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  • 1
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 136, No. 6 ( 1997-06), p. 608-616
    Abstract: The present study was performed to examine the effect of natural menopause on serum levels of IGF-I, IGF-binding protein (IGFBP-2) and -3 as well as on bone mass and lipid metabolism in perimenopausal women. One hundred and twenty-one healthy Japanese women, who were 45–55 years old, were studied (71 premenopausal and 50 postmenopausal women 1–9 years after menopause). Bone mineral density (BMD) was measured at the middle third of the radius by using dual energy X-ray absorptiometry. Serum levels of IGF-I, but not those of IGFBP-2 or -3, were significantly reduced in the postmenopausal group compared with the premenopausal group. One year after menopause, serum IGF-I levels were significantly lower, and the biochemical markers of bone turnover, such as serum total alkaline phosphatase level and urinary calcium to creatinine ratio, were significantly higher than the premenopausal levels. Serum levels of IGF-I, but not those of IGFBP-2 or-3, were positively correlated with BMD. Serum levels of IGFBP-2, but not those of IGF-I or IGFBP-3, were negatively correlated with body mass index and body weight. Finally, serum levels of IGFBP-3, but not those of IGF-I, were positively correlated with serum levels of total cholesterol and triglyceride. The present findings suggest that a rapid decrease in serum IGF-I levels after menopause might be partly involved in bone loss following gonadal failure and that IGFBP-2 and -3 might be related to the regulation of body mass and lipid metabolism during perimenopause respectively, although the mechanisms remain unknown. European Journal of Endocrinology 136 608–616
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    RVK:
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 1997
    detail.hit.zdb_id: 1485160-X
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  • 2
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 153, No. 1 ( 2005-07), p. 57-65
    Abstract: Objectives : To investigate the effects of growth hormone (GH) treatment, using a dose-adjustment regimen based on serum insulin-like growth factor (IGF)-I concentrations, in adult Japanese hypopituitary patients with GH deficiency. Study design : Japanese patients who had initially been administered GH ( n = 31) or placebo ( n = 28) in a 24-week double-blind study received individualized GH treatment in an open-label study for 48 weeks. Body composition from dual-energy X-ray absorptiometry (DXA) and serum IGF-I, IGF-binding protein 3 (IGFBP-3) and lipid levels were determined centrally. Results : Significant increases in lean body mass (4.5%) and decreases in fat mass (−10.5%) were observed in the group that received individualized GH doses in the present open-label study following placebo in the double-blind study. This was comparable with the changes observed in these parameters (4.7 and −9.2%, respectively) with fixed-dose GH treatment in the double-blind study; this latter group maintained these improvements throughout the open-label study. Individualized dose adjustment allowed for more moderate dose increases than the fixed-dose titration method. Individualized dosing also resulted in a lower mean dose for adult-onset compared with childhood-onset GH-deficient patients (0.032±0.019 versus 0.061±0.023 mg/kg per week for patients treated with GH for 48 weeks in the open-label study following placebo in the double-blind study). Dosing patterns in the two groups were paralleled by the changes in IGF-I and IGFBP-3. The incidence of oedema and cases with high IGF-I level were less frequent under the IGF-I controlled regimen compared with those during the fixed-dose titration method. Conclusion : Individualized GH administration based on IGF-I levels was safe and effective. This regimen demonstrated differences in dose requirements between adult- and childhood-onset patients. An individualized dose regimen is recommended in adult Japanese GH-deficient patients.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    RVK:
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2005
    detail.hit.zdb_id: 1485160-X
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  • 3
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 156, No. 6 ( 2007-06), p. 637-645
    Abstract: Objective : To examine the responsiveness of quality of life (QoL) associated with changes in clinical indices relevant to GH deficiency (GHD) in Japanese hypopituitary adults. Design and methods : QoL was determined using the Short Form (SF)-36 in Japanese adults with adult-(AO; n = 27) or childhood- (CO; n = 37) onset GHD in a 24-week double-blind placebo-controlled study with a fixed GH dose, and a subsequent 48-week open-label extension study with GH doses individualized using serum IGF-I levels. Results : Baseline QoL was significantly decreased from the Japanese national reference in both onset types, more so in AO patients. Throughout the study, AO patients showed a trend for an increase in physical functioning and general health ( P = 0.0564 and 0.0999 respectively), whereas CO patients showed no changes in these domains. Fat mass changes negatively correlated with the changes in physical functioning and general health in AO patients ( r = −0.42 and −0.64 respectively), but to a lesser degree in CO patients ( r = −0.36 and −0.32 respectively). CO patients displayed significant decreases in social functioning ( P = 0.0305) and mental health ( P = 0.0442) and a decreasing trend in bodily pain ( P = 0.0769), although no correlation between these decreases and any measured clinical index was observed, except between changes in bodily pain and IGF-I levels ( r = −0.43). Conclusions : QoL impairment was evident in Japanese adults with GHD, particularly in AO patients. In AO patients, general health and physical functioning domains were responsive to fat mass changes during GH treatment; this association was not evident in CO patients. These relationships between QoL and body composition warrant verification.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    RVK:
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2007
    detail.hit.zdb_id: 1485160-X
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  • 4
    In: Acta Endocrinologica, Oxford University Press (OUP), Vol. 128, No. 4 ( 1993-04), p. 367-372
    Abstract: The individual and combined effects of intact PTH, amino-terminal, and a series of truncated carboxyl-terminal PTH fragments on alkaline phosphatase activity were examined in dexamethasone-treated rat osteoblastic osteosarcoma cells ROS 17/2.8. Dexamethasone-induced alkaline phosphatase activity was inhibited not only by hPTH(1–84) and amino-terminal PTH fragment hPTH(1–34), but also by carboxyl-terminal PTH fragment hPTH(69–84) in a dose-related fashion. At 10 −7 mol/1, hPTH(1–84) completely abolished dexamethasone-induced alkaline phosphatase activity, while hPTH(1–34) and hPTH(69–84) reduced alkaline phosphatase activity to 0.16±0.02 and 0.80±0.03 fold, respectively, of the control value obtained in the absence of PTH peptides. The combination of hPTH(1–34) and hPTH(69—84) resulted in reduction of alkaline phosphatase activity to the level obtained by hPTH(1-84). The shorter carboxyl-terminal PTH fragment hPTH(71–84) did not affect alkaline phosphatase activity or modulate the action of hPTH(1–34). The longer carboxyl-terminal PTH fragment hPTH(53-84) stimulated alkaline phosphatase activity up to 1.23±0.03 fold and partially blunted the inhibitory effect of hPTH(1–34) on alkaline phosphatase activity. These findings suggest that carboxyl-terminal PTH fragments could exert diverse effects on the target cells, depending on the length of deletion of amino-terminal amino acids of PTH molecule, and interact with amino-terminal PTH fragment. The two amino-terminal amino acids of hPTH(69–84) and the 53–68 portion of hPTH(53–84) might be responsible for the respective inhibitory and stimulatory effects of the peptides on alkaline phosphatase activity.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    RVK:
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 1993
    detail.hit.zdb_id: 1485160-X
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  • 5
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 1994
    In:  European Journal of Endocrinology Vol. 131, No. 6 ( 1994-12), p. 646-651
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 131, No. 6 ( 1994-12), p. 646-651
    Abstract: Arao M, Yamaguchi T, Sugimoto T, Fukase M, Chihara K. Involvement of protein kinase C in sodiumdependent phosphate transport by parathyroid hormone in osteoblast-like cells. Eur J Endocrinol 1994;131:646–51. ISSN 0804–4643 The rat osteosarcoma cell line UMR-106 has an osteoblast-like phenotype and possesses parathyroid hormone (PTH)-responsive dual signal transduction systems [adenosine 3′,5′-cyclic monophosphatedependent protein kinase (PKA) and calcium-protein kinase C (Ca-PKC)]. These cells transport inorganic phosphate (P i ) by a Na + -dependent carrier under stimulation by PTH. The present study aimed to clarify PTH-responsive signal transduction mechanisms in the regulation of Na + -dependent P i transport by PTH in UMR-106 cells. Exposure of these cells to 10 −7 mol/l PTH induced a significant increase in P i uptake within 30 min of incubation and it became maximal after 2 h. Parathyroid hormone (10 −9 –10 −7 mol/l) stimulated P i uptake dose dependently. Activation of PKC by 12-O-tetradecanoyl phorbol- 13-acetate (TPA) also increased P i uptake in time- and dose-dependent manners similar to PTH In contrast, neither PKA activation by 10 mol/l forskolin or by 10 −4 mol/l dibutyryladenosine 3′,5′-cyclic monophosphate nor calcium ionophore treatment with 10 −7 mol/l A23187 or with 10 −7 mol/l ionomycin during 3-h incubations affect P i uptake, except its increase by 10 −4 mol/l forskolin at a 3-h incubation. These agents had no influence on P i uptake even in combined treatments with TPA. The PTH-induced increase in P i uptake was abolished almost completely by pretreating cells with PKC inhibitors, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride (H-7) (50 μmol/l) or staurosporin (10 and 50 nmol/l), and by down-regulating PKC with a prolonged TPA treatment. These results indicate that the messenger system mediated by PKC, rather than by PKA or by cytosolic calcium, plays a crucial role in the regulation of Na + -dependent P i transport by PTH within a few hours of exposure of the hormone in the osteoblast-like cells. Toru Yamaguchi, Third Division, Department of Medicine, Kobe University School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650, Japan
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    RVK:
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 1994
    detail.hit.zdb_id: 1485160-X
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  • 6
    In: Cancer Chemotherapy and Pharmacology, Springer Science and Business Media LLC, Vol. 37, No. 4 ( 1996-1-10), p. 297-304
    Type of Medium: Online Resource
    ISSN: 0344-5704 , 1432-0843
    Language: Unknown
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1996
    detail.hit.zdb_id: 1458488-8
    SSG: 15,3
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  • 7
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2001
    In:  Journal of Neurology Vol. 248, No. 10 ( 2001-10-1), p. 856-860
    In: Journal of Neurology, Springer Science and Business Media LLC, Vol. 248, No. 10 ( 2001-10-1), p. 856-860
    Type of Medium: Online Resource
    ISSN: 0340-5354 , 1432-1459
    RVK:
    Language: Unknown
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2001
    detail.hit.zdb_id: 1421299-7
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  • 8
    In: International Journal of Molecular Medicine, Spandidos Publications, ( 2004-03-01)
    Type of Medium: Online Resource
    ISSN: 1107-3756 , 1791-244X
    Language: Unknown
    Publisher: Spandidos Publications
    Publication Date: 2004
    detail.hit.zdb_id: 2083937-6
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  • 9
    Online Resource
    Online Resource
    Bioscientifica ; 2005
    In:  Journal of Endocrinology Vol. 185, No. 1 ( 2005-04), p. 131-138
    In: Journal of Endocrinology, Bioscientifica, Vol. 185, No. 1 ( 2005-04), p. 131-138
    Abstract: Central in the pathogenesis of glucocorticoid (GC)-induced osteoporosis is the effects of GC on bone formation. However, the mechanism of GC-inhibited bone formation is not well known. Transforming growth factor (TGF)-β is most abundant in bone matrix compared with other tissues, and we have recently proposed that Smad3, a TGF-β signaling molecule, is important for promoting bone formation. However, no reports have been available about the effects of GC on Smad3 in osteoblasts. In the present study, we investigated whether dexamethasone (Dex), an active GC analog, would affect the expression and activity of Smad3 in mouse osteoblastic MC3T3-E1 and rat osteoblastic UMR-106 cells. Dex significantly suppressed Smad3-stimulated alkaline phosphatase (ALP) activity, although it did not affect TGF-β-inhibited ALP activity in MC3T3-E1 cells. Moreover, pretreatment with Dex suppressed TGF-β-enhanced expression of type I collagen in MC3T3-E1 and UMR-106 cells. In the luciferase assay using p3TP-Lux with a Smad3-specific response element, Dex significantly suppressed the transcriptional activity induced by TGF-β as well as Smad3. However, Dex did not affect the expression of Smad3 in these cells at both mRNA and protein levels. In conclusion, the present study indicates that Dex inhibits ALP activity and type I collagen expression, presumably by suppressing Smad3-induced transcriptional activity but not by modulating Smad3 expression in osteoblastic cells.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2005
    detail.hit.zdb_id: 1474892-7
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  • 10
    Online Resource
    Online Resource
    Bioscientifica ; 1974
    In:  Journal of Endocrinology Vol. 62, No. 3 ( 1974-09), p. 687-688
    In: Journal of Endocrinology, Bioscientifica, Vol. 62, No. 3 ( 1974-09), p. 687-688
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1974
    detail.hit.zdb_id: 1474892-7
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