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  • 1
    Online Resource
    Online Resource
    Treatment with the PPARγ agonist rosiglitazone downregulates interleukin-1 receptor antagonist in individuals with metabolic syndrome
    Oxford University Press (OUP) ; 2010
    In:  European Journal of Endocrinology Vol. 162, No. 2 ( 2010-02), p. 267-273
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 162, No. 2 ( 2010-02), p. 267-273
    Abstract: Thiazolidinediones (TZDs) reduce insulin resistance, but also have pleiotropic properties including effects on inflammation. The balance between protective and proatherogenic effects may differ in various patient populations. We studied the effect of rosiglitazone on inflammatory markers in patients with metabolic syndrome (MetSyn). Methods In a cross-over randomized controlled trial, 23 subjects with MetSyn were assigned to treatment with rosiglitazone that was uptitrated from 4 mg/day for 6 weeks followed by 8 mg/day for 6 weeks or matching placebo for 12 weeks, and then to the opposite treatment for 12 weeks. Plasma levels of inflammatory and metabolic markers were measured during follow-up. Results Our main findings were i) compared to placebo, rosiglitazone significantly decreased the plasma levels of the naturally occurring interleukin (IL)1 inhibitor, IL1 receptor antagonist (IL1Ra; P =0.001), potentially reflecting inflammatory effects on the IL1 system; ii) parallel to this, rosiglitazone decreased plasma levels of IL10 ( P =0.029) further suggesting inflammatory effects; iii) rosiglitazone decreased uric acid levels ( P =0.001), and monocyte chemoattractant protein-1 ( P =0.05) and C-reactive protein ( P =0.06) tended to be lower after rosiglitazone than placebo, suggesting potential pro- and anti-inflammatory effects simultaneously and iv) in vitro , rosiglitazone enhanced IL1Ra and decreased IL1β in THP-1 monocytes, illustrating the complex effects of these medications, potentially exhibiting anti-inflammatory effects on the IL1 system in certain tissues or cells at least at certain concentrations. Conclusion Our findings suggest inflammatory effects on the IL1 system during rosiglitazone therapy in MetSyn. However, anti-inflammatory effects were also observed, and the net effect of TZDs in MetSyn should be further investigated.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/EJE-09-0706
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2010
    detail.hit.zdb_id: 1485160-X
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  • 2
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    Online Resource
    Umbilical cord levels of sclerostin, placental weight, and birth weight are predictors of total bone mineral content in neonates
    Oxford University Press (OUP) ; 2013
    In:  European Journal of Endocrinology Vol. 168, No. 3 ( 2013-03), p. 371-378
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 168, No. 3 ( 2013-03), p. 371-378
    Abstract: During pregnancy, changes occur in the maternal calcium homeostasis to fulfill fetal demand. We hypothesized that the fibroblast growth factor 23 (FGF23) system and Wnt signaling pathway are important for normal skeletal development in the offspring. Aims Circulating α-klotho, FGF23, sclerostin, and 25-hydroxyvitamin D (25(OH)D) at the fetal and maternal sides of the placenta were measured to investigate associations with newborn bone mass independent of maternal BMI, calcium and phosphate levels, placental weight, and birth weight. Methods In a prospective cohort of healthy pregnant women, the total body bone mineral content (BMC) in 202 newborns was measured by dual-energy X-ray absorptiometry. Maternal circulating levels of the biomarkers were measured at gestational weeks 30–32 and in umbilical cord plasma (UCP) at birth. Results Mean α-klotho and sclerostin concentrations in the UCP were significantly higher than maternal levels (3004 vs 1077 pg/ml; P 〈 0.001 and 629 vs 346 pg/ml; P 〈 0.001 respectively), and mean 25(OH)D was lower (31 vs 45 nmol/l; P 〈 0.001). The UCP and maternal FGF23 levels were similar. No significant effects of maternal biomarkers on BMC were found in regression analyses. Among UCP biomarkers, only UCP sclerostin was significantly associated with BMC in univariate analyses, and the effect remained significant after adjustment for birth weight and other confounders. Conclusions We found that UCP sclerostin levels, birth weight, and placental weight were significant predictors of neonatal BMC but found no evidence for a main role of maternal levels of α-klotho, FGF23, sclerostin, or 25(OH)D nor of UCP levels of α-klotho, FGF23, or 25(OH)D.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/EJE-12-0531
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2013
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  • 3
    Online Resource
    Online Resource
    TXNIP is highly regulated in bone biopsies from patients with endogenous Cushing's syndrome and related to bone turnover
    Oxford University Press (OUP) ; 2012
    In:  European Journal of Endocrinology Vol. 166, No. 6 ( 2012-06), p. 1039-1048
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 166, No. 6 ( 2012-06), p. 1039-1048
    Abstract: Patients with endogenous Cushing's Syndrome (CS), as long-time treated patients with exogenous glucocorticoids (GCs), have severe systemic manifestations including secondary osteoporosis and low-energy fractures. The aim of the present study was to investigate the functional role of TXNIP in bone with focus on osteoblast (OB) differentiation and OB-mediated osteoclast activity and function in vitro . Design and methods Nine bone biopsies from CS before and after surgical treatment were screened for expressional candidate genes. Microarray analyses revealed that the gene encoding TXNIP ranked among the most upregulated genes. Subsequent in vitro and in vivo studies were performed. Results We found that TXNIP gene in bone is downregulated in CS following surgical treatment. Furthermore, our in vivo data indicate novel associations between thioredoxin and TXNIP . Our in vitro studies showed that silencing TXNIP in OBs was followed by increased differentiation and expression and secretion of osteocalcin as well as enhanced activity of alkaline phosphatase. Moreover, treating osteoclasts with silenced TXNIP OB media showed an increased osteoclast activity. Conclusions TXNIP expression in bone is highly regulated during the treatment of active CS, and by GC in bone cells in vitro . Our data indicate that TXNIP may mediate some of the detrimental effects of GC on OB function as well as modulate OB-mediated osteoclastogenesis by regulating the OPG/RANKL ratio.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/EJE-11-1082
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2012
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  • 4
    Online Resource
    Online Resource
    Increased serum and bone matrix levels of transforming growth factor β1 in patients with GH deficiency in response to GH treatment
    Oxford University Press (OUP) ; 2011
    In:  European Journal of Endocrinology Vol. 165, No. 3 ( 2011-09), p. 393-400
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 165, No. 3 ( 2011-09), p. 393-400
    Abstract: Patients with adult onset GH deficiency (aoGHD) have secondary osteoporosis, which is reversed by long-term GH substitution. Transforming growth factor β1 (TGFβ1 or TGFB1) is abundant in bone tissue and could mediate some effects of GH/IGFs on bone. We investigated its regulation by GH/IGF1 in vivo and in vitro . Design and methods The effects of GH substitution (9–12 months, placebo controlled) on circulating and cortical bone matrix contents of TGFβ1 were investigated in patients with aoGHD. The effects of GH/IGF1 on TGFβ1 secretion in osteoblasts (hFOB), adipocytes, and THP-1 macrophages as well as the effects on release from platelets were investigated in vitro . Results In vivo GH substitution increased TGFβ1 protein levels in cortical bone and serum. In vitro , GH/IGF1 stimulation induced a significant increase in TGFβ1 secretion in hFOB. In contrast, no major effect of GH/IGF1 on TGFβ1 was found in adipocytes and THP-1 macrophages. Finally, a minor modifying effect on SFLLRN-stimulated platelet release of TGFβ1 was observed in the presence of IGF1. Conclusion GH substitution increases TGFβ1 in vivo and in vitro , and this effect could contribute to improved bone metabolism during such therapy, potentially reflecting direct effect of GH/IGF1 on bone cells.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/EJE-11-0442
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2011
    detail.hit.zdb_id: 1485160-X
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  • 5
    Online Resource
    Online Resource
    Inflammatory adipokines contribute to insulin resistance in active acromegaly and respond differently to different treatment modalities
    Oxford University Press (OUP) ; 2014
    In:  European Journal of Endocrinology Vol. 170, No. 1 ( 2014-01), p. 39-48
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 170, No. 1 ( 2014-01), p. 39-48
    Abstract: Active acromegaly is associated with insulin resistance, but it is uncertain whether inflammation in adipose tissue is a contributing factor. Aim To test if GH/IGF1 promotes inflammation in adipocytes, and if this is relevant for systemic insulin resistance in acromegaly. Furthermore, to investigate the effect of treatment modalities (transsphenoidal surgery (TS), somatostatin analogs (SAs), and pegvisomant (PGV)) on glucose metabolism and inflammatory biomarkers in acromegaly. Methods The in vitro effects of GH/IGF1 on gene expression of adipokines in human adipocytes were investigated. Body composition, glucose metabolism, and circulating adipokines (adiponectin (AD), high-molecular weight AD (HMWAD), leptin, vascular endothelial growth factor-A (VEGF-A), monocyte chemotactic protein 1 (MCP1), and thioredoxin (TRX)) were measured in 37 patients with active acromegaly before and after treatment. Results In vitro GH, but not IGF1, increased VEGF and MCP1 in human adipocytes. In all treatment groups, body fat increased and IGF1 decreased to the same extent. Fasting glucose decreased in the TS ( P =0.016) and PGV ( P =0.042) groups, but tended to increase in the SA group ( P =0.078). Insulin and HOMA-IR decreased in both TS and SA groups, while the PGV group showed no changes. Serum VEGF and MCP1 decreased significantly in the TS group only ( P =0.010, P =0.002), while HMWAD increased with PGV treatment only ( P =0.018). A multivariate analysis model identified the changes in GH and VEGF as predictors of improvement in HOMA-IR after treatment ( R 2 =0.39, P =0.002). Conclusions i) GH directly promotes inflammation of human adipocytes by increasing VEGF and MCP1 levels; ii) glucose metabolism and inflammation (VEGF and MCP1) improve to some extent after treatment, despite an increase in adipose tissue mass; and iii) the decrease in insulin resistance after therapy in acromegaly depends, to some extent, on treatment modalities.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/EJE-13-0523
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2014
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  • 6
    Online Resource
    Online Resource
    Metabolic improvement after treatment of acromeglay is determined by the increase of gynoid fat mass and the decrease of serum vaspin and IGF1
    Bioscientifica ; 2014
    In:  Endocrine Abstracts ( 2014-04-17)
    Details
    In: Endocrine Abstracts, Bioscientifica, ( 2014-04-17)
    Type of Medium: Online Resource
    ISSN: 1479-6848
    URL: Article
    DOI: 10.1530/endoabs.35.OC8.1
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2014
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