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砷暴露可降低高脂肪喂养期间的肥胖程度。

Arsenic Exposure Decreases Adiposity During High-Fat Feeding.

机构信息

Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA.

Committee on Molecular Pathogenesis and Molecular Medicine, University of Chicago, Chicago, Illinois, USA.

出版信息

Obesity (Silver Spring). 2020 May;28(5):932-941. doi: 10.1002/oby.22770. Epub 2020 Mar 20.

DOI:10.1002/oby.22770
PMID:32196994
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7180103/
Abstract

OBJECTIVE

Arsenic is an endocrine-disrupting chemical associated with diabetes risk. Increased adiposity is a significant risk factor for diabetes and its comorbidities. Here, the impact of chronic arsenic exposure on adiposity and metabolic health was assessed in mice.

METHODS

Male C57BL/6J mice were provided ad libitum access to a normal or high-fat diet and water +/- 50 mg/L of sodium arsenite. Changes in body weight, body composition, insulin sensitivity, energy expenditure, and locomotor activity were measured. Measures of adiposity were compared with accumulated arsenic in the liver.

RESULTS

Despite uniform arsenic exposure, internal arsenic levels varied significantly among arsenic-exposed mice. Hepatic arsenic levels in exposed mice negatively correlated with overall weight gain, individual adipose depot masses, and hepatic triglyceride accumulation. No effects were observed in mice on a normal diet. For mice on a high-fat diet, arsenic exposure reduced fasting insulin levels, homeostatic model assessment of insulin resistance and β-cell function, and systemic insulin resistance. Arsenic exposure did not alter energy expenditure or activity.

CONCLUSIONS

Collectively, these data indicate that arsenic is antiobesogenic and that concentration at the source poorly predicts arsenic accumulation and phenotypic outcomes. In future studies, investigators should consider internal accumulation of arsenic rather than source concentration when assessing the outcomes of arsenic exposure.

摘要

目的

砷是一种与糖尿病风险相关的内分泌干扰化学物质。肥胖是糖尿病及其并发症的一个重要危险因素。在此,评估了慢性砷暴露对小鼠肥胖和代谢健康的影响。

方法

雄性 C57BL/6J 小鼠自由获得正常或高脂肪饮食和水+/-50mg/L 的亚砷酸钠。测量体重、身体成分、胰岛素敏感性、能量消耗和运动活性的变化。将肥胖测量值与肝脏中的累积砷进行比较。

结果

尽管砷暴露均匀,但暴露于砷的小鼠体内砷水平差异显著。暴露于砷的小鼠的肝脏砷水平与总体体重增加、个体脂肪沉积质量和肝甘油三酯积累呈负相关。在正常饮食的小鼠中未观察到影响。对于高脂肪饮食的小鼠,砷暴露降低了空腹胰岛素水平、胰岛素抵抗和β细胞功能的稳态模型评估以及全身胰岛素抵抗。砷暴露并未改变能量消耗或活性。

结论

总的来说,这些数据表明砷具有抗肥胖作用,而来源浓度不能很好地预测砷积累和表型结果。在未来的研究中,研究人员在评估砷暴露的结果时,应考虑砷的体内积累,而不是来源浓度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/b271afdff396/nihms-1559331-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/e834450eda95/nihms-1559331-f0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/120c46628d42/nihms-1559331-f0003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/8abbd23ee39a/nihms-1559331-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/b271afdff396/nihms-1559331-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/e834450eda95/nihms-1559331-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/4a3f2584c766/nihms-1559331-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/120c46628d42/nihms-1559331-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/f65cbe48a36a/nihms-1559331-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/8abbd23ee39a/nihms-1559331-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8e/7180103/b271afdff396/nihms-1559331-f0006.jpg

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Developmental exposure to the endocrine disruptor tolylfluanid induces sex-specific later-life metabolic dysfunction.发育暴露于内分泌干扰物甲苯氟磺胺会导致性别特异性的晚年代谢功能障碍。
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The Role of the Nuclear Receptor FXR in Arsenic-Induced Glucose Intolerance in Mice.核受体FXR在小鼠砷诱导的葡萄糖不耐受中的作用
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Is Arsenic Exposure a Risk Factor for Metabolic Syndrome? A Review of the Potential Mechanisms.砷暴露是否是代谢综合征的危险因素?潜在机制的综述。
Front Endocrinol (Lausanne). 2022 May 16;13:878280. doi: 10.3389/fendo.2022.878280. eCollection 2022.
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