TXNIP is highly regulated in bone biopsies from patients with endogenous Cushing's syndrome and related to bone turnover

Lekva, Tove; Ueland, Thor; Bøyum, Hege; Evang, Johan Arild; Godang, Kristin; Bollerslev, Jens

doi:10.1530/eje-11-1082

Cited by 32 publications

(39 citation statements)

References 21 publications

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“…For longitudinal parameters, baseline group differences were evaluated using unpaired t-tests; endpoints collected during the study were assessed using 1-way repeated measures ANOVA. Significant interactions were examined 15 using both paired (time effect) and unpaired (treatment effect) t-tests, For non-longitudinal data, group differences (M versus C) were evaluated using unpaired t-tests.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, GCs suppress the osteoblastic bone forming activity through the osteoclast [12]. The effects on osteoclasts are controversial, as GCs may suppress [13] or enhance [14] osteoclastogenesis in vitro, while human biopsy data generally suggest a neutral effect on bone turnover [15]. Altered localized biomechanical parameters at the osteocytecanalicular level consequently to reduced bone vascularity has been reported [16].…”

Section: Introductionmentioning

confidence: 99%

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Sclerostin antibody and interval treadmill training effects in a rodent model of glucocorticoid-induced osteopenia

Achiou

Toumi

Touvier

et al. 2015

Bone

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sclerostin antibody and interval treadmill training effects in a rodent model of glucocorticoid-induced osteopenia

Achiou

Toumi

Touvier

et al. 2015

Bone

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“…These processes are considered to contribute to the pro-diabetic, immunosuppressive, and osteoporotic actions of glucocorticoids. Glucocorticoids induce the expressions of thioredoxin-interacting protein (TXNIP) in all these cells [61][62][63] , and the induction of TXNIP is found to be required for glucocorticoid-induced apoptosis [61,62] . TXNIP binds to thioredoxin, which in turn causes the dissociation of apoptosis signal-regulating kinase 1 (ASK1) from thioredoxin.…”

Section: Pancreatic β-Cell Deathmentioning

confidence: 99%

Competitive and compensatory effects of androgen signaling and glucocorticoid signaling

Harada

Inui

Yamaji

2015

Receptor Clin Invest

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Androgens and glucocorticoids have competitive and compensatory effects in several physiological and pathophysiological processes. Although blood androgen levels affect blood glucocorticoid levels and vice versa, it does not fully explain the relationship between the effects of androgens and glucocorticoids. Androgens and glucocorticoids exert their functions through binding to androgen receptor (AR) and glucocorticoid receptor (GR), respectively. AR homodimer and GR homodimer bind to the androgen response element (ARE) and glucocorticoid response element (GRE), respectively, where they positively or negatively regulate transcription. AR/GR heterodimer can also form but whether it has a physiological role is unclear. Notably, some ARE/GRE sites are recognized by both AR and GR. This review focuses on the functional interventions between androgen signaling and glucocorticoid signaling in target cells that are involved in muscle atrophy, lipid metabolism in adipocytes and hepatocytes, and pancreatic β-cell death. Androgens and glucocorticoids exert opposite effects by differentially regulating key genes (e.g., insulin-like growth factor-1, atrogin-1, and thioredoxin-interacting protein) involved in these physiological processes. We also review functional compensation between these steroids in the development of castration-resistant prostate cancer in which glucocorticoids compensate for the castration-induced loss of AR function by activating key genes (e.g., serum/glucocorticoid-regulated kinase 1). The gene expressions regulated by androgens and glucocorticoids are regulated through at least three different mechanisms in target cells: (i) regulation of applicable ligand levels by modulation of steroid metabolite enzyme levels, (ii) regulation of each other's receptor levels, and (iii) competitive binding between AR and GR on ARE/GRE sites. Recent findings shed light on the complicated relationship between androgen signaling and glucocorticoid signaling in various cellular processes.

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“…Because of rapid loss of trabecular bone, BMD loss in the lumbar spine is significantly higher than in femoral neck, which consists mainly of cortical bone [41,45]. It was observed that patients with ACTH-secreting adenoma have significant lower Z-score as compared with controls.…”

Section: Bone Mineral Densitymentioning

confidence: 99%

Osteoporosis in pituitary diseases: lessons for the clinic

Bolanowski¹,

Jawiarczyk-Przybyłowska

Halupczok-Żyła

2014

Expert Review of Endocrinology & Metabolism

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Osteoporosis is a systemic disease characterized by bone mass and density loss leading to fragility fractures. Osteoporosis due to endocrine disorders is an example of secondary osteoporosis. The harmful effects on bones are common in patients harboring pituitary tumors (acromegaly, prolactinoma, Cushing's disease) and suffering from hypopituitarism. Increased fracture risk and high healthcare costs of fractured patients are their consequences. The coexistence of some of these disorders and hypogonadism results in severe osteoporosis. The influence of the certain diseases, their activity and therapy and accompanying hypogonadism on bone turnover, bone mineral density and fracture incidence is presented. KEYWORDS: acromegaly • bone density • bone turnover • Cushing's syndrome • fractures • hypopituitarism • prolactinoma • secondary osteoporosisOsteoporosis in pituitary diseases: lessons for the clinic Osteoporosis is a generalized disease defined as a loss of bone mass and strength that leads to fragility fractures [1]. Bone strength is a component of bone mineral density (BMD) and bone quality. In general, certain factors can influence bone metabolism and evoke osteoporosis. These factors include aging, lifestyle, exercise, diet, calcium intake and adverse effect of medications. Furthermore, secondary osteoporosis is caused by numerous diseases such as endocrine system diseases, disorders of the gastrointestinal or biliary tract, renal diseases and neoplasms. It is also known that pituitary adenoma can affect bone metabolism through the hypersecretion of certain hormones or secondary hypopituitarism [2]. In this study, we would like to present the association between the loss of bone mass and pituitary diseases such as acromegaly, hyperprolactinemia, Cushing's syndrome (CS) and hypopituitarism. It is important to know that these disorders not always have the same effects in individual patients, because of different age, sex and associated conditions. Coexistence of several of these diseases might result in severe osteoporosis. AcromegalyAcromegaly is a rare disease caused by hypersecretion of growth hormone (GH), mainly from a pituitary tumor. It is known that patients with acromegaly have increased bone turnover as determined by changes in biochemical markers, calcium kinetics and histomorphometry [3]. Increased bone turnover suggests that acromegaly leads to the activation of both osteoblasts and osteoclasts [4]. Moreover, increased bone turnover was correlated with disease activity but was independent of gonadal status. In some in vitro experiments on human bone cells, it was shown that GH and IGF-1 may stimulate bone resorption by direct and indirect influence on formation, differentiation and activity of osteoclasts. On the other hand, it was shown that both GH and IGF-1 influence proliferation of osteoblasts but their differentiation is regulated only by IGF-1 and a lot of effects are the consequence of local secretion of IGFs [5]. In pre-pubertal period, GH is responsible for longitudinal bone growth. Duri...

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TXNIP is highly regulated in bone biopsies from patients with endogenous Cushing's syndrome and related to bone turnover

Cited by 32 publications

References 21 publications

Sclerostin antibody and interval treadmill training effects in a rodent model of glucocorticoid-induced osteopenia

Sclerostin antibody and interval treadmill training effects in a rodent model of glucocorticoid-induced osteopenia

Competitive and compensatory effects of androgen signaling and glucocorticoid signaling

Osteoporosis in pituitary diseases: lessons for the clinic

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