Chemerin alleviates the placental oxidative stress and improves fetal overgrowth of gestational diabetes mellitus mice induced by high fat diet
Evidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is indispensable to the progression of this condition. Adipokine chemerin was linked with GDM, yet the roles of chemerin in placental oxidative stress and its underlyi...
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Published in | Molecular medicine (Cambridge, Mass.) Vol. 30; no. 1; pp. 239 - 16 |
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30.11.2024
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Abstract | Evidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is indispensable to the progression of this condition. Adipokine chemerin was linked with GDM, yet the roles of chemerin in placental oxidative stress and its underlying effects on GDM in vivo remain elusive.
We firstly analyzed the disparities of oxidative stress levels in placenta between GDM and normoglycaemic pregnant women, and then added recombinant active chemerin to the high-glucose treated human trophoblastic cells to investigate effects of chemerin on reactive oxygen species (ROS), total antioxidant capacity (T-AOC) and intake of glucose. Finally, a GDM animal model induced by high-fat diet (HFD) was established and the impacts of chemerin on oxidative stress of placenta and fetal growth of GDM were explored.
Analysis of human samples showed that the extent of lipid peroxidation in placenta was significantly elevated in GDM patients compared with their normoglycaemic counterparts. In the high glucose cell model, active chemerin lessened the content of ROS, heightened the index of T-AOC and stimulated glucose uptake in a concentration-dependent manner. Importantly, we successfully constructed a GDM mouse model through HFD. The treatment of chemerin was found to alleviate the high blood glucose levels in these HFD-fed pregnant mice and attenuate the excessive growth of their offspring. Our data also revealed that chemerin might counteract placental oxidative stress in HFD mice by improving the activity of superoxide dismutase.
The present study further elucidated the molecular biology of chemerin, which plays a pivotal role in ameliorating oxidative stress and hyperglycemia, resulting in improved fetal overgrowth in GDM. |
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AbstractList | Evidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is indispensable to the progression of this condition. Adipokine chemerin was linked with GDM, yet the roles of chemerin in placental oxidative stress and its underlying effects on GDM in vivo remain elusive.
We firstly analyzed the disparities of oxidative stress levels in placenta between GDM and normoglycaemic pregnant women, and then added recombinant active chemerin to the high-glucose treated human trophoblastic cells to investigate effects of chemerin on reactive oxygen species (ROS), total antioxidant capacity (T-AOC) and intake of glucose. Finally, a GDM animal model induced by high-fat diet (HFD) was established and the impacts of chemerin on oxidative stress of placenta and fetal growth of GDM were explored.
Analysis of human samples showed that the extent of lipid peroxidation in placenta was significantly elevated in GDM patients compared with their normoglycaemic counterparts. In the high glucose cell model, active chemerin lessened the content of ROS, heightened the index of T-AOC and stimulated glucose uptake in a concentration-dependent manner. Importantly, we successfully constructed a GDM mouse model through HFD. The treatment of chemerin was found to alleviate the high blood glucose levels in these HFD-fed pregnant mice and attenuate the excessive growth of their offspring. Our data also revealed that chemerin might counteract placental oxidative stress in HFD mice by improving the activity of superoxide dismutase.
The present study further elucidated the molecular biology of chemerin, which plays a pivotal role in ameliorating oxidative stress and hyperglycemia, resulting in improved fetal overgrowth in GDM. BackgroundEvidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is indispensable to the progression of this condition. Adipokine chemerin was linked with GDM, yet the roles of chemerin in placental oxidative stress and its underlying effects on GDM in vivo remain elusive.MethodsWe firstly analyzed the disparities of oxidative stress levels in placenta between GDM and normoglycaemic pregnant women, and then added recombinant active chemerin to the high-glucose treated human trophoblastic cells to investigate effects of chemerin on reactive oxygen species (ROS), total antioxidant capacity (T-AOC) and intake of glucose. Finally, a GDM animal model induced by high-fat diet (HFD) was established and the impacts of chemerin on oxidative stress of placenta and fetal growth of GDM were explored.ResultsAnalysis of human samples showed that the extent of lipid peroxidation in placenta was significantly elevated in GDM patients compared with their normoglycaemic counterparts. In the high glucose cell model, active chemerin lessened the content of ROS, heightened the index of T-AOC and stimulated glucose uptake in a concentration-dependent manner. Importantly, we successfully constructed a GDM mouse model through HFD. The treatment of chemerin was found to alleviate the high blood glucose levels in these HFD-fed pregnant mice and attenuate the excessive growth of their offspring. Our data also revealed that chemerin might counteract placental oxidative stress in HFD mice by improving the activity of superoxide dismutase.ConclusionsThe present study further elucidated the molecular biology of chemerin, which plays a pivotal role in ameliorating oxidative stress and hyperglycemia, resulting in improved fetal overgrowth in GDM. Evidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is indispensable to the progression of this condition. Adipokine chemerin was linked with GDM, yet the roles of chemerin in placental oxidative stress and its underlying effects on GDM in vivo remain elusive.BACKGROUNDEvidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is indispensable to the progression of this condition. Adipokine chemerin was linked with GDM, yet the roles of chemerin in placental oxidative stress and its underlying effects on GDM in vivo remain elusive.We firstly analyzed the disparities of oxidative stress levels in placenta between GDM and normoglycaemic pregnant women, and then added recombinant active chemerin to the high-glucose treated human trophoblastic cells to investigate effects of chemerin on reactive oxygen species (ROS), total antioxidant capacity (T-AOC) and intake of glucose. Finally, a GDM animal model induced by high-fat diet (HFD) was established and the impacts of chemerin on oxidative stress of placenta and fetal growth of GDM were explored.METHODSWe firstly analyzed the disparities of oxidative stress levels in placenta between GDM and normoglycaemic pregnant women, and then added recombinant active chemerin to the high-glucose treated human trophoblastic cells to investigate effects of chemerin on reactive oxygen species (ROS), total antioxidant capacity (T-AOC) and intake of glucose. Finally, a GDM animal model induced by high-fat diet (HFD) was established and the impacts of chemerin on oxidative stress of placenta and fetal growth of GDM were explored.Analysis of human samples showed that the extent of lipid peroxidation in placenta was significantly elevated in GDM patients compared with their normoglycaemic counterparts. In the high glucose cell model, active chemerin lessened the content of ROS, heightened the index of T-AOC and stimulated glucose uptake in a concentration-dependent manner. Importantly, we successfully constructed a GDM mouse model through HFD. The treatment of chemerin was found to alleviate the high blood glucose levels in these HFD-fed pregnant mice and attenuate the excessive growth of their offspring. Our data also revealed that chemerin might counteract placental oxidative stress in HFD mice by improving the activity of superoxide dismutase.RESULTSAnalysis of human samples showed that the extent of lipid peroxidation in placenta was significantly elevated in GDM patients compared with their normoglycaemic counterparts. In the high glucose cell model, active chemerin lessened the content of ROS, heightened the index of T-AOC and stimulated glucose uptake in a concentration-dependent manner. Importantly, we successfully constructed a GDM mouse model through HFD. The treatment of chemerin was found to alleviate the high blood glucose levels in these HFD-fed pregnant mice and attenuate the excessive growth of their offspring. Our data also revealed that chemerin might counteract placental oxidative stress in HFD mice by improving the activity of superoxide dismutase.The present study further elucidated the molecular biology of chemerin, which plays a pivotal role in ameliorating oxidative stress and hyperglycemia, resulting in improved fetal overgrowth in GDM.CONCLUSIONSThe present study further elucidated the molecular biology of chemerin, which plays a pivotal role in ameliorating oxidative stress and hyperglycemia, resulting in improved fetal overgrowth in GDM. Abstract Background Evidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is indispensable to the progression of this condition. Adipokine chemerin was linked with GDM, yet the roles of chemerin in placental oxidative stress and its underlying effects on GDM in vivo remain elusive. Methods We firstly analyzed the disparities of oxidative stress levels in placenta between GDM and normoglycaemic pregnant women, and then added recombinant active chemerin to the high-glucose treated human trophoblastic cells to investigate effects of chemerin on reactive oxygen species (ROS), total antioxidant capacity (T-AOC) and intake of glucose. Finally, a GDM animal model induced by high-fat diet (HFD) was established and the impacts of chemerin on oxidative stress of placenta and fetal growth of GDM were explored. Results Analysis of human samples showed that the extent of lipid peroxidation in placenta was significantly elevated in GDM patients compared with their normoglycaemic counterparts. In the high glucose cell model, active chemerin lessened the content of ROS, heightened the index of T-AOC and stimulated glucose uptake in a concentration-dependent manner. Importantly, we successfully constructed a GDM mouse model through HFD. The treatment of chemerin was found to alleviate the high blood glucose levels in these HFD-fed pregnant mice and attenuate the excessive growth of their offspring. Our data also revealed that chemerin might counteract placental oxidative stress in HFD mice by improving the activity of superoxide dismutase. Conclusions The present study further elucidated the molecular biology of chemerin, which plays a pivotal role in ameliorating oxidative stress and hyperglycemia, resulting in improved fetal overgrowth in GDM. Graphical abstract |
ArticleNumber | 239 |
Author | Wang, Zizhuo Wei, Lijie Fang, Chenyun Du, Yuanyuan Zhang, Huiting Ding, Wencheng Li, Weikun Jiang, Yi Zhang, Liangnan Zhou, Xuan He, Zhenzhen He, Mengzhou Feng, Ling Su, Rui Zhu, Shenglan Tan, Weidong Wang, Shaoshuai Yu, Jun |
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Cites_doi | 10.1016/j.mce.2021.111369 10.1113/JP280593 10.3390/ijms222111578 10.3390/antiox12030658 10.1631/jzus.B2000432 10.2337/dc24-S002 10.3390/antiox12101812 10.1016/j.phrs.2021.105987 10.3390/biomedicines10082018 10.4093/dmj.2021.0216 10.1016/j.redox.2022.102554 10.3390/ijms21103570 10.1016/j.apsb.2021.05.011 10.1038/s41401-023-01216-1 10.1096/fj.202201611R 10.1038/s42003-020-0986-1 10.1096/fj.202000326RR 10.1038/s41574-022-00734-y 10.1038/s41467-020-20665-4 10.3390/biomedicines12040924 10.1016/j.bbadis.2020.165967 10.1186/s10020-023-00669-8 10.1097/FM9.0000000000000044 10.7150/ijbs.84890 10.1530/JOE-18-0174 10.3390/nu15132878 10.1007/s00018-024-05192-5 10.1186/s10020-023-00707-5 10.1146/annurev-nutr-082018-124228 10.3390/antiox10030405 10.1016/j.redox.2021.101964 10.1016/j.peptides.2020.170422 10.1186/s10020-023-00615-8 10.1136/bmj.m1361 10.3390/ijms21249408 10.1111/1440-1681.13172 10.1136/bmj-2021-067946 10.2337/dbi18-0052 |
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Keywords | Chemerin Fetal growth Gestational diabetes mellitus Animal model Oxidative stress Placenta |
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References | JF Hebert (1007_CR17) 2021; 1867 J Gong (1007_CR15) 2024; 20 E Vounzoulaki (1007_CR31) 2020; 369 JJ Fisher (1007_CR13) 2020; 47 M Ruszała (1007_CR26) 2021; 22 J Fang (1007_CR11) 2023; 29 JJ Fisher (1007_CR14) 2021; 599 XQ Hu (1007_CR20) 2021; 10 X Zhou (1007_CR43) 2020; 2 P Gutaj (1007_CR16) 2020; 21 J Bai (1007_CR5) 2019; 68 X Tang (1007_CR29) 2023; 47 G Helfer (1007_CR19) 2018; 238 KA Cojocaru (1007_CR7) 2023; 12 X An (1007_CR2) 2020; 135 M Yang (1007_CR32) 2024; 45 Y Yin (1007_CR35) 2022; 175 WS Blaner (1007_CR6) 2021; 41 L Jiang (1007_CR21) 2022; 18 J Zaugg (1007_CR36) 2024; 81 L Zhao (1007_CR40) 2024; 12 K Zorena (1007_CR45) 2020; 21 J Bai (1007_CR4) 2020; 3 L Li (1007_CR23) 2023; 29 X Zhou (1007_CR44) 2023; 37 L Tan (1007_CR28) 2023; 15 1007_CR1 C Lennicke (1007_CR22) 2021; 42 AM Valent (1007_CR30) 2021; 35 H Zhou (1007_CR41) 2021; 12 R Saucedo (1007_CR27) 2023; 12 Y Deng (1007_CR9) 2023; 29 W Ye (1007_CR33) 2022; 377 X Zhou (1007_CR42) 2020; 21 P Fang (1007_CR12) 2021; 535 L Zhao (1007_CR39) 2022; 10 PK Oduro (1007_CR24) 2022; 12 J Zhang (1007_CR37) 2022; 58 |
References_xml | – volume: 535 start-page: 111369 year: 2021 ident: 1007_CR12 publication-title: Mol Cell Endocrinol doi: 10.1016/j.mce.2021.111369 – volume: 599 start-page: 1291 issue: 4 year: 2021 ident: 1007_CR14 publication-title: J Physiol doi: 10.1113/JP280593 – volume: 22 start-page: 11578 issue: 21 year: 2021 ident: 1007_CR26 publication-title: Int J Mol Sci doi: 10.3390/ijms222111578 – volume: 12 start-page: 658 issue: 3 year: 2023 ident: 1007_CR7 publication-title: Antioxid (Basel) doi: 10.3390/antiox12030658 – volume: 21 start-page: 990 issue: 12 year: 2020 ident: 1007_CR42 publication-title: J Zhejiang Univ Sci B doi: 10.1631/jzus.B2000432 – ident: 1007_CR1 doi: 10.2337/dc24-S002 – volume: 12 start-page: 1812 issue: 10 year: 2023 ident: 1007_CR27 publication-title: Antioxid (Basel) doi: 10.3390/antiox12101812 – volume: 175 start-page: 105987 year: 2022 ident: 1007_CR35 publication-title: Pharmacol Res doi: 10.1016/j.phrs.2021.105987 – volume: 10 start-page: 2018 issue: 8 year: 2022 ident: 1007_CR39 publication-title: Biomedicines doi: 10.3390/biomedicines10082018 – volume: 47 start-page: 267 issue: 2 year: 2023 ident: 1007_CR29 publication-title: Diabetes Metab J doi: 10.4093/dmj.2021.0216 – volume: 58 start-page: 102554 year: 2022 ident: 1007_CR37 publication-title: Redox Biol doi: 10.1016/j.redox.2022.102554 – volume: 21 start-page: 3570 issue: 10 year: 2020 ident: 1007_CR45 publication-title: Int J Mol Sci doi: 10.3390/ijms21103570 – volume: 12 start-page: 50 issue: 1 year: 2022 ident: 1007_CR24 publication-title: Acta Pharm Sin B doi: 10.1016/j.apsb.2021.05.011 – volume: 45 start-page: 777 issue: 4 year: 2024 ident: 1007_CR32 publication-title: Acta Pharmacol Sin doi: 10.1038/s41401-023-01216-1 – volume: 37 start-page: e22806 issue: 3 year: 2023 ident: 1007_CR44 publication-title: FASEB J doi: 10.1096/fj.202201611R – volume: 3 start-page: 257 issue: 1 year: 2020 ident: 1007_CR4 publication-title: Commun Biol doi: 10.1038/s42003-020-0986-1 – volume: 35 start-page: e21423 issue: 3 year: 2021 ident: 1007_CR30 publication-title: FASEB J doi: 10.1096/fj.202000326RR – volume: 18 start-page: 760 issue: 12 year: 2022 ident: 1007_CR21 publication-title: Nat Rev Endocrinol doi: 10.1038/s41574-022-00734-y – volume: 12 start-page: 326 issue: 1 year: 2021 ident: 1007_CR41 publication-title: Nat Commun doi: 10.1038/s41467-020-20665-4 – volume: 12 start-page: 924 issue: 4 year: 2024 ident: 1007_CR40 publication-title: Biomedicines doi: 10.3390/biomedicines12040924 – volume: 1867 start-page: 165967 issue: 1 year: 2021 ident: 1007_CR17 publication-title: Biochim Biophys Acta Mol Basis Dis doi: 10.1016/j.bbadis.2020.165967 – volume: 29 start-page: 82 issue: 1 year: 2023 ident: 1007_CR23 publication-title: Mol Med doi: 10.1186/s10020-023-00669-8 – volume: 2 start-page: 131 issue: 3 year: 2020 ident: 1007_CR43 publication-title: Maternal-Fetal Med doi: 10.1097/FM9.0000000000000044 – volume: 20 start-page: 152 issue: 1 year: 2024 ident: 1007_CR15 publication-title: Int J Biol Sci doi: 10.7150/ijbs.84890 – volume: 238 start-page: R79 issue: 2 year: 2018 ident: 1007_CR19 publication-title: J Endocrinol doi: 10.1530/JOE-18-0174 – volume: 15 start-page: 2878 issue: 13 year: 2023 ident: 1007_CR28 publication-title: Nutrients doi: 10.3390/nu15132878 – volume: 81 start-page: 151 issue: 1 year: 2024 ident: 1007_CR36 publication-title: Cell Mol Life Sci doi: 10.1007/s00018-024-05192-5 – volume: 29 start-page: 115 issue: 1 year: 2023 ident: 1007_CR9 publication-title: Mol Med doi: 10.1186/s10020-023-00707-5 – volume: 41 start-page: 105 year: 2021 ident: 1007_CR6 publication-title: Annu Rev Nutr doi: 10.1146/annurev-nutr-082018-124228 – volume: 10 start-page: 405 issue: 3 year: 2021 ident: 1007_CR20 publication-title: Antioxid (Basel) doi: 10.3390/antiox10030405 – volume: 42 start-page: 101964 year: 2021 ident: 1007_CR22 publication-title: Redox Biol doi: 10.1016/j.redox.2021.101964 – volume: 135 start-page: 170422 year: 2020 ident: 1007_CR2 publication-title: Peptides doi: 10.1016/j.peptides.2020.170422 – volume: 29 start-page: 23 issue: 1 year: 2023 ident: 1007_CR11 publication-title: Mol Med doi: 10.1186/s10020-023-00615-8 – volume: 369 start-page: m1361 year: 2020 ident: 1007_CR31 publication-title: BMJ doi: 10.1136/bmj.m1361 – volume: 21 start-page: 9408 issue: 24 year: 2020 ident: 1007_CR16 publication-title: Int J Mol Sci doi: 10.3390/ijms21249408 – volume: 47 start-page: 176 issue: 1 year: 2020 ident: 1007_CR13 publication-title: Clin Exp Pharmacol Physiol doi: 10.1111/1440-1681.13172 – volume: 377 start-page: e067946 year: 2022 ident: 1007_CR33 publication-title: BMJ doi: 10.1136/bmj-2021-067946 – volume: 68 start-page: 1099 issue: 6 year: 2019 ident: 1007_CR5 publication-title: Diabetes doi: 10.2337/dbi18-0052 |
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Snippet | Evidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is indispensable to the... BackgroundEvidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is indispensable... Abstract Background Evidence has shown that oxidative stress induced by high glucose microenvironment in placenta of gestational diabetes mellitus (GDM) is... |
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SubjectTerms | Adult Animal model Animals Antioxidants Biotechnology Cell culture Chemerin Chemokines - metabolism Diabetes, Gestational - metabolism Diet Diet, High-Fat - adverse effects Disease Models, Animal Female Females Fetal growth Gestational diabetes Gestational diabetes mellitus Glucose Humans Insulin resistance Intercellular Signaling Peptides and Proteins Kinases Laboratory animals Mice Oxidative Stress Placenta Placenta - metabolism Pregnancy Proteins Reactive oxygen species Reactive Oxygen Species - metabolism |
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Title | Chemerin alleviates the placental oxidative stress and improves fetal overgrowth of gestational diabetes mellitus mice induced by high fat diet |
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