p38 MAPK regulates calcium signal-mediated lipid accumulation through changing VDR expression in primary preadipocytes of mice

Sun, Cheng; Qi, Renli; Wang, Li; Yan, Jun; Wang, Yong

doi:10.1007/s11033-011-1084-8

Cited by 39 publications

(28 citation statements)

References 19 publications

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“…It has been indicated that L-VGCC, an important calcium influx channel in the plasma membrane, is involved in [Ca 2+ ] o -mediated adipogenesis of mice primary preadipocytes [33]. Similarly, we found that L-VGCC blocker Nifidipine prevented the increase of [Ca ] i was found to promote adipogenesis of mice BMSCs [12,26] and to boost the late stage of differentiation and lipid filling in human adipocyte differentiation [34].…”

Section: Discussionsupporting

confidence: 63%

Calcium Supplementation Enhanced Adipogenesis and Improved Glucose Homeostasis Through Activation of Camkii and PI3K/Akt Signaling Pathway in Porcine Bone Marrow Mesenchymal Stem Cells (pBMSCs) and Mice Fed High Fat Diet (HFD)

Zhang

Meng

et al. 2018

Cell Physiol Biochem

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Background/Aims: It has been implicated that calcium supplementation is involved in reducing body weight/fat and improving glucose homeostasis. However, the underlying mechanisms are still not fully understood. Here, we investigated the effects of calcium supplementation on adipogenesis and glucose homeostasis in porcine bone marrow mesenchymal stem cells (pBMSCs) and high fat diet (HFD)-fed mice and explored the involved signaling pathways. Methods: In vitro, pBMSCs were treated with 4 mM extracellular calcium ([Ca²⁺]_o) and/or 1 μM nifedipine, 0.1 μM BAPTA-AM, 1 μM KN-93, 50 nM wortmannin for 10 days. The intracellular calcium ([Ca²⁺]_i) levels were measured using Fluo 3-AM by flow cytometry. The adipogenic differentiation of pBMSCs was determined by Oil Red-O staining and triglyceride assay. The expression of marker genes involved in adipogenesis (peroxisome proliferator activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα)) and glucose uptake (glucose transporter 4 (GLUT4)), as well as the activation of Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) and PI3K/Akt-FoxO1/AS160 signaling pathways were determined by Western blotting. Glucose uptake and utilization were examined using 2-NBDG assay and glucose content assay, respectively. In vivo, C57BL/6J male mice were fed a HFD (containing 1.2% calcium) without or with 0.6% (w/w) calcium chloride in drinking water for 13 weeks. The adipogenesis, glucose homeostasis and the involvement of CaMKII and PI3K/Akt signaling pathway were also assessed. Results: In vitro, [Ca²⁺]_o stimulated pBMSCs adipogenesis by increasing [Ca²⁺]_i level and activating CaMKII and PI3K/Akt-FoxO1 pathways. In addition, [Ca²⁺]_o promoted glucose uptake/utilization by enhancing AS160 phosphorylation, GLUT4 expression and translocation. However, the stimulating effects of [Ca²⁺]_o on pBMSCs adipogenesis and glucose uptake/utilization were abolished by L-VGCC blocker Nifedipine, [Ca²⁺]_i chelator BAPTA-AM, CaMKII inhibitor KN-93, or PI3K inhibitor Wortmannin. In vivo, calcium supplementation decreased body weight and fat content, increased adipocyte number, and improved glucose homeostasis, with elevated PPARγ and GLUT4 expression and PI3K/Akt activation in iWAT. Conclusion: calcium supplementation enhanced adipogenesis and glucose uptake in pBMSCs, which was coincident with the increased adipocyte number and improved glucose homeostasis in HFD-fed mice, and was associated with activation of CaMKII and PI3K/Akt-FoxO1/AS160 pathways. These data provided a broader understanding of the mechanisms underlying calcium-induced body weight/fat loss and glycemic control.

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Section: Discussionsupporting

confidence: 63%

Calcium Supplementation Enhanced Adipogenesis and Improved Glucose Homeostasis Through Activation of Camkii and PI3K/Akt Signaling Pathway in Porcine Bone Marrow Mesenchymal Stem Cells (pBMSCs) and Mice Fed High Fat Diet (HFD)

Zhang

Meng

et al. 2018

Cell Physiol Biochem

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“…Others have, however, found that protein levels of CYP27B1 and VDR measured by western blotting were consistent with mRNA levels. 53,56 In conclusion, we found a high prevalence of low VD levels in obese women scheduled for bariatric surgery. We found that AT expresses the enzymes forboth the formation of 25OHD and of the active form, 1,25(OH) 2 D, and for degradation of VD.…”

Section: Discussionmentioning

confidence: 53%

Expression of vitamin D-metabolizing enzymes in human adipose tissue—the effect of obesity and diet-induced weight loss

et al. 2012

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OBJECTIVE: Low vitamin D (VD) levels are common in obesity. We hypothesized that this may be due to metabolism of VD in adipose tissue (AT). Thus, we studied (1) whether the VD-metabolizing enzymes were expressed differently in AT of lean and obese individuals and in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT), and (2) whether their expression was influenced by weight loss. METHODS: Samples of SAT and VAT were analyzed for expression of the vitamin-D-25-hydroxylases CYP2R1, CYP2J2, CYP27A1 and CYP3A4, the 25-vitamin-D-1a-hydroxylase CYP27B1, the catabolic vitamin-D-24-hydroxylase CYP24A1, and the vitamin D receptor, using reverse transcriptase-PCR. Moreover, plasma 25-hydroxy-vitamin D (25OHD) level was measured and related to the expression of these enzymes. Samples of SAT and VAT from 20 lean women and 20 obese women, and samples of SAT from 17 obese subjects before and after a 10% weight loss were analyzed. RESULTS: A plasma 25OHD level o50 nmol l À 1 was highly prevalent in both lean (45%) and obese (90%) women (Po0.01). Plasma 25OHD increased by 27% after weight loss in the obese individuals (Po0.05). Expression levels of the 25-hydroxylase CYP2J2 and the 1a-hydroxylase CYP27B1 were decreased by 71% (Po0.0001) and 49% (Po0.05), respectively, in SAT of the obese. CYP24A1 did not differ between lean and obese women, but the expression was increased by 79% (Po0.05) after weight loss. CONCLUSION: Obesity is characterized by a decreased expression of the 25-hydroxylase CYP2J2 and the 1a-hydroxylase CYP27B1 in SAT, whereas the catabolic CYP24A1 does not differ between lean and obese women. However, the expression of CYP24A1 is increased after weight loss. Accordingly, AT has the capacity to metabolize VD locally, and this can be dynamically altered during obesity and weight loss. INTRODUCTIONLow levels of circulating 25-hydroxy-vitamin D (25OHD) are associated with increased fat mass and body mass index, 1-5 but the underlying mechanism for this association is not fully elucidated. 6 Vitamin D (VD) is stored in adipose tissue (AT), and release of VD from AT is proposed to serve as an endogenous source of VD during the winter, when cutaneous production is low or absent in several parts of the world. 7 As low circulating levels of 25OHD are common in association with the obese state, 8 several studies have examined the effect of weight loss on circulating levels of 25OHD. However, results are inconsistent. After diet-and exercise-induced weight loss, both increased 9-11 and unaltered 12,13 circulating levels of 25OHD have been reported. Likewise, after major weight loss by bariatric surgery, both temporary 14-16 and long-term increases [16][17][18] in circulating levels of 25OHD have been reported, along with reports of no changes one year after surgery. 13,19 Taken together, these findings indicate that body weight is an important factor for circulating 25OHD levels. Several other explanations for the low levels of 25OHD in obesity have been proposed: a decreased exposure to sun light, 20 ...

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“…Further studies have shown that SOCS2 is a negative regulator of GH signaling, resulting in inhibition of intestinal epithelial cell proliferation, which is induced by GH and IGF-1 (Miller et al, 2004), the negative action of estrogen on GH signaling, which is caused by an upregulation of SOCS2 (Leung et al, 2003), and the blocking of GH-dependent inhibition of neural stem cell differentiation (Turnley, 2005). It is also known that glucocorticoids have negative effects on somatic growth and enhance GH-induced SOCS2 expression in primary hepatocytes (Tollet-Egnell et al, 1999;Sun et al, 2012b), suggesting SOCS2 as the mediator of the negative effects of glucocorticoids on GH action.…”

Section: Discussionmentioning

confidence: 99%

Construction of suppressor of cytokine signaling 2 (SOCS2) adenoviral overexpression vector and its impact on growth-hormone-induced lipolysis in swine primary adipocytes

Yang¹,

Yan²,

Feng³

et al. 2013

Genet. Mol. Res.

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ABSTRACT.We investigated the effect of overexpression suppressor of cytokine signaling 2 (SOCS2) on lipolysis in swine primary adipocytes (pAd) induced by growth hormone (GH). We constructed pAd-SOCS2 adenoviral overexpression vectors to infect HEK293 cells for virus packaging and propagation. Cultured swine primary adipocytes were infected with virus particles; after 48 h the infected adipocytes were treated with 500 ng GH/mL in the growth medium. Lipometabolismrelated gene expressions were detected at 0, 0.25, 0.5, 1, 2, and 4 h, by measuring mRNA and protein levels. The pAd-SOCS2 overexpression vector was successfully constructed and the concentration of titrated virus was 1.2 x 10 9 PFU/mL. We found that virus infection significantly increased SOCS2 mRNA and protein levels in swine primary adipocytes. Overexpression of SOCS2 significantly inhibited the increase in fatty acid synthase, adipose triglyceride lipase mRNA, and protein expression at 0.5 h. However, after 0.5 h, this inhibition was not significant. We concluded that overexpression of SOCS2 inhibited the increase in lipolysis induced by GH in swine primary adipocytes; this could provide a basis for studies of lipometabolism.

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p38 MAPK regulates calcium signal-mediated lipid accumulation through changing VDR expression in primary preadipocytes of mice

Cited by 39 publications

References 19 publications

Calcium Supplementation Enhanced Adipogenesis and Improved Glucose Homeostasis Through Activation of Camkii and PI3K/Akt Signaling Pathway in Porcine Bone Marrow Mesenchymal Stem Cells (pBMSCs) and Mice Fed High Fat Diet (HFD)

Calcium Supplementation Enhanced Adipogenesis and Improved Glucose Homeostasis Through Activation of Camkii and PI3K/Akt Signaling Pathway in Porcine Bone Marrow Mesenchymal Stem Cells (pBMSCs) and Mice Fed High Fat Diet (HFD)

Expression of vitamin D-metabolizing enzymes in human adipose tissue—the effect of obesity and diet-induced weight loss

Construction of suppressor of cytokine signaling 2 (SOCS2) adenoviral overexpression vector and its impact on growth-hormone-induced lipolysis in swine primary adipocytes

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