• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

全氟烷基物质与β细胞缺陷型糖尿病

Perfluoroalkyl substances and beta cell deficient diabetes.

作者信息

Conway Baqiyyah, Innes Karen E, Long Dustin

机构信息

Department of Epidemiology, West Virginia University, P.O. Box 9127, Morgantown, WV 26505.

Department of Epidemiology, West Virginia University, P.O. Box 9127, Morgantown, WV 26505.

出版信息

J Diabetes Complications. 2016 Aug;30(6):993-8. doi: 10.1016/j.jdiacomp.2016.05.001. Epub 2016 May 4.

DOI:10.1016/j.jdiacomp.2016.05.001
PMID:27311784
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5556924/
Abstract

AIMS

Perfluoroalkyl substances (PFAS) are synthetic hydrocarbons shown to preserve pancreatic islet cell viability and reduce islet cell hypoxia and apoptosis. We investigated the relationship of serum PFAS with diabetes, and whether this varied by diabetes type.

METHODS

6,460 individuals with and 60,439 without diabetes from the C8 Health Project, were categorized into three groups: type 1 (n=820), type 2 (n=4,291), or uncategorized diabetes (n=1,349, missing data on diabetes type or diabetes based on blood sugar at study entry). Four PFAS were investigated: perfluorohexane sulfonate (PFHxS), perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), and perfluorononaoic acid (PFNA).

RESULTS

PFAS levels were significantly lower in those with diabetes, and lowest in those with type 1 diabetes. In age and sex adjusted analyses, ORs (CI) for type 1, type 2, and uncategorized diabetes compared to no diabetes were 0.59 (0.54-0.64), 0.74 (0.71-0.77), 0.84 (0.78-0.90), respectively for PFHxS; 0.69 (0.65-0.74), 0.87 (0.89-0.91), 0.92 (0.88-0.97), respectively for PFOA; 0.65 (0.61-0.70), 0.86 (0.82-0.90), 0.93 (0.86-1.03), respectively for PFOS; and 0.65 (0.57-0.74), 0.94 (0.88-1.00), 0.95 (0.85-1.06), respectively for PFNA. Further adjustment for eGFR and other covariates did not eliminate these inverse associations.

CONCLUSIONS

PFAS levels were negatively associated with diabetes. This inverse relationship was strongest for type 1 diabetes, suggesting the relationship with serum PFAS may vary with the severity of islet cell deficiency.

摘要

目的

全氟烷基物质(PFAS)是一类合成碳氢化合物,已被证明可维持胰岛细胞活力,减少胰岛细胞缺氧和凋亡。我们研究了血清PFAS与糖尿病的关系,以及这种关系是否因糖尿病类型而异。

方法

来自C8健康项目的6460名糖尿病患者和60439名非糖尿病患者被分为三组:1型糖尿病(n = 820)、2型糖尿病(n = 4291)或未分类糖尿病(n = 1349,研究入组时糖尿病类型或基于血糖的糖尿病数据缺失)。研究了四种PFAS:全氟己烷磺酸(PFHxS)、全氟辛酸(PFOA)、全氟辛烷磺酸(PFOS)和全氟壬酸(PFNA)。

结果

糖尿病患者的PFAS水平显著较低,1型糖尿病患者的PFAS水平最低。在年龄和性别调整分析中,与无糖尿病相比,PFHxS的1型、2型和未分类糖尿病的OR(CI)分别为0.59(0.54 - 0.64)、0.74(0.71 - 0.77)、0.84(0.78 - 0.90);PFOA的分别为0.69(0.65 - 0.74)、0.87(0.89 - 0.91)、0.92(0.88 - 0.97);PFOS的分别为0.65(0.61 - 0.70)、0.86(0.82 - 0.90)、0.93(0.86 - 1.03);PFNA的分别为0.65(0.57 - 0.74)、0.94(0.88 - 1.00)、0.95(0.85 - 1.06)。进一步调整估算肾小球滤过率(eGFR)和其他协变量并未消除这些负相关关系。

结论

PFAS水平与糖尿病呈负相关。这种负相关关系在1型糖尿病中最为明显,表明与血清PFAS的关系可能随胰岛细胞缺乏的严重程度而变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2501/5556924/4ee485e9c808/nihms786901f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2501/5556924/4ee485e9c808/nihms786901f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2501/5556924/4ee485e9c808/nihms786901f1.jpg

相似文献

1
Perfluoroalkyl substances and beta cell deficient diabetes.全氟烷基物质与β细胞缺陷型糖尿病
J Diabetes Complications. 2016 Aug;30(6):993-8. doi: 10.1016/j.jdiacomp.2016.05.001. Epub 2016 May 4.
2
Perfluoroalkyl substances are inversely associated with coronary heart disease in adults with diabetes.全氟烷基物质与糖尿病成人的冠心病呈负相关。
J Diabetes Complications. 2019 Jun;33(6):407-412. doi: 10.1016/j.jdiacomp.2019.02.004. Epub 2019 Feb 20.
3
Perfluoroalkyl substances and likelihood of stroke in persons with and without diabetes.全氟烷基物质与糖尿病患者和非糖尿病患者中风概率的关系。
Diab Vasc Dis Res. 2020 Jan-Feb;17(1):1479164119892223. doi: 10.1177/1479164119892223. Epub 2019 Dec 16.
4
Perfluoroalkyl Substances, Sex Hormones, and Insulin-like Growth Factor-1 at 6-9 Years of Age: A Cross-Sectional Analysis within the C8 Health Project.6至9岁儿童的全氟烷基物质、性激素和胰岛素样生长因子-1:C8健康项目中的横断面分析
Environ Health Perspect. 2016 Aug;124(8):1269-75. doi: 10.1289/ehp.1509869. Epub 2016 Jan 22.
5
PFOA is associated with diabetes and metabolic alteration in US men: National Health and Nutrition Examination Survey 2003-2012.全氟辛酸(PFOA)与美国男性糖尿病和代谢改变有关:2003-2012 年全国健康和营养调查。
Sci Total Environ. 2018 Jun 1;625:566-574. doi: 10.1016/j.scitotenv.2017.12.186. Epub 2017 Dec 30.
6
Association of Perfluoroalkyl Substances, Bone Mineral Density, and Osteoporosis in the U.S. Population in NHANES 2009-2010.2009 - 2010年美国国家健康与营养检查调查(NHANES)中全氟烷基物质、骨密度与骨质疏松症的关联
Environ Health Perspect. 2016 Jan;124(1):81-7. doi: 10.1289/ehp.1307909. Epub 2015 Jun 9.
7
Perfluoroalkyl substances follow inverted U-shaped distributions across various stages of glomerular function: Implications for future research.全氟烷基物质在肾小球功能的各个阶段呈倒 U 型分布:对未来研究的启示。
Environ Res. 2019 Feb;169:476-482. doi: 10.1016/j.envres.2018.11.033. Epub 2018 Nov 27.
8
Environmental perfluoroalkyl acid exposures are associated with liver disease characterized by apoptosis and altered serum adipocytokines.环境中全氟烷基酸暴露与以凋亡和改变的血清脂肪细胞因子为特征的肝脏疾病有关。
Environ Pollut. 2019 Apr;247:1055-1063. doi: 10.1016/j.envpol.2019.01.064. Epub 2019 Jan 18.
9
Roles of gender and obesity in defining correlations between perfluoroalkyl substances and lipid/lipoproteins.性别和肥胖在定义全氟烷基物质与脂质/脂蛋白之间相关性中的作用。
Sci Total Environ. 2019 Feb 25;653:74-81. doi: 10.1016/j.scitotenv.2018.10.362. Epub 2018 Oct 29.
10
Prenatal exposure to perfluoroalkyl substances and birth outcomes in a Spanish birth cohort.孕期暴露于全氟烷基物质与西班牙出生队列的出生结局。
Environ Int. 2017 Nov;108:278-284. doi: 10.1016/j.envint.2017.09.006.

引用本文的文献

1
Temporal changes in per and polyfluoroalkyl substances and their associations with type 2 diabetes.全氟和多氟烷基物质的时间变化及其与2型糖尿病的关联。
Sci Rep. 2025 Jul 1;15(1):22026. doi: 10.1038/s41598-025-05422-1.
2
Associations of PFAS and OH-PCBs with risk of multiple sclerosis onset and disability worsening.全氟烷基和多氟烷基物质(PFAS)与羟基多氯联苯(OH-PCBs)与多发性硬化症发病风险及残疾恶化的关联。
Nat Commun. 2025 Feb 27;16(1):2014. doi: 10.1038/s41467-025-57172-3.
3
All-cause, cardiovascular disease and cancer mortality in the population of a large Italian area contaminated by perfluoroalkyl and polyfluoroalkyl substances (1980-2018).

本文引用的文献

1
Perfluorooctanoate exposure and major birth defects.全氟辛酸暴露与主要出生缺陷
Reprod Toxicol. 2014 Aug;47:15-20. doi: 10.1016/j.reprotox.2014.04.006. Epub 2014 May 4.
2
Influence of in vitro and in vivo oxygen modulation on β cell differentiation from human embryonic stem cells.体外和体内氧调节对人胚胎干细胞向β细胞分化的影响。
Stem Cells Transl Med. 2014 Mar;3(3):277-89. doi: 10.5966/sctm.2013-0160. Epub 2013 Dec 27.
3
Circulating levels of perfluoroalkyl substances and prevalent diabetes in the elderly.全氟烷基物质的循环水平与老年人的常见糖尿病。
意大利一个受全氟烷基和多氟烷基物质污染的地区人群的全因、心血管疾病和癌症死亡率(1980-2018 年)。
Environ Health. 2024 Apr 16;23(1):42. doi: 10.1186/s12940-024-01074-2.
4
Prenatal Exposure to Metabolism-Disrupting Chemicals, Cord Blood Transcriptome Perturbations, and Birth Weight in a Belgian Birth Cohort.比利时出生队列研究中孕期暴露于代谢干扰化学物质、脐血细胞转录组紊乱与出生体重
Int J Mol Sci. 2023 Apr 20;24(8):7607. doi: 10.3390/ijms24087607.
5
Associations between per- and polyfluoroalkyl substances (PFAS) and diabetes in two population-based cohort studies from Sweden.两项来自瑞典的基于人群的队列研究中全氟和多氟烷基物质(PFAS)与糖尿病之间的关联。
J Expo Sci Environ Epidemiol. 2023 Sep;33(5):748-756. doi: 10.1038/s41370-023-00529-x. Epub 2023 Mar 24.
6
Critical Overview on Endocrine Disruptors in Diabetes Mellitus.糖尿病中内分泌干扰物的关键综述。
Int J Mol Sci. 2023 Feb 25;24(5):4537. doi: 10.3390/ijms24054537.
7
Early-life exposure to per- and polyfluoroalkyl substances and infant gut microbial composition.生命早期接触全氟和多氟烷基物质与婴儿肠道微生物组成
Environ Epidemiol. 2022 Dec 14;7(1):e238. doi: 10.1097/EE9.0000000000000238. eCollection 2023 Feb.
8
Exposure to persistent organic pollutants alters the serum metabolome in non-obese diabetic mice.暴露于持久性有机污染物会改变非肥胖型糖尿病小鼠的血清代谢组。
Metabolomics. 2022 Nov 3;18(11):87. doi: 10.1007/s11306-022-01945-0.
9
Exposure to per- and polyfluoroalkyl substances (PFAS) and type 2 diabetes risk.接触全氟和多氟烷基物质(PFAS)与 2 型糖尿病风险。
Front Endocrinol (Lausanne). 2022 Aug 5;13:965384. doi: 10.3389/fendo.2022.965384. eCollection 2022.
10
Persistent organic pollutants and β-cell toxicity: a comprehensive review.持久性有机污染物与β细胞毒性:全面综述。
Am J Physiol Endocrinol Metab. 2022 May 1;322(5):E383-E413. doi: 10.1152/ajpendo.00358.2021. Epub 2022 Feb 14.
Diabetologia. 2014 Mar;57(3):473-9. doi: 10.1007/s00125-013-3126-3. Epub 2013 Dec 14.
4
Incidence of type II diabetes in a cohort with substantial exposure to perfluorooctanoic acid.大量接触全氟辛酸的队列人群中 II 型糖尿病的发病率。
Environ Res. 2014 Jan;128:78-83. doi: 10.1016/j.envres.2013.11.003. Epub 2013 Dec 2.
5
Perfluorooctanoic acid (PFOA) exposures and incident cancers among adults living near a chemical plant.全氟辛酸(PFOA)暴露与居住在化工厂附近的成年人癌症发病情况。
Environ Health Perspect. 2013 Nov-Dec;121(11-12):1313-8. doi: 10.1289/ehp.1306615. Epub 2013 Sep 5.
6
Prevention of autoimmune diabetes and induction of β-cell proliferation in NOD mice by hyperbaric oxygen therapy.高压氧治疗预防 NOD 小鼠自身免疫性糖尿病和诱导β细胞增殖。
Diabetes. 2012 Jul;61(7):1769-78. doi: 10.2337/db11-0516. Epub 2012 May 7.
7
Pancreas preservation for pancreas and islet transplantation: a minireview.用于胰腺和胰岛移植的胰腺保存:一篇综述
Transplant Proc. 2011 Nov;43(9):3398-401. doi: 10.1016/j.transproceed.2011.09.052.
8
Perfluorocarbon emulsions prevent hypoxia of pancreatic β-cells.全氟碳乳剂可防止胰岛β细胞缺氧。
Cell Transplant. 2012;21(4):657-69. doi: 10.3727/096368911X593136. Epub 2011 Sep 22.
9
The role of perfluorocarbon in organ preservation.全氟碳化物在器官保存中的作用。
Transplantation. 2010 May 27;89(10):1169-75. doi: 10.1097/TP.0b013e3181da6064.
10
Association of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) with uric acid among adults with elevated community exposure to PFOA.社区高水平暴露于全氟辛烷酸(PFOA)的成年人中,全氟辛酸(PFOA)和全氟辛烷磺酸(PFOS)与尿酸的关系。
Environ Health Perspect. 2010 Feb;118(2):229-33. doi: 10.1289/ehp.0900940.