Wanqi Zhang

Prof. Wanqi Zhang

orcid

Research Focus & Metrics

Academic Career Length

25Years (2002-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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23 April 2014 in The FASEB Journal
Verified
Journal Article
Open access
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RBRaymond F. Burk
Raymond F. Burk
KHKristina E. Hill
Kristina E. Hill
AMAmy K. Motley
Amy K. Motley
VWVirginia P. Winfrey
Virginia P. Winfrey
SKSuguru Kurokawa
Suguru Kurokawa
WZWanqi Zhang
Wanqi Zhang
Selenoprotein P (Sepp1) and its receptor, apolipoprotein E receptor 2 (apoER2), account for brain retaining selenium better than other tissues. The primary sources of Sepp1 in plasma and brain are hepatocytes and astrocytes, respectively. ApoER2 is expressed in varying amounts by tissues; within the brain it is expressed primarily by neurons. Knockout of Sepp1 or apoER2 lowers brain selenium from ~120 to ~50 ng/g and leads to severe neurodegeneration and death in mild selenium deficiency. Interactions of Sepp1 and apoER2 that protect against this injury have not been characterized. We studied Sepp1, apoER2, and brain selenium in knockout mice. Immunocytochemistry showed that apoER2 mediates Sepp1 uptake at the blood‐brain barrier. When Sepp1 –/– or apoER2 –/– mice developed severe neurodegeneration caused by mild selenium deficiency, brain selenium was ~35 ng/g. In extreme selenium deficiency, however, brain selenium of ~12 ng/g was tolerated when both Sepp1 and apoER2 were intact in the brain. These findings indicate that tandem Sepp1‐apoER2 interactions supply selenium for maintenance of brain neurons. One interaction is at the blood‐brain barrier, and the other is within the brain. We postulate that Sepp1 inside the blood‐brain barrier is taken up by neurons via apoER2, concentrating brain selenium in them.—Burk, R. F., Hill, K. E., Motley, A. K., Winfrey, V. P., Kurokawa, S., Mitchell, S. L., Zhang, W. Selenoprotein P and apolipoprotein E receptor‐2 interact at the blood‐brain barrier and also within the brain to maintain an essential selenium pool that protects against neurodegeneration. FASEB J. 28, 3579–3588 (2014). www.fasebj.org

1 November 2019 in Journal of Endocrinology
Verified
Journal Article
Closed access
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CYChunxia Yu
Chunxia Yu
SLSujuan Liu
Sujuan Liu
LCLiqin Chen
Liqin Chen
JSJun Shen
Jun Shen
YNYanmei Niu
Yanmei Niu
LFLi Fu
Li Fu
The composition and activity of the gut microbiota depend on the host genome, nutrition, and lifestyle. Exercise and sodium butyrate (NaB) exert metabolic benefits in both mice and humans. However, the underlying mechanisms have not been fully elucidated. This study aimed to examine the effect of exercise training and dietary supplementation of butyrate on the composition of gut microbiota and whether the altered gut microbiota can stimulate differential production of short-chain fatty acids (SCFAs), which promote the expression of SESN2 and CRTC2 to improve metabolic health and protect against obesity. C57BL/6J mice were used to study the effect of exercise and high-fat diet (HFD) with or without NaB on gut microbiota. Bacterial communities were assayed in fecal samples using pyrosequencing of 16S rRNA gene amplicons. Western blot was performed using relevant antibodies to detect the protein expressions in liver and HepG2 cell extracts. Exercise and butyrate administration significantly reversed metabolic dysfunctions induced by HFD (P < 0.05). The number of Firmicutes and the proportion of Firmicutes to Bacteroidetes order were predominant in all HFD groups (P = 0.001). Exercise and butyrate supplementation significantly inhibited the relative abundance of lipopolysaccharide-producing phyla (P = 0.001). SESN2 and CRTC2 expression in the liver of mice were significantly increased after exercise (P < 0.05) and/or supplementation of butyrate (P < 0.05). Exercise enhances butyrate-producing fecal bacteria and increases butyrate production and consequently improves lipid metabolism through the butyrate-SESN2/CRTC2 pathway. Excess butyrate may reduce the proportion of probiotics and reverse the metabolic effects.

1 August 2012 in The Journal of Clinical Endocrinology & Metabolism
Verified
Journal Article
Open access
PDF file
ZSZhongNa Sang
ZhongNa Sang
WWWei Wei
Wei Wei
NZNa Zhao
Na Zhao
GZGuiQin Zhang
GuiQin Zhang
WCWen Chen
Wen Chen
WZWanqi Zhang
Wanqi Zhang
Context: Adequate iodine intake during pregnancy is essential for both the synthesis of maternal thyroid hormones and the maintenance of normal fetal brain development. Scant evidence is available on the effects of excessive iodine intake during pregnancy. Objective: The study assesses the relationship between iodine nutritional status and thyroid function of pregnant women with excessive iodine intake during late gestation. Design and Participants: A cross-sectional study of 384 pregnant women was carried out in Tianjin and Haixing from April to October in 2010. Main Outcome Measures: Morning urine samples and blood samples were obtained from all subjects. Serum levels of free T3, free T4, and sensitive TSH and urinary iodine concentration were measured. Results: The median urinary iodine concentration of pregnant women with excessive iodine intake was significantly higher than those with adequate iodine intake (P < 0.001). The prevalence of thyroid disease, especially subclinical hypothyroidism, in pregnant women with excessive iodine intake was significantly higher than in those with adequate iodine intake (P < 0.05). Subclinical hypothyroidism was the most frequent pattern of thyroid disease for pregnant women and those with positive or negative thyroid autoantibodies. Living with high water iodine content and having urinary iodine concentration higher than 250 μg/liter are associated risk factors for subclinical hypothyroidism in pregnant women (OR1 = 41.822, OR2 = 6.202; P < 0.05, where OR1 is the odds ratio for living with high water iodine content and hypothyroidism and OR2 is the odds ratio for urinary iodine concentration >250 μg/liter and hypothyroidism). Conclusions: Excessive iodine intake during late pregnancy may lead to maternal thyroid dysfunction, particularly subclinical hypothyroidism. The appropriate measurements should be performed to monitor the onset of hypothyroidism in pregnant women with excessive iodine intake.

2 July 2018 in Scientific Reports
Verified
Journal Article
Open access
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KWKunling Wang
Kunling Wang
HWHongyan Wei
Hongyan Wei
WZWanqi Zhang
Wanqi Zhang
ZLZhen Li
Zhen Li
LDLi Ding
Li Ding
MZMei Zhu
Mei Zhu
Trace elements, such as iodine and selenium, are closely related to autoimmune thyroiditis and thyroid function. Low serum magnesium is associated with several chronic diseases; however, its associations with autoimmune thyroiditis and thyroid function are unclear. We investigated the relationships between low serum magnesium, autoimmune thyroiditis, and thyroid function in 1,257 Chinese participants. Demographic data were collected via questionnaires, and levels of serum thyroid stimulating hormone, anti-thyroid peroxidase antibody, anti-thyroglobulin antibody (TGAb), free thyroxine, serum magnesium, serum iodine, and urinary iodine concentration were measured. Participants were divided into serum magnesium level quartiles (≤0.55, 0.551–0.85, 0.851–1.15, and >1.15 mmol/L). The median serum magnesium level was 0.89 (0.73–1.06) mmol/L; levels ≤0.55 mmol/L were considered severely low (5.9% of participants). The risks of TGAb positivity and Hashimoto thyroiditis (HT) diagnosed using ultrasonography in the lowest quartile group were higher than those in the adequate magnesium group (0.851–1.15 mmol/L) (p < 0.01, odds ratios [ORs] = 2.748–3.236). The risks of total and subclinical-only hypothyroidism in the lowest quartile group were higher than those in the adequate magnesium group (0.851–1.15 mmol/L) (p < 0.01, ORs = 4.482–4.971). Severely low serum magnesium levels are associated with an increased rate of TGAb positivity, HT, and hypothyroidism.

1 January 2017 in The American Journal of Clinical Nutrition
Verified
Journal Article
Open access
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WCWen Chen
Wen Chen
XLXiang Li
Xiang Li
YWYalan Wu
Yalan Wu
JBJianchao Bian
Jianchao Bian
JSJun Shen
Jun Shen
WZWanqi Zhang
Wanqi Zhang
Background: Excessive iodine intake may have adverse effects on the thyroid, particularly in children, but the safe upper iodine intake concentration

1 December 2013 in The Journal of Nutrition
Verified
Journal Article
Open access
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SZSang Zhongna
Sang Zhongna
CWChen Wen
Chen Wen
SJShen Jun
Shen Jun
TLTan Long
Tan Long
ZNZhao Na
Zhao Na
WZWanqi Zhang
Wanqi Zhang
Previous studies have indicated an association between iodine excess and increased incidence of thyroid dysfunction in adults. However, there have be