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- Author: Guang Ning x
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School of Medicine, State Key Laboratory for Medical Genomics, Laboratory of Development and Diseases, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Disease
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Chromogranin A (CHGA), a protein participating in the biogenesis of dense core secretory granules in various neuroendocrine tissues, plays a critical role in the release of hormones/peptides and the pathogenesis of pheochromocytoma. However, little is known about the developmental origin of CHGA-expressing cells during embryogenesis. Here, we report the structural characterization and spatio-temporal expression pattern of zebrafish (Danio rerio) ortholog of mammalian CHGA. The earliest expression of chga transcripts was observed at 16 h post fertilization in the developing cranial ganglia as six distinct cellular masses arranged bilaterally as strings of beads in the dorsal root ganglia (DRG) precursors along the dorsal trunk. With development advancing, the chga transcripts were expressed abundantly in diencephalon, mesencephalon, and rhombencephalon as well as in the DRG. Interestingly, double in situ hybridization assay of chga with genes expressed in pronephros (Wilms' tumor suppressor 1, wt1), adrenal cortex (side-chain cleavage enzyme, scc), and sympathoadrenal neuron/chromaffin cell (dopamine-β-hydroxylase, dbh), respectively, showed that the chga-expressing cells are spatially separated from wt1-, scc-, and dbh-positive cell populations during early embryonic development. The pronephros region does not express chga even up to 7 days post fertilization, while chga positive-staining cells bind in the brain and DRG, indicating that chga may play an important role in nervous system development during the early embryonic stages.
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Department of Endocrinology, East Hospital, Tongji University School of Medicine, Shanghai, China
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An increasing amount of evidence suggests that the delayed effect of antibiotics (abx) on gut microbiota after its cessation is not as favorable as its immediate effect on host metabolism. However, it is not known how the diverse abx-dependent metabolic effects influence diabetic subjects and how gut microbiota is involved. Here, we treated db/db mice with abx cocktail for 12 days and discontinued for 24 days. We found that db/db mice showed decreased body weight and blood glucose after abx treatment, which rapidly caught up after abx cessation. Twenty-four days after abx withdrawal, db/db mice exhibit increased plasma, hepatic total cholesterol (TC) levels and liver weight. The gut microbiota composition at that time showed decreased relative abundances (RAs) of Desulfovibrionaceae and Rikenellaceae, increased RA of Erysipelotrichaceae and Mogibacteriaceae, which were correlating with the reduced short-chain fatty acids (SCFAs) in gut content, such as propionic acid and valeric acid and with the elevated fecal taurine-conjugated bile acids (BAs) levels. The molecular biology studies showed inhibited hepatic BA synthesis from cholesterol, impeded intracellular transportation and biliary excretion of cholesterol that all conferred to liver TC accumulation. The associations among alterations of gut microbiota composition, microbial metabolite profiles and host phenotypes suggested the existence of gut microbiota-linked mechanisms that mediate the unfavorable delayed effects of abx on db/db mice cholesterol metabolism. Thus, we call upon the caution of applying abx in diabetic animal models for studying microbiota-host interaction and in type 2 diabetes subjects for preventing chronic cardiovascular consequences.
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.
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SIRT1, a class III histone/protein deacetylase (HDAC), has been associated with autoimmune diseases. There is a paucity of data about the role of SIRT1 in Graves’ disease. The aim of this study was to investigate the role of SIRT1 in the pathogenesis of GD. Here, we showed that SIRT1 expression and activity were significantly decreased in GD patients compared with healthy controls. The NF-κB pathway was activated in the peripheral blood of GD patients. The reduced SIRT1 levels correlated strongly with clinical parameters. In euthyroid patients, SIRT1 expression was markedly upregulated and NF-κB downstream target gene expression was significantly reduced. SIRT1 inhibited the NF-κB pathway activity by deacetylating P65. These results demonstrate that reduced SIRT1 expression and activity contribute to the activation of the NF-κB pathway and may be involved in the pathogenesis of GD.
