Adipokines and free fatty acids regulate insulin sensitivity by increasing microRNA-21 expression in human mature adipocytes
Obesity is a global public health concern and may lead to a variety of complications. Previous studies have indicated that adipokines and energy-source materials contribute to obesity and obesity-associated insulin resistance. MicroRNAs (miRs) are endogenous 20- to 25-nucleotide non-coding RNAs asso...
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| Veröffentlicht in: | Molecular medicine reports 2017-08, Vol.16 (2), p.2254-2258 |
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| creator | Zhang, Nannan Zhang, Naijian Song, Leilei Xie, Hui Zhao, Chao Li, Sujuan Zhao, Wenxi Zhao, Yaping Gao, Chunlin Xu, Guangfeng |
| description | Obesity is a global public health concern and may lead to a variety of complications. Previous studies have indicated that adipokines and energy-source materials contribute to obesity and obesity-associated insulin resistance. MicroRNAs (miRs) are endogenous 20- to 25-nucleotide non-coding RNAs associated with fat metabolism. It has been indicated that miR-21 is associated with adipogenesis and metabolic syndrome. In the present study, the expression of miR-21 in human mature adipocytes was analyzed using reverse transcription quantitative-polymerase chain reaction following treatment with adipokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, leptin, resistin and energy source materials, including free fatty acids (FFAs) and glucose. The current study demonstrated that the expression of miR-21 in human mature adipocytes was upregulated following treatment with TNF-α, IL-6, leptin, resistin and FFAs. However, low- and high-glucose did not have an effect on miR-21 expression. These results confirmed that TNF-α, IL-6, leptin, resistin and FFAs may contribute to obesity and obesity-associated insulin resistance via upregulating miR-21 in human mature adipocytes. Therefore, miR-21 may be a key regulatory factor of obesity and obesity-associated insulin resistance, and represents a potential therapeutic target for the treatment of these disorders. |
| doi_str_mv | 10.3892/mmr.2017.6769 |
| format | Article |
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Previous studies have indicated that adipokines and energy-source materials contribute to obesity and obesity-associated insulin resistance. MicroRNAs (miRs) are endogenous 20- to 25-nucleotide non-coding RNAs associated with fat metabolism. It has been indicated that miR-21 is associated with adipogenesis and metabolic syndrome. In the present study, the expression of miR-21 in human mature adipocytes was analyzed using reverse transcription quantitative-polymerase chain reaction following treatment with adipokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, leptin, resistin and energy source materials, including free fatty acids (FFAs) and glucose. The current study demonstrated that the expression of miR-21 in human mature adipocytes was upregulated following treatment with TNF-α, IL-6, leptin, resistin and FFAs. However, low- and high-glucose did not have an effect on miR-21 expression. These results confirmed that TNF-α, IL-6, leptin, resistin and FFAs may contribute to obesity and obesity-associated insulin resistance via upregulating miR-21 in human mature adipocytes. Therefore, miR-21 may be a key regulatory factor of obesity and obesity-associated insulin resistance, and represents a potential therapeutic target for the treatment of these disorders.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.6769</identifier><identifier>PMID: 28627656</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adipocytes ; Adipocytes - cytology ; Adipocytes - drug effects ; Adipocytes - metabolism ; Adipogenesis ; adipokines ; Adipokines - pharmacology ; Cell Line ; Diabetes ; Experiments ; Fat metabolism ; Fatty acids ; Fatty Acids, Nonesterified - pharmacology ; free fatty acids ; Gene expression ; Genetic aspects ; Glucose ; Glucose - pharmacology ; Health aspects ; Humans ; Insulin ; Insulin resistance ; Interleukin 6 ; Interleukin-6 - pharmacology ; Laboratories ; Leptin ; Leptin - pharmacology ; Metabolic syndrome ; MicroRNA ; microRNA-21 ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Obesity ; Obesity - metabolism ; Obesity - pathology ; Physiological aspects ; Polymerase chain reaction ; Public health ; Resistin - pharmacology ; Reverse transcription ; Risk factors ; Statistical analysis ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Up-Regulation - drug effects</subject><ispartof>Molecular medicine reports, 2017-08, Vol.16 (2), p.2254-2258</ispartof><rights>Copyright © 2017, Spandidos Publications</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-70b08b7b1d8188dc1235817ed59390b2a336d78013ac47dbde422343adba80fe3</citedby><cites>FETCH-LOGICAL-c459t-70b08b7b1d8188dc1235817ed59390b2a336d78013ac47dbde422343adba80fe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28627656$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Nannan</creatorcontrib><creatorcontrib>Zhang, Naijian</creatorcontrib><creatorcontrib>Song, Leilei</creatorcontrib><creatorcontrib>Xie, Hui</creatorcontrib><creatorcontrib>Zhao, Chao</creatorcontrib><creatorcontrib>Li, Sujuan</creatorcontrib><creatorcontrib>Zhao, Wenxi</creatorcontrib><creatorcontrib>Zhao, Yaping</creatorcontrib><creatorcontrib>Gao, Chunlin</creatorcontrib><creatorcontrib>Xu, Guangfeng</creatorcontrib><title>Adipokines and free fatty acids regulate insulin sensitivity by increasing microRNA-21 expression in human mature adipocytes</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Obesity is a global public health concern and may lead to a variety of complications. Previous studies have indicated that adipokines and energy-source materials contribute to obesity and obesity-associated insulin resistance. MicroRNAs (miRs) are endogenous 20- to 25-nucleotide non-coding RNAs associated with fat metabolism. It has been indicated that miR-21 is associated with adipogenesis and metabolic syndrome. In the present study, the expression of miR-21 in human mature adipocytes was analyzed using reverse transcription quantitative-polymerase chain reaction following treatment with adipokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, leptin, resistin and energy source materials, including free fatty acids (FFAs) and glucose. The current study demonstrated that the expression of miR-21 in human mature adipocytes was upregulated following treatment with TNF-α, IL-6, leptin, resistin and FFAs. However, low- and high-glucose did not have an effect on miR-21 expression. These results confirmed that TNF-α, IL-6, leptin, resistin and FFAs may contribute to obesity and obesity-associated insulin resistance via upregulating miR-21 in human mature adipocytes. Therefore, miR-21 may be a key regulatory factor of obesity and obesity-associated insulin resistance, and represents a potential therapeutic target for the treatment of these disorders.</description><subject>Adipocytes</subject><subject>Adipocytes - cytology</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - metabolism</subject><subject>Adipogenesis</subject><subject>adipokines</subject><subject>Adipokines - pharmacology</subject><subject>Cell Line</subject><subject>Diabetes</subject><subject>Experiments</subject><subject>Fat metabolism</subject><subject>Fatty acids</subject><subject>Fatty Acids, Nonesterified - pharmacology</subject><subject>free fatty acids</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Glucose - pharmacology</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - pharmacology</subject><subject>Laboratories</subject><subject>Leptin</subject><subject>Leptin - pharmacology</subject><subject>Metabolic syndrome</subject><subject>MicroRNA</subject><subject>microRNA-21</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Obesity - pathology</subject><subject>Physiological aspects</subject><subject>Polymerase chain reaction</subject><subject>Public health</subject><subject>Resistin - pharmacology</subject><subject>Reverse transcription</subject><subject>Risk factors</subject><subject>Statistical analysis</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Up-Regulation - drug effects</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkcuL1TAUh4sozkOXbiXgQje9k1ebZnkZxgcMCoOuQ9qcXjO2ac1JBy_4x0_KvY6MSBYJh-_8cjhfUbxidCMazS_GMW44ZWpTq1o_KU6Z0qwUlMqnxzfXWp0UZ4i3lNYVr_Tz4oQ3NVd1VZ8Wv7fOz9MPHwCJDY70EYD0NqU9sZ13SCLslsEmID7gMvhAEAL65O98Rtp9LncRLPqwI6Pv4nTzeVtyRuDXHAHRTyET5Psy2kBGm5YIxK4_dvsE-KJ41tsB4eXxPi--vb_6evmxvP7y4dPl9rrsZKVTqWhLm1a1zDWsaVzHuKgapsBVWmjacitE7VRDmbCdVK51IDkXUljX2ob2IM6Ld4fcOU4_F8BkRo8dDIMNMC1omGaMU82kzuibf9DbaYkhT5epOm8v56q_1M4OYHzopxRtt4aabUWlkKxiMlOb_1D5OMirmgL0PtcfNZSHhrxHxAi9maMfbdwbRs1q22TbZrVtVtuZf30cdmlHcA_0H70ZeHsAcM5yvZvwgclJJatLykvOKynuAaFBsfE</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Zhang, Nannan</creator><creator>Zhang, Naijian</creator><creator>Song, Leilei</creator><creator>Xie, Hui</creator><creator>Zhao, Chao</creator><creator>Li, Sujuan</creator><creator>Zhao, Wenxi</creator><creator>Zhao, Yaping</creator><creator>Gao, Chunlin</creator><creator>Xu, Guangfeng</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20170801</creationdate><title>Adipokines and free fatty acids regulate insulin sensitivity by increasing microRNA-21 expression in human mature adipocytes</title><author>Zhang, Nannan ; Zhang, Naijian ; Song, Leilei ; Xie, Hui ; Zhao, Chao ; Li, Sujuan ; Zhao, Wenxi ; Zhao, Yaping ; Gao, Chunlin ; Xu, Guangfeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-70b08b7b1d8188dc1235817ed59390b2a336d78013ac47dbde422343adba80fe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adipocytes</topic><topic>Adipocytes - cytology</topic><topic>Adipocytes - drug effects</topic><topic>Adipocytes - metabolism</topic><topic>Adipogenesis</topic><topic>adipokines</topic><topic>Adipokines - pharmacology</topic><topic>Cell Line</topic><topic>Diabetes</topic><topic>Experiments</topic><topic>Fat metabolism</topic><topic>Fatty acids</topic><topic>Fatty Acids, Nonesterified - pharmacology</topic><topic>free fatty acids</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Glucose</topic><topic>Glucose - pharmacology</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - pharmacology</topic><topic>Laboratories</topic><topic>Leptin</topic><topic>Leptin - pharmacology</topic><topic>Metabolic syndrome</topic><topic>MicroRNA</topic><topic>microRNA-21</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Obesity</topic><topic>Obesity - metabolism</topic><topic>Obesity - pathology</topic><topic>Physiological aspects</topic><topic>Polymerase chain reaction</topic><topic>Public health</topic><topic>Resistin - pharmacology</topic><topic>Reverse transcription</topic><topic>Risk factors</topic><topic>Statistical analysis</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Nannan</creatorcontrib><creatorcontrib>Zhang, Naijian</creatorcontrib><creatorcontrib>Song, Leilei</creatorcontrib><creatorcontrib>Xie, Hui</creatorcontrib><creatorcontrib>Zhao, Chao</creatorcontrib><creatorcontrib>Li, Sujuan</creatorcontrib><creatorcontrib>Zhao, Wenxi</creatorcontrib><creatorcontrib>Zhao, Yaping</creatorcontrib><creatorcontrib>Gao, Chunlin</creatorcontrib><creatorcontrib>Xu, Guangfeng</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Nannan</au><au>Zhang, Naijian</au><au>Song, Leilei</au><au>Xie, Hui</au><au>Zhao, Chao</au><au>Li, Sujuan</au><au>Zhao, Wenxi</au><au>Zhao, Yaping</au><au>Gao, Chunlin</au><au>Xu, Guangfeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adipokines and free fatty acids regulate insulin sensitivity by increasing microRNA-21 expression in human mature adipocytes</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2017-08-01</date><risdate>2017</risdate><volume>16</volume><issue>2</issue><spage>2254</spage><epage>2258</epage><pages>2254-2258</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Obesity is a global public health concern and may lead to a variety of complications. Previous studies have indicated that adipokines and energy-source materials contribute to obesity and obesity-associated insulin resistance. MicroRNAs (miRs) are endogenous 20- to 25-nucleotide non-coding RNAs associated with fat metabolism. It has been indicated that miR-21 is associated with adipogenesis and metabolic syndrome. In the present study, the expression of miR-21 in human mature adipocytes was analyzed using reverse transcription quantitative-polymerase chain reaction following treatment with adipokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, leptin, resistin and energy source materials, including free fatty acids (FFAs) and glucose. The current study demonstrated that the expression of miR-21 in human mature adipocytes was upregulated following treatment with TNF-α, IL-6, leptin, resistin and FFAs. However, low- and high-glucose did not have an effect on miR-21 expression. These results confirmed that TNF-α, IL-6, leptin, resistin and FFAs may contribute to obesity and obesity-associated insulin resistance via upregulating miR-21 in human mature adipocytes. Therefore, miR-21 may be a key regulatory factor of obesity and obesity-associated insulin resistance, and represents a potential therapeutic target for the treatment of these disorders.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28627656</pmid><doi>10.3892/mmr.2017.6769</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adipocytes Adipocytes - cytology Adipocytes - drug effects Adipocytes - metabolism Adipogenesis adipokines Adipokines - pharmacology Cell Line Diabetes Experiments Fat metabolism Fatty acids Fatty Acids, Nonesterified - pharmacology free fatty acids Gene expression Genetic aspects Glucose Glucose - pharmacology Health aspects Humans Insulin Insulin resistance Interleukin 6 Interleukin-6 - pharmacology Laboratories Leptin Leptin - pharmacology Metabolic syndrome MicroRNA microRNA-21 MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Obesity Obesity - metabolism Obesity - pathology Physiological aspects Polymerase chain reaction Public health Resistin - pharmacology Reverse transcription Risk factors Statistical analysis Tumor necrosis factor Tumor Necrosis Factor-alpha - pharmacology Tumor necrosis factor-TNF Tumor necrosis factor-α Up-Regulation - drug effects |
| title | Adipokines and free fatty acids regulate insulin sensitivity by increasing microRNA-21 expression in human mature adipocytes |
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