Involvement of regucalcin in lipid metabolism and diabetes

Yamaguchi, Masayoshi; Murata, Takeshi

doi:10.1016/j.metabol.2013.01.023

Cited by 52 publications

(35 citation statements)

References 42 publications

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“…There are evidences linking higher expression of regucalcin to adipogenesis in adipocytes [43], and also alterations in lipid and glucose metabolism in vivo [44], which are predisposing factors to obesity and diabetes. Overexpression of regucalcin was also found to enhance glucose utilization and lipid production in the cloned rat hepatoma H4-II-E cells in vitro [44,45]. Concomitant with a decrease in regucalcin on a high n -3 PUFA diet was a significant decrease in plasma TG concentrations as compared to mice fed a low n -3 PUFA diet (Figure 2A).…”

Section: Resultsmentioning

confidence: 99%

Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach

et al. 2014

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BackgroundOmega-3 polyunsaturated fatty acids (n-3 PUFA) have been shown to alleviate the symptoms of metabolic disorders, such as heart disease, diabetes, obesity and insulin resistance. Several putative mechanisms by which n-3 PUFA elicit beneficial health effects have been proposed; however, there is still a shortage of knowledge on the proteins and pathways that are regulated by n-3 PUFA.MethodsUsing two dimensional polyacrylamide gel electrophoresis (2D-PAGE) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis, we investigated the effects of diets high or low in n-3 PUFA on hepatic proteomic profile of C57BL/6 mice.ResultsThe findings show for the first time that high dietary n-3 PUFA reduced the expression of regucalcin, adenosine kinase and aldehyde dehydrogenase. On the other hand, diets high in n-3 PUFA increased the expression of apolipoprotein A-I, S-adenosylmethionine synthase, fructose-1, 6-bisphosphatase, ketohexokinase, malate dehydrogenase, GTP-specific succinyl CoA synthase, ornithine aminotransferase and protein disulfide isomerase-A3.ConclusionsOur findings revealed for the first time that n-3 PUFA causes alterations in several novel functional proteins involved in regulating lipid, carbohydrate, one-carbon, citric acid cycle and protein metabolism, suggesting integrated regulation of metabolic pathways. These novel proteins are potential targets to develop therapeutic strategies against metabolic disorders.

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Section: Resultsmentioning

confidence: 99%

Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach

et al. 2014

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“…Regucalcin has been demonstrated to possess a pathophysiological role in metabolic disorders (16)(17)(18). In addition, regucalcin has been demonstrated to be involved in carcinogenesis (19).…”

Section: Introductionmentioning

confidence: 99%

Exogenous regucalcin suppresses the proliferation of human breast cancer MDA-MB-231 bone metastatic cells in vitro

Yamaguchi

Murata

2015

Molecular Medicine Reports

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Regucalcin serves a pivotal role as a suppressor protein in signal transduction in various types of cells and tissues. The regucalcin gene, which is localized on the X chromosome, consists of seven exons and six introns. Reductions in the gene expression of regucalcin have been suggested to serve a role in hepatocarcinogenesis in animal models and human patients, indicating a potential role as a suppressor protein in cancer. The aim of the current study was to investigate the effect of exogenous regucalcin on cell proliferation in the cloned human breast cancer MDA-MB-231 bone metastatic cell line in vitro. The proliferation of MDA-MB-231 cells was suppressed following the addition of regucalcin (0.1-10 nM) in vitro. The suppression of proliferation was not enhanced in the presence of tumor necrosis factor-α, PD98059, staurosporine, Bay K8644, wortmannin, 5,6-dichloro-1-β-D-ribofuranosylbenzimidazole or gemcitabine. Exogenous regucalcin did not induce cell death in MDA-MB-231 cells in vitro. These data suggest that exogenous regucalcin possesses suppressive effects on the proliferation of human breast cancer MDA-MB-231 bone metastatic cells, and that this effect may be mediated through various intracellular signaling pathways in vitro. Exogenous regucalcin is suggested to function as a suppressor in cancer cell proliferation.

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“…Regucalcin has been found to stimulate adipogenesis in bone marrow mesenchymal stem cells (48), and overexpressed regucalcin was demonstrated to cause diabetes and lipid metabolic disorders with hyperlipidemia in vivo (49,50). RGPR-p117 is speculated to partly participate in lipid metabolic disorder, which is mediated through regucalcin.…”

Section: Involvement Of Rgpr-p117/sec16b In Human Obesitymentioning

confidence: 99%

Involvement of regucalcin gene promoter region-related protein-p117, a transcription factor, in human obesity

Yamaguchi

Murata

2017

Biomedical Reports

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Abstract. Regucalcin gene promoter region-related protein-p117 (RGPR-p117; gene symbol, rgpr-117) was identified in 2001 as a novel transcription factor that specifically binds to a nuclear factor I consensus motif, TTGGC(N) 6 CC in the promoter region of the regucalcin (rgn) gene. The human RGPR-p117 gene consists of 26 exons spanning ~4.1 kbp and is localized on chromosome 1q25.2. The nuclear translocation of cytoplasm RGPR-p117 is mediated via the protein kinase C-dependent signaling pathway. Overexpression of RGPR-p117 enhances the transcription activity of rgn, and a protective effect on cell death by inhibition of gene expression levels of caspase-3, caspase-8 and FADD proteins that possess the TTGGC motif in the promoter region of those genes was revealed. RGPR-p117 has a crucial role as a transcription factor. Notably, RGPR-p117 was shown to localize in the plasma membranes, mitochondria and microsomes (endoplasmic reticulum; ER). RGPR-p117, which is located in the ER, was also shown to have a role as an ER export factor implicated in the transports of proteins and lipids. As a result of this finding, it was proposed in 2007 that RGPR-p117 is renamed SEC 16 homolog B, endoplasmic reticulum export factor (SEC16B). Recently, there is increasing evidence that RGPR-p117/SEC16B may be involved in human obesity. Thus, the current review presents data regarding the involvement of RGPR-p117 in human obesity.

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Involvement of regucalcin in lipid metabolism and diabetes

Cited by 52 publications

References 42 publications

Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach

Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach

Exogenous regucalcin suppresses the proliferation of human breast cancer MDA-MB-231 bone metastatic cells in vitro

Involvement of regucalcin gene promoter region-related protein-p117, a transcription factor, in human obesity

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