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Cadmium exposure impairs pancreatic β-cell function and exaggerates diabetes by disrupting lipid metabolism
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Highlights Cd exposure induces pancreatic β-cell dysfunction and promotes the development of diabetes. Cd exposure disrupts lipid metabolism and induces lipid accumulation in MIN6 cells. Cd exposure promotes inflammation by increasing the weight of inflammatory bioactive lipids.
Abstract Cadmium is known as an environmental pollutant that contributes to pancreatic damage and the pathogenesis of diabetes. However, less attention has been devoted to elucidating the mechanisms underlying Cd-induced pancreatic β-cell dysfunction and the role of Cd toxicity in the development of diabetes. In this study, we demonstrated that exposure to Cd caused remarkable pancreatic β-cell dysfunction and death, both in vitro and in vivo. Lipidomic analysis of Cd-exposed pancreatic β-cells using high-resolution mass spectrometry revealed that Cd exposure altered the profile and abundance of lipids. Cd exposure induced intracellular lipid accumulation, promoted lipid biogenesis, elevated pro-inflammatory lipid contents and inhibited lipid degradation. Furthermore, Cd exposure upregulated the expression levels of TNF-α, IL-1β and IL-6 in pancreatic β-cells and elevated the TNF-α, IL1-β and IL-6 levels in the serum and pancreas. Taken together, the results of our study demonstrated that environmental relevant Cd exposure causes pro-inflammatory lipids elevation and insulin secretion dysfunction in β-cells and hence exaggerates diabetes development. Combined exposure to environmental hazardous chemicals might markedly increase the probability of developing diabetes in humans. This study provides new metabolic and pharmacological targets for antagonizing Cd toxicity.
Cadmium exposure impairs pancreatic β-cell function and exaggerates diabetes by disrupting lipid metabolism
Graphical abstract Display Omitted
Highlights Cd exposure induces pancreatic β-cell dysfunction and promotes the development of diabetes. Cd exposure disrupts lipid metabolism and induces lipid accumulation in MIN6 cells. Cd exposure promotes inflammation by increasing the weight of inflammatory bioactive lipids.
Abstract Cadmium is known as an environmental pollutant that contributes to pancreatic damage and the pathogenesis of diabetes. However, less attention has been devoted to elucidating the mechanisms underlying Cd-induced pancreatic β-cell dysfunction and the role of Cd toxicity in the development of diabetes. In this study, we demonstrated that exposure to Cd caused remarkable pancreatic β-cell dysfunction and death, both in vitro and in vivo. Lipidomic analysis of Cd-exposed pancreatic β-cells using high-resolution mass spectrometry revealed that Cd exposure altered the profile and abundance of lipids. Cd exposure induced intracellular lipid accumulation, promoted lipid biogenesis, elevated pro-inflammatory lipid contents and inhibited lipid degradation. Furthermore, Cd exposure upregulated the expression levels of TNF-α, IL-1β and IL-6 in pancreatic β-cells and elevated the TNF-α, IL1-β and IL-6 levels in the serum and pancreas. Taken together, the results of our study demonstrated that environmental relevant Cd exposure causes pro-inflammatory lipids elevation and insulin secretion dysfunction in β-cells and hence exaggerates diabetes development. Combined exposure to environmental hazardous chemicals might markedly increase the probability of developing diabetes in humans. This study provides new metabolic and pharmacological targets for antagonizing Cd toxicity.
Cadmium exposure impairs pancreatic β-cell function and exaggerates diabetes by disrupting lipid metabolism
Hong, Huihui (author) / Xu, Yudong (author) / Xu, Jia (author) / Zhang, Jingjing (author) / Xi, Yu (author) / Pi, Huifeng (author) / Yang, Lingling (author) / Yu, Zhengping (author) / Wu, Qingqian (author) / Meng, Zhuoxian (author)
2021-01-13
Article (Journal)
Electronic Resource
English
Cadmium , Pancreatic β-cells , Diabetes , Lipid metabolism , Inflammation , AcCa , Acyl carnitine , ATGL , Adipose triglyceride lipase , Cer , Ceramides , CerG1/CerG2 , Simple Glc series , Cd , ChE , Cholesterol ester , Co , Coenzyme , DG , Diglyceride , FA , Fatty acid , GM3 , Gangliosides , GSIS , Glucose-stimulated insulin secretion , HDL-C , High-density lipoproteincholesterol , H&E , Hematoxylin-Eosin , HSL , Hormone-sensitive lipase , IpGTT , Intraperitoneal glucose tolerance test , LCFA , Long chain fatty acid , LD , Lipid droplet , LDL-C , Low-density lipoproteincholesterol , LPC , Lysophosphatidylcholine , LPE , Lysophosphatidylethanolamine , LPG , Lysophosphatidylglycerol , LPI , Lysophosphatidylinositol , LPS , Lysophosphatidylserine , MGDG , Monogalactosyldiacylglycerol , MTBE , Methyl <italic>tert</italic>-butyl ether , OAHFA , (O-acyl)-1-hydroxy fatty acid , OPLS-DA , Orthogonal partial least-squares-discriminant analysis , PC , Phosphatidylcholine , PCA , Principal component analysis , PE , Phosphatidylethanolamine , PFA , Paraformaldehyde , PG , Phosphatidylglycerol , PI/PIP , Phosphatidylinositol , PLS-DA , Partial least-squares-discriminant analysis , PS , Phosphatidylserine , RF , Radiofrequency , RSD , Relative standard deviation , RT , Retention time , SM , Sphingomyelin , So , Sphingosine , SQDG , Sulfoquinovosyldiacylglycerol , SQMG , Sulfoquinovosylmonoacylglycerol , STZ , Streptozotocin , S1P , Sphongosine1-phosphate , TG , Triglyceride , TC , Total Cholesterol , UHPLC-HRMS , Ultrahigh-performance liquid chromatography coupled with high-resolution mass spectrometry , VLCFA , Very long chain fatty acid , VIP , Variable Importance for the Projection
| British Library Online Contents | 2017
| Elsevier | 2024