid receptors, strongly indicates that the effects of progesterone on GH and Prl production are mediated through the progesterone receptors.


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