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- Author: Xiaoying Li x
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Department of Endocrinology, FuJian Union hospital, Fuzhou, P R China
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The cellular and molecular mechanisms of glucose-stimulated β-cell proliferation are poorly understood. Recently, secreted frizzled-related protein 5 (encoded by Sfrp5; a Wnt signaling inhibitor) has been demonstrated to be involved in β-cell proliferation in obesity. A previous study demonstrated that glucose enhanced Wnt signaling to promote cell proliferation. We hypothesized that inhibition of SFRP5 contributes to glucose-stimulated β-cell proliferation. In this study, we found that the Sfrp5 level was significantly reduced in high glucose-treated INS-1 cells, primary rat β-cells, and islets isolated from glucose-infused rats. Overexpression of SFRP5 diminished glucose-stimulated proliferation in both INS-1 cells and primary β-cells, with a concomitant inhibition of the Wnt signaling pathway and decreased cyclin D2 expression. In addition, we showed that glucose-induced Sfrp5 suppression was modulated by the PI3K/AKT pathway. Therefore, we conclude that glucose inhibits Sfrp5 expression via the PI3K/AKT pathway and hence promotes rat pancreatic β-cell proliferation.
Shanghai Key Laboratory of Endocrine Tumor, Division of Endocrinology and Metabolism, Shanghai Jiao-Tong University School of Medicine, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui-Jin Hospital, 197 Rui-Jin 2nd Road, Shanghai 200025, People's Republic of China
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Shanghai Key Laboratory of Endocrine Tumor, Division of Endocrinology and Metabolism, Shanghai Jiao-Tong University School of Medicine, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui-Jin Hospital, 197 Rui-Jin 2nd Road, Shanghai 200025, People's Republic of China
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Shanghai Key Laboratory of Endocrine Tumor, Division of Endocrinology and Metabolism, Shanghai Jiao-Tong University School of Medicine, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui-Jin Hospital, 197 Rui-Jin 2nd Road, Shanghai 200025, People's Republic of China
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Shanghai Key Laboratory of Endocrine Tumor, Division of Endocrinology and Metabolism, Shanghai Jiao-Tong University School of Medicine, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui-Jin Hospital, 197 Rui-Jin 2nd Road, Shanghai 200025, People's Republic of China
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Shanghai Key Laboratory of Endocrine Tumor, Division of Endocrinology and Metabolism, Shanghai Jiao-Tong University School of Medicine, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui-Jin Hospital, 197 Rui-Jin 2nd Road, Shanghai 200025, People's Republic of China
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Shanghai Key Laboratory of Endocrine Tumor, Division of Endocrinology and Metabolism, Shanghai Jiao-Tong University School of Medicine, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui-Jin Hospital, 197 Rui-Jin 2nd Road, Shanghai 200025, People's Republic of China
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Shanghai Key Laboratory of Endocrine Tumor, Division of Endocrinology and Metabolism, Shanghai Jiao-Tong University School of Medicine, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui-Jin Hospital, 197 Rui-Jin 2nd Road, Shanghai 200025, People's Republic of China
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Genipin, a compound derived from Gardenia jasminoides Ellis fruits, has been used over the years in traditional Chinese medicine to treat symptoms of type 2 diabetes. However, the molecular basis for its antidiabetic effect has not been fully revealed. In this study, we investigated the effects of genipin on glucose uptake and signaling pathways in C2C12 myotubes. Our study demonstrates that genipin stimulated glucose uptake in a time- and dose-dependent manner. The maximal effect was achieved at 2 h with a concentration of 10 μM. In myotubes, genipin promoted glucose transporter 4 (GLUT4) translocation to the cell surface, which was observed by analyzing their distribution in subcellular membrane fraction, and increased the phosphorylation of insulin receptor substrate-1 (IRS-1), AKT, and GSK3β. Meanwhile, genipin increased ATP levels, closed KATP channels, and then increased the concentration of calcium in the cytoplasm in C2C12 myotubes. Genipin-stimulated glucose uptake could be blocked by both the PI3-K inhibitor wortmannin and calcium chelator EGTA. Moreover, genipin increases the level of reactive oxygen species and ATP in C2C12 myotubes. These results suggest that genipin activates IRS-1, PI3-K, and downstream signaling pathway and increases concentrations of calcium, resulting in GLUT4 translocation and glucose uptake increase in C2C12 myotubes.
Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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The ectopic ACTH syndrome is caused by abnormal expression of the POMC gene product arising from non-pituitary tumors in response to the ectopic activation of the pituitary-specific promoter of this gene. It has been proved that methylation of the CpG island in the promoter region is associated with silencing of some genes. Using bisulphite sequencing, we identified hypermethylation in the 5′ promoter region of the POMC gene in three normal thymuses and one large cell lung cancer, and hypomethylation in five thymic carcinoid tumors resected from patients with ectopic ACTH syndrome. The region undergoing hypermethylation was narrowed to coordinates −417 to −260 of the POMC promoter. Furthermore, we observed that the levels of POMC expression correlated with the methylation density at −417 to −260 bp across the E2 transcription factor binding region of the POMC promoter. It is concluded that hypomethylation of the POMC promoter in thymic carcinoids correlates with POMC overexpression and the ectopic ACTH syndrome.
