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| 1 | Effect of methyl tert-butyl ether on adipogenesis and glucose metabolism in vitro and in vivo显示文摘Methyl tert-butyl ether (MTBE),as a widely used gasoline additive,is suspected of being environmentally toxic.MTBE accumulates mainly in adipose tissue,but its effect on obesity or obesity-related metabolic disorders has not been well understood yet.Therefore,we examined the effect of MTBE on the adipose function and the related metabolic processes with both 3T3-L1 cell line and C57BL/6J mice model.We found that exposure to MTBE at the environmental relevant concentration (100 μmol/L) could significantly induce differentiation of preadipocyte and disturb insulin-stimulated glucose uptake of mature adipocyte.The in vivo observation in male mice showed a positive correlation of visceral white adipose tissue (vWAT) expansion and cell size increase with MTBE treatment in 14 weeks.Glucose tolerance and insulin sensitivity tests demonstrated that MTBE at 1000 μg/(kg·day) disturbed the systemic glucose metabolism in a gender-specific manner,which might be partly attributed to the alterations of gut microbiota community at genus level with respect to Akkermansia,Clostridium XIVb,and Megamonas.In summary,our study characterized the effect of MTBE on adipose tissue function and glucose homeostasis in vitro and in vivo,and revealed that systemic disorders of the glucose metabolism might be modulated by the related gut microbiota. | Yue Tang Qidong Ren Qing Wen Caixia Yu Xinni Xie Qing Hu Yuguo Du | 2019 | Journal of Environmental Sciences2019，31，11： | 4 |
| 2 | Methyl tertiary-butyl ether inhibits THP-1 macrophage cholesterol efflux in vitro and accelerates atherosclerosis in ApoE-deficient mice in vivo显示文摘The biosafety of methyl tertiary-butyl ether(MTBE),mainly used as a gasoline additive,has long been a contentious topic.In addition to its routine toxicities,MTBE has been demonstrated to disrupt glucose and lipid metabolism and contribute to the development of type2 diabetes as well as obesity.As one of the morbidities related to dyslipidemia,atherosclerosis is worthy of being investigated under MTBE exposure.Since foam cells derived from macrophages play pivotal roles during atherosclerosis development,we studied the effects of MTBE on macrophages in vitro and assessed the effect of MTBE on atherosclerosis plaque formation with the ApoE^(-/-)mouse model in uiuo for the first time.Our results demonstrated that exposure to MTBE at environmentally relevant concentrations decreased the expression of ABCA1 and ABCG1,which are responsible for macrophage cholesterol efflux,at both mRNA and protein levels in THP-1 macrophages.Consequently,treatment with MTBE inhibited the transport of cholesterol from macrophages to High-density lipoprotein.ApoE^(-/-)mice exposed to MTBE at environmentally relevant concentrations(100,1000μg/kg)displayed significant increases in lesion area in the aorta and aortic root compared to vehicletreated ones.Further analysis indicated that MTBE exposure enhanced the macrophagespecific marker Mac-2 contents within plaques in the aortic root,implying that MTBE could promote macrophage-derived foam cell formation and thus accelerate atherosclerosis plaque formation.We for the first time demonstrated the pro-atherogenic effect of MTBE via eliciting disruption of macrophage cholesterol efflux and accelerating foam cell formation and atherosclerosis plaque development. | Qidong Ren Xinni Xie Yue Tang Qing Hu Yuguo Du | 2021 | Journal of Environmental Sciences2021，33，3： | 1 |
| 3 | Multi-scaling hierarchical structure analysis on the sequence of E.coli complete genome显示文摘We have applied the newly developed hierarchical structure theory for complex systems to analyze the multi-scaling structures of the nucleotide density distribution along a linear DNA sequence from the complete Escherichia coli genome. The hierarchical symmetry in the nucleotide density distribution was demonstrated. In particular, we have shown that the G, C density distribution that represents a strong H-bonding between the two DNA chains is more coherent with smaller similarity parameter compared to that of A, T density distribution, indicating a better organized multi-scaling fluctuation field for G, C density distributionalong the genome sequence. The biological significance of these findings is under investigation. | WANG Jin ZHANG Qidong REN Kui SHE Zhensu | 2001 | Chinese Science Bulletin2001，46，23： | 1 |
| 4 | Graphene oxide-decorated Fe2(MoO4)3 microflowers as a promising anode for lithium and sodium storage显示文摘 | Chunhua Han Xiaoji Ren Qidong Li Wen Luo Lei Huang Liang Zhou Liqiang Mai | 2018 | Nano Research2018，11，3： | 0 |
| 5 | Differential expression of a cDNA clone in human liverversus hepatic cancer-highly homologous to aryl-dialkyl-phosphatase显示文摘We applied the technique of mRNA differential display to normal liver tissue and hepatoma cell line Hep3B. One of the isolated cDNA clones was expressed in human normal liver tissue but not in the human hepatocarcinoma cell line. Northern Blot analysis confirmed that high level of mRNA was expressed in human normal liver tissue but the level was decreased in non-cancerous liver tissue from hepatoma patients. Low level or no expression was observed in human hepatoma tissue. One of these transcripts was about 1.8 kb in length. Southern Blot analysis showed that it was a single copy gene. We obtained a full length cDNA clone of 2,395 bp by screening human liver 5’-stretch plus cDNA library. Nucleotide sequence indicated that this clone was highly homologous to aryldialkyl-phosphatase and possessed two polymorphic sites. Aryl-dialkyl--phosphatase which has a prominent role in the metabolism of several toxic, synthetic compounds, may be potentially related to human hepatocarcinoma susceptibility. The biological significance of its differential expression in normal versus malignant tissue is discussed. | WANG KAN KAN DA FANG WAN XIAO KUN QIU PEI XIN LU JIAN REN GU(National La6oratory for Oncogenes and Related Genes Shanghai Cancer Institute, Shanghai 200032)(Qidong Cancer Institute, Jiangsu 226200) | 1997 | Cell Research1997，7，1： | 0 |
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