Bone and Metabolism: A Complex Crosstalk

Lieben, Liesbet; Callewaert, Filip; Bouillon, Roger

doi:10.1159/000178056

Cited by 28 publications

(25 citation statements)

References 41 publications

(29 reference statements)

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“…The following metabolic risk factors were evaluated separately: smoking status, BMI (≥30), elevated WC (≥88 cm), elevated FPG (≥100 mg/dl), elevated blood pressure (≥130 mm Hg SBP or ≥85 mm Hg DBP), antihypertensive drug treatment in a patient with a history of hypertension, elevated TG (≥150 mg/dl), reduced HDL-C (<50 mg/dl) and elevated LDL-C level (≥130 mg/dl) [19,20,21]. The features of metabolic syndrome were identified [19].…”

Section: Methodsmentioning

confidence: 99%

The Association of Osteocalcin and Adiponectin with Glucose Metabolism in Nondiabetic Postmenopausal Women

Çağlar¹,

Özdemir²,

Kiseli³

et al. 2014

Gynecol Obstet Invest

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Background/Aim: This study was designed to determine if osteocalcin is associated with insulin resistance, metabolic risk factors and adiponectin levels in nondiabetic postmenopausal women. Methods: A total of 87 menopausal nondiabetic subjects were enrolled into the study. Levels of fasting plasma glucose (FPG), insulin and serum lipids were determined. To estimate insulin sensitivity, homeostasis model assessment (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI) were used. Serum total osteocalcin and adiponectin levels were measured and the features of metabolic syndrome were identified. Results: The mean age of the patients was 54.7 years. Among the participants, 28.7% were obese (body mass index, BMI, ≥30). Insulin resistance was detected by HOMA-IR in 42.5% and by the QUICKI index in 63.2% of the cases. Metabolic syndrome was present in 29.8% of the patients. Neither the baseline characteristics nor the metabolic risk factors were correlated with osteocalcin or adiponectin levels (p > 0.05). When the patients were analyzed regarding BMI, osteocalcin levels were significantly lower in overweight women. Serum adiponectin levels were significantly lower in women with metabolic syndrome. Conclusion: No correlation between total osteocalcin and FPG, fasting insulin and insulin resistance parameters was found in nondiabetic postmenopausal women. Serum levels of adiponectin were associated with metabolic syndrome.

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Section: Methodsmentioning

confidence: 99%

The Association of Osteocalcin and Adiponectin with Glucose Metabolism in Nondiabetic Postmenopausal Women

Çağlar¹,

Özdemir²,

Kiseli³

et al. 2014

Gynecol Obstet Invest

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confidence: 99%

Elevated Fra-1 expression causes severe lipodystrophy

Luther

Drießler

Megges

et al. 2011

Journal of Cell Science

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Research Article 1465Introduction A reciprocal interaction between bone and energy metabolism has been described, whereby a hormone secreted by adipocytes influences bone formation and a factor produced by osteoblasts regulates fat metabolism (Lieben et al., 2009;Rosen, 2008). The crucial factor in this systemic loop is leptin, because its deficiency causes obesity and increases bone formation in the mouse (Ducy et al., 2000). Leptin is produced by white adipocytes and acts via the hypothalamus to regulate appetite and to favor energy expenditure. Bone formation is also negatively regulated by leptin through a second hypothalamic pathway, the -adrenergic sympathetic nervous system (Takeda et al., 2002). This pathway increases ATF-4-dependent expression of Esp (protein tyrosine phosphatase, receptor type, V; Ptprv) in osteoblasts, which leads to an inhibition of osteocalcin bioactivity. By contrast, insulin signaling in osteoblasts promotes the production of bioactive osteocalcin via acidification of the extracellular bone matrix as a consequence of increased bone resorption by osteoclasts (Ferron et al., 2010;Fulzele et al., 2010). In turn, osteocalcin, a hormone secreted by osteoblasts, modulates fat metabolism via the stimulation of pancreatic -cell proliferation and insulin secretion and thus, can indirectly, via adiponectin, lower insulin resistance (Hinoi et al., 2008;Yoshizawa et al., 2009). Thus, a common neuroendocrine systemic co-regulation of bone and adipose mass is established.In addition to this systemic regulation of bone and fat metabolism, a local control of cell fates balancing osteoblast and adipocyte differentiation, which is still poorly understood, must exist to integrate the systemic messages. Indeed, osteoblasts share with adipocytes a common mesenchymal progenitor, the mesenchymal stromal or stem cell (MSC) from which also arise other mesenchymal cell lineages such as chondrocytes, fibroblasts and myoblasts (Caplan, 2007). Mesenchymal cell fate decisions are driven by key transcription factors that confer identity to the cell. The major transcription factors regulating MSC differentiation to osteoblasts are -catenin and Runx2, both of which are required for the differentiation to pre-osteoblasts and osterix that drives osteoblast maturation (Karsenty, 2008;Komori, 2006). Similarly, adipocyte differentiation occurs first by activation of C/EBP and C/EBP, resulting in expression of PPAR2 and C/EBP, which then regulate late stages of adipogenesis (Lefterova and Lazar, 2009). Furthermore, a number of additional factors such as bone morphogenic proteins (BMPs) and signaling, for instance through the WNT pathway, have been described to regulate cell fate decisions between osteoblasts and adipocytes by promoting commitment or differentiation into one lineage at the expense of the other (Takada et al., 2007). All these observations strongly argue in favor of a cell-autonomous locally controlled relationship between osteoblastogenesis and adipogenesis. SummaryA shift from osteoblastogenesis...

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“…1 However, studies in animal models show that bone cells regulate glucose and fat metabolism via osteocalcin. 2,3 Osteocalcin is a small noncollagen protein of 49 amino acids found mainly in bone and dentine tissue produced by mature osteoblasts, odontoblasts, and hypertrophic chondrocytes. It is characterized by the presence of three residues of the calcium-binding amino acid, F-carboxyglutamic acid, which regulates calcium homeostasis during bone mineralization.…”

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confidence: 99%