Published Papers - GU Ping

Butylparaben induces glycolipid metabolic disorders in mice via disruption of gut microbiota and FXR signaling

Du H., Cui L., Zhao X., Yu Z., He T., Zhang B., Fan X., Zhao M., Zhu R., Zhang Z., Li M., Li J., Oh Y., Gu Ning

Journal of Hazardous Materials   474   2024.08  [Refereed]

Lambda-cyhalothrin induces lipid accumulation in mouse liver is associated with AMPK inactivation

Daqian Yang, Xiaotong Sun, Xiangjuan Wei, Boya Zhang, Xingpei Fan, Haining Du, Ruijiao Zhu, Yuri Oh, Ning Gu

Food and Chemical Toxicology ( Elsevier BV )  172   113563 - 113563   2023.02  [Refereed]

DOI

High-fat diet and palmitate inhibits FNDC5 expression via AMPK-Zfp57 pathway in mouse muscle cells

Qian Guo, Boya Zhang, Haining Du, Ruijiao Zhu, Xiaotong Sun, Xingpei Fan, Xiangjuan Wei, DaQian Yang, Yuri Oh, Lei Fan, Changlin Wang, Ning Gu

Chemico-Biological Interactions ( Elsevier BV )  369   110265 - 110265   2023.01  [Refereed]

DOI

Probiotics protect against hepatic steatosis in tris (2-chloroethyl) phosphate-induced metabolic disorder of mice via FXR signaling

Yang D, Wei X, Zhang B, Zhu R, Hu H, Fan X, Du H, Chen X, Zhang Z, Zhao M, Oh Y, Gu Ning

Food Chem Toxicol   169 ( 113440 )   2022.11  [Refereed]

DOI

Malting barley carbon dots-mediated oxidative stress promotes insulin resistance in mice via NF-κB pathway and MAPK cascade.

Zhang B, Yu L, Zhu R, Wei X, Fan X, Hu H, Yang D, Du H, Zhao M, Li L, Oh Y, Feng Y, Gu Ning

J Nanobiotechnology   20 ( 331 ) 1 - 19   2022.07  [Refereed]

DOI

Thiamethoxam induces nonalcoholic fatty liver disease in mice via methionine metabolism disturb via nicotinamide N-methyltransferase overexpression

Daqian Yang, Xiaoting Zhang, Lei Yue, Hailong Hu, Xiangjuan Wei, Qian Guo, Boya Zhang, Xingpei Fan, Yuan Xin, Yuri Oh, Ning Gu

Chemosphere ( Elsevier BV )  273   129727 - 129727   2021.06  [Refereed]

DOI

Effects of oral administration of polystyrene nanoplastics on plasma glucose metabolism in mice

Xingpei Fan, Xiangjuan Wei, Hailong Hu, Boya Zhang, Daqian Yang, Haining Du, Ruijiao Zhu, Xiaotong Sun, Yuri Oh, Ning Gu

Chemosphere ( Elsevier Ltd )    2021

　View Summary

Microplastic (MP) and nanoplastic (NP) induce neurotoxicity, cytotoxicity, and reproductive system toxicity in mammals. However, the impacts of NPs on the endocrine system are obscure. Here, monodisperse polystyrene nanoplastics (PS-NPs) were prepared by emulsion polymerization and the accumulation of fluorescent PS-NPs in various organs, including the liver, kidney, spleen, and pancreas, was examined. The oral administration of PS-NPs induced visceral organ injury, and the main toxicities were damage to hepatic function and the abnormity of lipid metabolism. Global transcriptome sequencing (RNA-Seq) revealed the impact of PS-NPs on the genes involved in reactive oxygen species (ROS) generation and the PI3K/Akt signaling pathway, which is associated with glucose metabolism in mice. Chronic exposure to PS-NPs significantly increased plasma glucose levels and ROS levels, but did not affect plasma insulin secretion. The phosphorylation of insulin receptor substrate (IRS)-1 at Ser307 was raised, which decreased the phosphorylation of Akt (at Ser473) in the PI3K/Akt pathway. Collectively, these findings suggested that the oral administration of PS-NPs significantly increased ROS, hepatic triglycerides, and cholesterol accumulation. The high levels of ROS disturbed the PI3K/Akt pathway, causing insulin resistance and increased plasma glucose in the mouse liver.

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Probiotics protect against hepatic steatosis in tris (2-chloroethyl) phosphate-induced metabolic disorder of mice via FXR signaling

Yang D, Wei X, Zhang B, Zhu R, Hu H, Fan X, Du H, Chen X, Zhang Z, Zhao M, Oh Y, Gu Ning

  169 ( 113440 )   2020.09  [Refereed]

DOI

The toxic effects of titanium dioxide nanoparticles on plasma glucose metabolism are more severe in developing mice than in adult mice

Hailong Hu, Boya Zhang, Li Li, Qian Guo, Daqian Yang, Xiangjuan Wei, Xingpei Fan, Jing Liu, Qiong Wu, Yuri Oh, Yujie Feng, Kun Chen, Changlin Wang, Liping Hou, Ning Gu

Environmental Toxicology ( John Wiley and Sons Inc. )  35 ( 4 ) 443 - 456   2020.04

　View Summary

Titanium dioxide nanoparticles (TiO2 NPs) are authorized food additives, and children have the highest exposure. Therefore, children are likely more susceptible to the adverse effects of TiO2 NPs than adults. Previous study showed that oral administration of 50 mg/kg body weight (bw) TiO2 NPs increase plasma glucose in mice. However, few studies have directly compared the adverse effects of exposure to TiO2 NPs on plasma glucose metabolism of different age groups. In this study, the developing (age 3 weeks) and adult mice (age 10 weeks) were orally administered with 50 mg/kg bw TiO2 NPs per day. The TiO2 NPs induced hyperglycemia earlier in the developing mice than in the adult mice. Then mechanisms were analyzed after mice were oral administration of TiO2 NPs for 8 weeks and 26 weeks, respectively. Results showed that the treatment with TiO2 NPs activated xenobiotic biodegradation in livers of both developing and adult mice at the early stage. However, only in the developing mice, TiO2 NPs induced endoplasmic reticulum (ER) stress in livers and increased reactive oxygen species in livers and sera in the early stage. The ER stress and ROS activated an inflammation response and mitogen-activated protein kinase pathways, thereby inducing insulin resistance in the livers of developing mice at the early stage. The response of the adult mice was delayed, and these changes were observed in the late stage of the study. The results of this study all suggest that children are more susceptible than adults to the toxicity of orally administered TiO2 NPs.

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Molecular mechanisms underlying zinc oxide nanoparticle induced insulin resistance in mice

Hu H, Guo Q, Fan X, Wei X, Yang D, Zhang B, Liu J, Wu Q, Oh Y, Feng Y, Chen K, Hou L, Gu N

Nanotoxicology.   14 ( 1 ) 59 - 76   2020.02  [Refereed]

The saturated fatty acid palmitate induces insulin resistance through Smad3-mediated down-regulation of FNDC5 in myotubes.

Qian Guo, Xiangjuan Wei, Hailong Hu, Daqian Yang, Boya Zhang, Xingpei Fan, Jing Liu, Hongjuan He, Yuli Oh, Qiong Wu, Yao Zhang, Chuanpeng Liu, Changlin Whang, Ning Gu

Biochemical and Biophysical Research Communications. Vol. 520(3):619-626, 2019.   5206 ( 3 ) 619 - 626   2019.12  [Refereed]

Mechanisms of titanium dioxide nanoparticle-induced oxidative stress and modulation of plasma glucose in mice

Hailong Hu, Xingpei Fan, Yao Yin, Qian Guo, Daqian Yang, Xiangjuan Wei, Boya Zhang, Jing Liu, Qiong Wu, Yuri Oh, Kun Chen, Yujie Feng, Liping Hou, Li Li, Ning Gu

Environmental Toxicology ( John Wiley and Sons Inc. )  34 ( 11 ) 1221 - 1235   2019.11

　View Summary

Titanium dioxide nanoparticles (TiO2 NPs) are reported to increase plasma glucose levels in mice at specific doses. The production and accumulation of reactive oxygen species (ROS) is potentially the most important factor underlying the biological toxicity of TiO2 NPs but the underlying mechanisms are unclear at present. Data from genome-wide analyses showed that TiO2 NPs induce endoplasmic reticulum (ER) stress and ROS generation, leading to the inference that TiO2 NP-induced ER stress contributes to enhancement of ROS in mice. Resveratrol (Res) effectively relieved TiO2 NP-induced ER stress and ROS generation by ameliorating expression of a common set of activated genes for both processes, signifying that ER stress and ROS are closely related. TiO2 NP-induced ER stress occurred earlier than ROS generation. Upon treatment with 4-phenylbutyric acid to relieve ER stress, plasma glucose levels tended toward normal and TiO2 NP increased ROS production was inhibited. These results suggest that TiO2 NP-induced ER stress promotes the generation of ROS, in turn, triggering increased plasma glucose levels in mice. In addition, Res that displays the ability to reduce ER stress presents a dietary polyphenol antioxidant that can effectively prevent the toxicological effects of TiO2 NPs on plasma glucose metabolism.

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Silicon dioxide nanoparticles induce insulin resistance through endoplasmic reticulum stress and generation of reactive oxygen species.

Hailong Hu, Xingpei Fan, Qian Guo, Xiangjuan Wei, Daqian Yang, Boya Zhang, Jing Liu, Qiong Wu, Yuri Oh, Yujie Feng, Kun Chen, Liping Hou, Ning Gu

Particle and Fibre Toxicology   Vol.16 ( 41 ) 1 - 18   2019.11  [Refereed]

C/EBPβ mediates palmitate-induced musclin expression via the regulation of PERK/ATF4 pathways in myotubes.

Qian Guo, Hailong Hu, Xiaohuan Liu, DaQian Yang, Yao Yin, Boya Zhang, Hongjuan He, Yuri Oh, Qiong Wu, Chuanpeng Liu, Ning Gu

Am J Physiol Endocrinol Metab.   316 ( 6 ) E1081-E1092 - E1092   2019.06  [Refereed]

Glucosamine induces increased musclin gene expression through endoplasmic reticulum stress-induced unfolding protein response signaling pathways in mouse skeletal muscle cells.

1) Qian Guo,Hailong Hu,Ying Zhoua,Yuheng Yan,Xiangjuan Wei,Xingpei Fan,Daqian Yang,Hongjuan He,Yuri Oh,Kun Chen,Qiong Wu,Chuanpeng Liu,Ning Gu.

Food Chem Toxicol,   125   95 - 105   2019.03  [Refereed]

RNA sequencing analysis shows that titanium dioxide nanoparticles induce endoplasmic reticulum stress, which has a central role in mediating plasma glucose in mice

Hailong Hu, Li Li, Qian Guo, He Zong, Yuheng Yan, Yao Yin, Yu Wang, Yuri Oh, Yujie Feng, Qiong Wu, Ning Gu

Nanotoxicology ( Taylor and Francis Ltd )  12 ( 4 ) 341 - 356   2018.04  [Refereed]

　View Summary

Titanium dioxide nanoparticles (TiO2NPs) constitute the top five NPs in use today. In this study, oral administration of 50, 100, and 200 mg/kg body weight (b.w.) TiO2NPs increases plasma glucose in mice, whereas 10 and 20 mg/kg b.w. TiO2NPs did not. RNA sequencing (RNA-seq) technology was used to investigate genome-wide effects of TiO2NPs. Clustering analysis of the RNA-seq data showed the most significantly enriched gene ontology terms and KEGG pathways related to the endoplasmic reticulum (ER) and ER stress. Molecular biology verification showed that 50 mg/kg b.w. and higher doses TiO2NPs activated a xenobiotic biodegradation response and increased expression of cytochrome P450 family genes in mouse livers, thus inducing ER stress in mice. ER stress-activated MAPK and NF-κB pathways and induced an inflammation response, resulting in phosphorylation of the insulin receptor substrate 1 and, consequently, insulin resistance. This was the main mechanism by which TiO2NPs increased plasma glucose in mice. Meanwhile, ER stress disturbed the monooxygenase system, and thus generated reactive oxygen species (ROS). Relief of ER stress with 4-phenylbutyric acid inhibited all the above effects of TiO2NPs, including the generation of ROS. Therefore, TiO2NP-induced ER stress was a decisive factor with a central role in plasma glucose disturbance in mice.

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Hypoxia in 3T3-L1 adipocytes suppresses adiponectin expression via the PERK and IRE1 unfolded protein response

Qian Guo, Sanli Jin, Hailong Hu, Ying Zhou, Yuheng Yan, He Zong, Yu Wang, Hongjuan He, Yuri Oh, Chuanpeng Liu, Ning Gu

Biochemical and Biophysical Research Communications ( Elsevier B.V. )  493 ( 1 ) 346 - 351   2017.11  [Refereed]

　View Summary

Adiponectin, an adipocytokine produced by adipocytes, functions as an anti-inflammatory and anti-apoptotic substance, while also enhancing insulin sensitivity. Patients or model animals with obesity or diabetes typically present attenuated expression of adiponectin. Moreover, obesity and diabetes are often accompanied with hypoxia in adipose tissue, which may result in endoplasmic reticulum (ER) stress as well as low expression of adiponectin. The purpose of this study was to investigate the specific role of the unfolded protein response (UPR) involved in the low expression of adiponectin induced by hypoxia. Subjecting 3T3-L1 adipocytes to hypoxia significantly reduced adiponectin expression and activated the PERK and IRE1 signaling pathways in a time-dependent manner. The ATF6 signaling pathway showed no obvious changes with hypoxia treatment under a similar time course. Moreover, the down-regulated expression of adiponectin induced by hypoxia was relieved once the PERK and IRE1 signaling pathways were suppressed by the inhibitors GSK2656157 and 4μ8C, respectively. Overall, these data demonstrate that hypoxia can suppress adiponectin expression and activate the PERK and IRE1 signaling pathways in differentiated adipocytes, and this two pathways are involved in the suppression of adiponectin expression induced by hypoxia.

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Growth of zinc sulfide by mist chemical vapor deposition depending on mist size and thermal conditions in susceptor: Growth of zinc sulfide by mist chemical vapor

Kazuyuki Uno, Yuichiro YAMASAKI、Gu PING, Ichiro Tanaka

physica status solidi (c)   13   7 - 9   2016.04  [Refereed]

A mechanistic study to increase understanding of titanium dioxide nanoparticles-increased plasma glucose in mece

Hu Hailong, Guo Qian, Wang Changlin, Ma Xiao, He Hongjuan, Oh Yuri, Feng Yujie, Wu Qiong, Ning Gu

Food and Chemical Toxicology   95   175 - 187   2016  [Refereed]

Growth of zinc sulfide by mist chemical vapor deposition depending on mist size and thermal conditions in susceptor

Kazuyuki Uno, Yuichiro Yamasaki, Ping Gu, Ichiro Tanaka

PHYSICA STATUS SOLIDI C: CURRENT TOPICS IN SOLID STATE PHYSICS, VOL 13 NO 7-9 ( WILEY-V C H VERLAG GMBH )  13 ( 7-9 ) 448 - 451   2016  [Refereed]

　View Summary

Zinc sulfide (ZnS) films were successfully grown by using mist chemical vapor deposition (mist-CVD) with fine-channel susceptor made of quartz. For the investigation of growth dynamics, two types of mist generators and two types of susceptors were prepared and distribution profiles of film thickness were examined. Thermal efficiency of susceptor depends on heat-penetration efficiency and line-velocity of the mists, which are influenced by the fine-channel gap-height of the susceptors. Using larger size of mists requires higher thermal efficiency in susceptor to obtain a flat thickness distribution. This result indicates that the optimization of the mist size and the susceptor structure is important for the film uniformity of grown films by the mist-CVD. (C) 201 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim

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