Aerobic Exercise Improves Synaptic-Related Proteins of Diabetic Rats by Inhibiting FOXO1/NF-κB/NLRP3 Inflammatory Signaling Pathway and Ameliorating PI3K/Akt Insulin Signaling Pathway
Diabetes mellitus is metabolic syndrome and a risk factor for cognitive dysfunction-related diseases such as dementia, especially Alzheimer’s disease (AD), which is associated with chronic inflammation and abnormal insulin signaling pathway. Exercise, a known potential therapy for diabetes, can also...
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description | Diabetes mellitus is metabolic syndrome and a risk factor for cognitive dysfunction-related diseases such as dementia, especially Alzheimer’s disease (AD), which is associated with chronic inflammation and abnormal insulin signaling pathway. Exercise, a known potential therapy for diabetes, can also alleviate neurodegeneration. We evaluated the effects of aerobic exercise on inflammation and insulin signaling pathway in the prefrontal cortex of diabetic rats. Male SD rats were fed with a normal diet or a high-fat diet (HFD) for 8 weeks. Then, part of the HFD rats was selected for aerobic exercise training. Our results show that aerobic exercise can improve the expression of synaptic plasticity-related proteins and reduce the phosphorylation of Tau by inhibiting the inflammatory signaling pathway and ameliorating the insulin signaling pathway in diabetic rats. |
doi_str_mv | 10.1007/s12031-019-01302-2 |
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Exercise, a known potential therapy for diabetes, can also alleviate neurodegeneration. We evaluated the effects of aerobic exercise on inflammation and insulin signaling pathway in the prefrontal cortex of diabetic rats. Male SD rats were fed with a normal diet or a high-fat diet (HFD) for 8 weeks. Then, part of the HFD rats was selected for aerobic exercise training. Our results show that aerobic exercise can improve the expression of synaptic plasticity-related proteins and reduce the phosphorylation of Tau by inhibiting the inflammatory signaling pathway and ameliorating the insulin signaling pathway in diabetic rats.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-019-01302-2</identifier><identifier>PMID: 31111330</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>1-Phosphatidylinositol 3-kinase ; Aerobics ; AKT protein ; Alzheimer's disease ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cognitive ability ; Dementia disorders ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - physiopathology ; Diet ; Exercise ; FOXO1 protein ; Health risks ; High fat diet ; Inflammation ; Insulin ; Insulin - metabolism ; Male ; Metabolic disorders ; Metabolic syndrome ; Nerve Tissue Proteins - metabolism ; Neurochemistry ; Neurodegeneration ; Neurology ; Neuronal Plasticity ; Neurosciences ; NF-kappa B - metabolism ; NF-κB protein ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Physical Conditioning, Animal ; Physical fitness ; Prefrontal cortex ; Prefrontal Cortex - metabolism ; Prefrontal Cortex - physiopathology ; Proteins ; Proteomics ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Sprague-Dawley ; Risk analysis ; Risk factors ; Rodents ; Signal Transduction ; Signaling ; Synaptic plasticity ; Tau protein ; tau Proteins - metabolism</subject><ispartof>Journal of molecular neuroscience, 2019-09, Vol.69 (1), p.28-38</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Journal of Molecular Neuroscience is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-a83a63c41881a7ea80f051be63b508cd004cebd10410f385c4f03f827e51c4003</citedby><cites>FETCH-LOGICAL-c375t-a83a63c41881a7ea80f051be63b508cd004cebd10410f385c4f03f827e51c4003</cites><orcidid>0000-0002-3237-2605</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-019-01302-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-019-01302-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31111330$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Qian</creatorcontrib><creatorcontrib>Hu, Jingyun</creatorcontrib><creatorcontrib>Liu, Yuran</creatorcontrib><creatorcontrib>Li, Jingjing</creatorcontrib><creatorcontrib>Liu, Beibei</creatorcontrib><creatorcontrib>Li, Mingming</creatorcontrib><creatorcontrib>Lou, Shujie</creatorcontrib><title>Aerobic Exercise Improves Synaptic-Related Proteins of Diabetic Rats by Inhibiting FOXO1/NF-κB/NLRP3 Inflammatory Signaling Pathway and Ameliorating PI3K/Akt Insulin Signaling Pathway</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>Diabetes mellitus is metabolic syndrome and a risk factor for cognitive dysfunction-related diseases such as dementia, especially Alzheimer’s disease (AD), which is associated with chronic inflammation and abnormal insulin signaling pathway. Exercise, a known potential therapy for diabetes, can also alleviate neurodegeneration. We evaluated the effects of aerobic exercise on inflammation and insulin signaling pathway in the prefrontal cortex of diabetic rats. Male SD rats were fed with a normal diet or a high-fat diet (HFD) for 8 weeks. Then, part of the HFD rats was selected for aerobic exercise training. Our results show that aerobic exercise can improve the expression of synaptic plasticity-related proteins and reduce the phosphorylation of Tau by inhibiting the inflammatory signaling pathway and ameliorating the insulin signaling pathway in diabetic rats.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Aerobics</subject><subject>AKT protein</subject><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cognitive ability</subject><subject>Dementia disorders</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Diet</subject><subject>Exercise</subject><subject>FOXO1 protein</subject><subject>Health risks</subject><subject>High fat diet</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Male</subject><subject>Metabolic disorders</subject><subject>Metabolic syndrome</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neurochemistry</subject><subject>Neurodegeneration</subject><subject>Neurology</subject><subject>Neuronal Plasticity</subject><subject>Neurosciences</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Physical Conditioning, Animal</subject><subject>Physical fitness</subject><subject>Prefrontal cortex</subject><subject>Prefrontal Cortex - metabolism</subject><subject>Prefrontal Cortex - physiopathology</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Synaptic plasticity</subject><subject>Tau protein</subject><subject>tau Proteins - 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metabolism</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Diet</topic><topic>Exercise</topic><topic>FOXO1 protein</topic><topic>Health risks</topic><topic>High fat diet</topic><topic>Inflammation</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Male</topic><topic>Metabolic disorders</topic><topic>Metabolic syndrome</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Neurochemistry</topic><topic>Neurodegeneration</topic><topic>Neurology</topic><topic>Neuronal Plasticity</topic><topic>Neurosciences</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Physical Conditioning, Animal</topic><topic>Physical fitness</topic><topic>Prefrontal cortex</topic><topic>Prefrontal Cortex - metabolism</topic><topic>Prefrontal Cortex - physiopathology</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Risk analysis</topic><topic>Risk factors</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Synaptic plasticity</topic><topic>Tau protein</topic><topic>tau Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Qian</creatorcontrib><creatorcontrib>Hu, Jingyun</creatorcontrib><creatorcontrib>Liu, Yuran</creatorcontrib><creatorcontrib>Li, Jingjing</creatorcontrib><creatorcontrib>Liu, Beibei</creatorcontrib><creatorcontrib>Li, Mingming</creatorcontrib><creatorcontrib>Lou, Shujie</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Qian</au><au>Hu, Jingyun</au><au>Liu, Yuran</au><au>Li, Jingjing</au><au>Liu, Beibei</au><au>Li, Mingming</au><au>Lou, Shujie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aerobic Exercise Improves Synaptic-Related Proteins of Diabetic Rats by Inhibiting FOXO1/NF-κB/NLRP3 Inflammatory Signaling Pathway and Ameliorating PI3K/Akt Insulin Signaling Pathway</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2019-09-01</date><risdate>2019</risdate><volume>69</volume><issue>1</issue><spage>28</spage><epage>38</epage><pages>28-38</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>Diabetes mellitus is metabolic syndrome and a risk factor for cognitive dysfunction-related diseases such as dementia, especially Alzheimer’s disease (AD), which is associated with chronic inflammation and abnormal insulin signaling pathway. Exercise, a known potential therapy for diabetes, can also alleviate neurodegeneration. We evaluated the effects of aerobic exercise on inflammation and insulin signaling pathway in the prefrontal cortex of diabetic rats. Male SD rats were fed with a normal diet or a high-fat diet (HFD) for 8 weeks. Then, part of the HFD rats was selected for aerobic exercise training. Our results show that aerobic exercise can improve the expression of synaptic plasticity-related proteins and reduce the phosphorylation of Tau by inhibiting the inflammatory signaling pathway and ameliorating the insulin signaling pathway in diabetic rats.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>31111330</pmid><doi>10.1007/s12031-019-01302-2</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-3237-2605</orcidid></addata></record> |
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subjects | 1-Phosphatidylinositol 3-kinase Aerobics AKT protein Alzheimer's disease Animals Biomedical and Life Sciences Biomedicine Cell Biology Cognitive ability Dementia disorders Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - physiopathology Diet Exercise FOXO1 protein Health risks High fat diet Inflammation Insulin Insulin - metabolism Male Metabolic disorders Metabolic syndrome Nerve Tissue Proteins - metabolism Neurochemistry Neurodegeneration Neurology Neuronal Plasticity Neurosciences NF-kappa B - metabolism NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Physical Conditioning, Animal Physical fitness Prefrontal cortex Prefrontal Cortex - metabolism Prefrontal Cortex - physiopathology Proteins Proteomics Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Sprague-Dawley Risk analysis Risk factors Rodents Signal Transduction Signaling Synaptic plasticity Tau protein tau Proteins - metabolism |
title | Aerobic Exercise Improves Synaptic-Related Proteins of Diabetic Rats by Inhibiting FOXO1/NF-κB/NLRP3 Inflammatory Signaling Pathway and Ameliorating PI3K/Akt Insulin Signaling Pathway |
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