&lt;b&gt;Steroid changes adipokine concentration in the blood and bone marrow &lt;/b&gt;&lt;b&gt;fluid &lt;/b&gt;

Fukushima, Tatsuya; Hozumi, Akira; Tomita, Masato; Yonekura, Akihiko; Miyata, Noriaki; Miyamoto, Takashi; Taguchi, Koichi; Goto, Hisataka; Tsuda, Keiichi; Osaki, Makoto

doi:10.2220/biomedres.37.215

Cited by 5 publications

(3 citation statements)

References 29 publications

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“…Lipid metabolic disorder and hypercoagulation are considered two important causes of femoral head osteonecrosis. Studies by Fukushima et al (2016) showed that increased secretion of various fat factors and an increased concentration of plasminogen activator inhibitor (pai-1) could significantly influence hemodynamic changes of the femoral head and the progression of bone osteonecrosis. Studies by Pritchett (2001) have shown that statins reduce the risk for osteonecrosis in steroid-treated patients.…”

Section: Discussionmentioning

confidence: 99%

Effects of angiotensin II combined with asparaginase and dexamethasone on the femoral head in mice: A model of steroid-induced femoral head osteonecrosis

Liu

Yang

et al. 2022

Front. Cell Dev. Biol.

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Background: To study the pathogenesis of steroid-induced femoral head osteonecrosis, an ideal animal model is very important. As experimental animals, mice are beneficial for studying the pathogenesis of disease. However, there are currently few mouse models of steroid-induced femoral head osteonecrosis, and there are many questions that require further exploration and research.Purposes: The purpose of this study was to establish a new model of osteonecrosis in mice using angiotensin II (Ang II) combined with asparaginase (ASP) and dexamethasone (DEX) and to study the effects of this drug combination on femoral head osteonecrosis in mice.Methods: Male BALB/c mice (n = 60) were randomly divided into three groups. Group A (normal control, NC) was treated with physiological saline and given a normal diet. Group B (DEX + ASP, DA) was given free access to food and water (containing 2 mg/L DEX) and subjected to intraperitoneal injection of ASP (1200 IU/kg twice/week for 8 weeks). Group C (DEX + ASP + Ang II, DAA) was treated the same as group B, it was also given free access to food and water (containing 2 mg/L DEX) and subjected to intraperitoneal injection of ASP (1200 IU/kg twice/week for 8 weeks), but in the 4th and 8th weeks, subcutaneous implantation of a capsule osmotic pump (0.28 mg/kg/day Ang II) was performed. The mice were sacrificed in the 4th and 8th weeks, and the model success rate, mouse mortality rate, body weight, blood lipids, coagulation factors, histopathology, and number of local vessels in the femoral head were evaluated.Results: DAA increased the model success rate [4th week, 30% (DA) vs. 40% (DAA) vs. 0% (NC); 8th week, 40% (DA) vs. 70% (DAA) vs. 0% (NC)]. There was no significant difference in mortality rate between the groups [4th week, 0% (DA) vs. 0% (DAA) vs. 0% (NC); 8th week, 5% (DA) vs. 10% (DAA) vs. 0% (NC)]. DAA affected mouse body weight and significantly affected blood lipids and blood coagulation factors. DAA reduces the number of blood vessels in the femoral head and destroys the local blood supply.Conclusion: Angiotensin II combined with asparaginase and dexamethasone can obviously promote the necrosis of femoral head and provide a new idea for the model and treatment of osteonecrosis.

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Section: Discussionmentioning

confidence: 99%

Effects of angiotensin II combined with asparaginase and dexamethasone on the femoral head in mice: A model of steroid-induced femoral head osteonecrosis

Liu

Yang

et al. 2022

Front. Cell Dev. Biol.

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“…Uchida et al reported that adiponectin levels were significantly augmented after glucocorticoid pulse therapy in patients with IgA nephropathy [ 32 ]. Furthermore, some reports have shown that steroids have no effect on the adiponectin level [ 33 , 34 ]. As mentioned above, the effects of steroid treatment on adiponectin are somewhat controversial, but many of studies suggest that steroid treatment increases adiponectin expression [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Distribution of serum adiponectin isoforms in pediatric patients with steroid-sensitive nephrotic syndrome

et al. 2021

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Background Serum adiponectin circulates in three multimeric isoforms: high-molecular-weight (HMW), middle-molecular-weight (MMW), and low-molecular-weight (LMW) isoforms. Potential change in the circulating adiponectin levels in patients with nephrotic syndrome (NS) remain unknown. This study aimed to assess the levels of total adiponectin and the distribution of its isoforms in pediatric patients with NS. Methods We sequentially measured total adiponectin and each adiponectin isoform levels at the onset of NS, initial remission, and during the remission period of the disease in 31 NS patients. We also calculated the ratios of HMW (%HMW), MMW (%MMW), and LMW (%LMW) to total adiponectin incuding 51 control subjects. Results The median of total serum adiponectin levels in patients were 36.7, 36.7, and 20.2 μg/mL at the onset, at initial remission, and during the remission period of NS, respectively. These values were significantly higher than those in control subjects. The median values of %HMW, %MMW, and %LMW values were 56.9/27.0/14.1 at the onset, 62.0/21.8/13.4 at the initial remission, and 58.1/21.7/17.5 at during the remission period of NS, respectively. Compared with control subjects, %HMW at initial remission and %MMW at the onset were high, and the %LMW values at the onset and at initial remission were low. Conclusions In patients with NS, total serum adiponectin levels increase at the onset of the disease, and the ratio of adiponectin isoforms changes during the course of the disease. Further studies are needed to delineate the mechanisms between proteinuria and adiponectin isoforms change.

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“…Uchida et al reported that adiponectin levels were signi cantly augmented after glucocorticoid pulse therapy in patients with IgA nephropathy [31]. Furthermore, some reports have shown that steroids have no effect on the adiponectin level [32,33]. As mentioned above, the effects of steroid treatment on adiponectin are somewhat controversial, but many of studies suggest that steroid treatment increases adiponectin expression [34].…”

Section: Discussionmentioning

confidence: 99%

Distribution of Serum Adiponectin Isoforms in Pediatric Patients with Steroid-Sensitive Nephrotic Syndrome

Tamai

Kamijo

Abe

et al. 2020

Preprint

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Background Serum adiponectin circulates in three multimeric isoforms: high-molecular-weight (HMW), middle-molecular-weight (MMW), and low-molecular-weight (LMW) isoforms. Potential change in the circulating adiponectin levels in patients with nephrotic syndrome (NS) remain unknown. Therefore, this study aimed to assess the levels of total adiponectin and the distribution of its isoforms in pediatric patients with NS.Methods We measured total adiponectin and each adiponectin isoform levels at the onset of NS, initial remission, and during the remission period of the disease in 31 patient with NS. We also calculated the ratios of HMW (%HMW), MMW (%MMW), and LMW (%LMW) to total adiponectin and all values in 31 with those of 51 control subjects.Results The mean total serum adiponectin levels in patients were 40.6 ± 16.0 µg/mL, 41.1 ± 18.5 µg/mL, and 25.5 ± 16.6 µg/mL at the onset of NS, at initial remission, and during the remission period of NS, respectively. These values were significantly higher than those in control subjects (12.6 ± 8.5 µg/mL). The mean values of %HMW, %MMW, and %LMW values were 57.0/28.0/14.2 at the onset of NS, 61.6/23.8/14.0 at the initial remission, and 58.1/21.7/17.7 at during the remission period, respectively. Compared with control subjects, %HMW at initial remission and %MMW at the onset of NS were high, and the %LMW values at the onset of NS and at initial remission were low.Conclusions In patients with NS, total serum adiponectin levels increase at the onset of the disease, and the ratio of adiponectin isoforms changes during the course of the disease. Further studies are needed to delineate the mechanisms between proteinuria and adiponectin isoforms.

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<b>Steroid changes adipokine concentration in the blood and bone marrow </b><b>fluid </b>

Cited by 5 publications

References 29 publications

Effects of angiotensin II combined with asparaginase and dexamethasone on the femoral head in mice: A model of steroid-induced femoral head osteonecrosis

Effects of angiotensin II combined with asparaginase and dexamethasone on the femoral head in mice: A model of steroid-induced femoral head osteonecrosis

Distribution of serum adiponectin isoforms in pediatric patients with steroid-sensitive nephrotic syndrome

Distribution of Serum Adiponectin Isoforms in Pediatric Patients with Steroid-Sensitive Nephrotic Syndrome

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