NYGGF4 (PID1) effects on insulin resistance are reversed by metformin in 3T3-L1 adipocytes
NYGGF4 (also called PID1 ) is a recently discovered gene that is involved in obesity-related insulin resistance (IR). We aimed in the present study to further elucidate the effects of NYGGF4 on IR and the underlying mechanisms through using metformin treatment in 3T3-L1 adipocytes. Our data showed t...
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| Veröffentlicht in: | Journal of bioenergetics and biomembranes 2012-12, Vol.44 (6), p.665-671 |
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| creator | Qiu, Jie Wang, Yu-mei Shi, Chun-mei Yue, Hong-ni Qin, Zhen-Ying Zhu, Guan-zhong Cao, Xin-guo Ji, Chen-bo Cui, Yan Guo, Xi-rong |
| description | NYGGF4
(also called
PID1
) is a recently discovered gene that is involved in obesity-related insulin resistance (IR). We aimed in the present study to further elucidate the effects of
NYGGF4
on IR and the underlying mechanisms through using metformin treatment in 3T3-L1 adipocytes. Our data showed that the metformin pretreatment strikingly enhanced insulin-stimulated glucose uptake through increasing GLUT4 translocation to the PM in
NYGGF4
overexpression adipocytes.
NYGGF4
overexpression resulted in significant inhibition of tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, whereas incubation with metformin strongly activated IRS-1 and Akt phosphorylation in
NYGGF4
overexpression adipocytes. The reactive oxygen species (ROS) levels in
NYGGF4
overexpression adipocytes were strikingly enhanced, which could be decreased by the metformin pretreatment. Our data also showed that metformin increased the expressions of PGC1-α, NRF-1, and TFAM, which were reduced in the
NYGGF4
overexpression adipocytes. These results suggest that
NYGGF4
plays a role in IR and its effects on IR could be reversed by metformin through activating IRS-1/PI3K/Akt and AMPK-PGC1-α pathways. |
| doi_str_mv | 10.1007/s10863-012-9472-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1220365587</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2823908411</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-431a0b538a59367f6c3122a89b321faca82fcca7554bc92170bbc73d5855435c3</originalsourceid><addsrcrecordid>eNp1kE9LwzAYh4Mobv75AF4k4EUP0bxJ06RHmTqFoR4mqJeQZql0rO1MWtm-vRlVEcFTePM-v1_Cg9AR0HOgVF4EoCrlhAIjWSIZWW2hIQjJSaoUbKMhhUSQRGbPA7QXwpxSqqigu2jAWJbGJB2i1_uX8fgmwaePd1dwhl1RONsG3NS4rEO3KGvsXShDa2rrsPEujh_OBzfD-RpXri0aX5UbGPMpJxPAZlYuG7tuXThAO4VZBHf4de6jp5vr6eiWTB7Gd6PLCbFcspYkHAzNBVdGZDyVRWo5MGZUlnMGhbFGscJaI4VIcpsxkDTPreQzoeINF5bvo9O-d-mb986FVldlsG6xMLVruqBjG-WpEEpG9OQPOm86X8ffaYBMgkxA8khBT1nfhOBdoZe-rIxfa6B6I1734nUUrzfi9Spmjr-au7xys5_Et-kIsB4IcVW_Of_r6X9bPwHGe4ti</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1197174173</pqid></control><display><type>article</type><title>NYGGF4 (PID1) effects on insulin resistance are reversed by metformin in 3T3-L1 adipocytes</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Qiu, Jie ; Wang, Yu-mei ; Shi, Chun-mei ; Yue, Hong-ni ; Qin, Zhen-Ying ; Zhu, Guan-zhong ; Cao, Xin-guo ; Ji, Chen-bo ; Cui, Yan ; Guo, Xi-rong</creator><creatorcontrib>Qiu, Jie ; Wang, Yu-mei ; Shi, Chun-mei ; Yue, Hong-ni ; Qin, Zhen-Ying ; Zhu, Guan-zhong ; Cao, Xin-guo ; Ji, Chen-bo ; Cui, Yan ; Guo, Xi-rong</creatorcontrib><description>NYGGF4
(also called
PID1
) is a recently discovered gene that is involved in obesity-related insulin resistance (IR). We aimed in the present study to further elucidate the effects of
NYGGF4
on IR and the underlying mechanisms through using metformin treatment in 3T3-L1 adipocytes. Our data showed that the metformin pretreatment strikingly enhanced insulin-stimulated glucose uptake through increasing GLUT4 translocation to the PM in
NYGGF4
overexpression adipocytes.
NYGGF4
overexpression resulted in significant inhibition of tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, whereas incubation with metformin strongly activated IRS-1 and Akt phosphorylation in
NYGGF4
overexpression adipocytes. The reactive oxygen species (ROS) levels in
NYGGF4
overexpression adipocytes were strikingly enhanced, which could be decreased by the metformin pretreatment. Our data also showed that metformin increased the expressions of PGC1-α, NRF-1, and TFAM, which were reduced in the
NYGGF4
overexpression adipocytes. These results suggest that
NYGGF4
plays a role in IR and its effects on IR could be reversed by metformin through activating IRS-1/PI3K/Akt and AMPK-PGC1-α pathways.</description><identifier>ISSN: 0145-479X</identifier><identifier>EISSN: 1573-6881</identifier><identifier>DOI: 10.1007/s10863-012-9472-x</identifier><identifier>PMID: 22968630</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>3T3-L1 Cells ; Adipocytes - metabolism ; Adipocytes - pathology ; Animal Anatomy ; Animal Biochemistry ; Animals ; Biochemistry ; Bioorganic Chemistry ; Body fat ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Cell Membrane - genetics ; Cell Membrane - metabolism ; Cell Membrane - pathology ; Chemistry ; Chemistry and Materials Science ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Glucose Transporter Type 4 - genetics ; Glucose Transporter Type 4 - metabolism ; High Mobility Group Proteins - genetics ; High Mobility Group Proteins - metabolism ; Histology ; Hypoglycemic Agents - pharmacology ; Insulin Receptor Substrate Proteins - genetics ; Insulin Receptor Substrate Proteins - metabolism ; Insulin Resistance ; Medical treatment ; Metformin - pharmacology ; Mice ; Morphology ; Nuclear Respiratory Factor 1 - genetics ; Nuclear Respiratory Factor 1 - metabolism ; Obesity ; Organic Chemistry ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation - drug effects ; Phosphorylation - genetics ; Protein Transport - drug effects ; Protein Transport - genetics ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Trans-Activators - genetics ; Trans-Activators - metabolism ; Transcription Factors ; Translocation</subject><ispartof>Journal of bioenergetics and biomembranes, 2012-12, Vol.44 (6), p.665-671</ispartof><rights>Springer Science+Business Media, LLC 2012</rights><rights>Springer Science+Business Media New York 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-431a0b538a59367f6c3122a89b321faca82fcca7554bc92170bbc73d5855435c3</citedby><cites>FETCH-LOGICAL-c372t-431a0b538a59367f6c3122a89b321faca82fcca7554bc92170bbc73d5855435c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10863-012-9472-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10863-012-9472-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22968630$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qiu, Jie</creatorcontrib><creatorcontrib>Wang, Yu-mei</creatorcontrib><creatorcontrib>Shi, Chun-mei</creatorcontrib><creatorcontrib>Yue, Hong-ni</creatorcontrib><creatorcontrib>Qin, Zhen-Ying</creatorcontrib><creatorcontrib>Zhu, Guan-zhong</creatorcontrib><creatorcontrib>Cao, Xin-guo</creatorcontrib><creatorcontrib>Ji, Chen-bo</creatorcontrib><creatorcontrib>Cui, Yan</creatorcontrib><creatorcontrib>Guo, Xi-rong</creatorcontrib><title>NYGGF4 (PID1) effects on insulin resistance are reversed by metformin in 3T3-L1 adipocytes</title><title>Journal of bioenergetics and biomembranes</title><addtitle>J Bioenerg Biomembr</addtitle><addtitle>J Bioenerg Biomembr</addtitle><description>NYGGF4
(also called
PID1
) is a recently discovered gene that is involved in obesity-related insulin resistance (IR). We aimed in the present study to further elucidate the effects of
NYGGF4
on IR and the underlying mechanisms through using metformin treatment in 3T3-L1 adipocytes. Our data showed that the metformin pretreatment strikingly enhanced insulin-stimulated glucose uptake through increasing GLUT4 translocation to the PM in
NYGGF4
overexpression adipocytes.
NYGGF4
overexpression resulted in significant inhibition of tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, whereas incubation with metformin strongly activated IRS-1 and Akt phosphorylation in
NYGGF4
overexpression adipocytes. The reactive oxygen species (ROS) levels in
NYGGF4
overexpression adipocytes were strikingly enhanced, which could be decreased by the metformin pretreatment. Our data also showed that metformin increased the expressions of PGC1-α, NRF-1, and TFAM, which were reduced in the
NYGGF4
overexpression adipocytes. These results suggest that
NYGGF4
plays a role in IR and its effects on IR could be reversed by metformin through activating IRS-1/PI3K/Akt and AMPK-PGC1-α pathways.</description><subject>3T3-L1 Cells</subject><subject>Adipocytes - metabolism</subject><subject>Adipocytes - pathology</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Bioorganic Chemistry</subject><subject>Body fat</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell Membrane - genetics</subject><subject>Cell Membrane - metabolism</subject><subject>Cell Membrane - pathology</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Glucose Transporter Type 4 - genetics</subject><subject>Glucose Transporter Type 4 - metabolism</subject><subject>High Mobility Group Proteins - genetics</subject><subject>High Mobility Group Proteins - metabolism</subject><subject>Histology</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Insulin Receptor Substrate Proteins - genetics</subject><subject>Insulin Receptor Substrate Proteins - metabolism</subject><subject>Insulin Resistance</subject><subject>Medical treatment</subject><subject>Metformin - pharmacology</subject><subject>Mice</subject><subject>Morphology</subject><subject>Nuclear Respiratory Factor 1 - genetics</subject><subject>Nuclear Respiratory Factor 1 - metabolism</subject><subject>Obesity</subject><subject>Organic Chemistry</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation - drug effects</subject><subject>Phosphorylation - genetics</subject><subject>Protein Transport - drug effects</subject><subject>Protein Transport - genetics</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription Factors</subject><subject>Translocation</subject><issn>0145-479X</issn><issn>1573-6881</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kE9LwzAYh4Mobv75AF4k4EUP0bxJ06RHmTqFoR4mqJeQZql0rO1MWtm-vRlVEcFTePM-v1_Cg9AR0HOgVF4EoCrlhAIjWSIZWW2hIQjJSaoUbKMhhUSQRGbPA7QXwpxSqqigu2jAWJbGJB2i1_uX8fgmwaePd1dwhl1RONsG3NS4rEO3KGvsXShDa2rrsPEujh_OBzfD-RpXri0aX5UbGPMpJxPAZlYuG7tuXThAO4VZBHf4de6jp5vr6eiWTB7Gd6PLCbFcspYkHAzNBVdGZDyVRWo5MGZUlnMGhbFGscJaI4VIcpsxkDTPreQzoeINF5bvo9O-d-mb986FVldlsG6xMLVruqBjG-WpEEpG9OQPOm86X8ffaYBMgkxA8khBT1nfhOBdoZe-rIxfa6B6I1734nUUrzfi9Spmjr-au7xys5_Et-kIsB4IcVW_Of_r6X9bPwHGe4ti</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Qiu, Jie</creator><creator>Wang, Yu-mei</creator><creator>Shi, Chun-mei</creator><creator>Yue, Hong-ni</creator><creator>Qin, Zhen-Ying</creator><creator>Zhu, Guan-zhong</creator><creator>Cao, Xin-guo</creator><creator>Ji, Chen-bo</creator><creator>Cui, Yan</creator><creator>Guo, Xi-rong</creator><general>Springer US</general><general>Springer Nature B.V</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>7QO</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20121201</creationdate><title>NYGGF4 (PID1) effects on insulin resistance are reversed by metformin in 3T3-L1 adipocytes</title><author>Qiu, Jie ; Wang, Yu-mei ; Shi, Chun-mei ; Yue, Hong-ni ; Qin, Zhen-Ying ; Zhu, Guan-zhong ; Cao, Xin-guo ; Ji, Chen-bo ; Cui, Yan ; Guo, Xi-rong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-431a0b538a59367f6c3122a89b321faca82fcca7554bc92170bbc73d5855435c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>3T3-L1 Cells</topic><topic>Adipocytes - metabolism</topic><topic>Adipocytes - pathology</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Bioorganic Chemistry</topic><topic>Body fat</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - metabolism</topic><topic>Cell Membrane - genetics</topic><topic>Cell Membrane - metabolism</topic><topic>Cell Membrane - pathology</topic><topic>Chemistry</topic><topic>Chemistry and Materials Science</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Glucose Transporter Type 4 - genetics</topic><topic>Glucose Transporter Type 4 - metabolism</topic><topic>High Mobility Group Proteins - genetics</topic><topic>High Mobility Group Proteins - metabolism</topic><topic>Histology</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Insulin Receptor Substrate Proteins - genetics</topic><topic>Insulin Receptor Substrate Proteins - metabolism</topic><topic>Insulin Resistance</topic><topic>Medical treatment</topic><topic>Metformin - pharmacology</topic><topic>Mice</topic><topic>Morphology</topic><topic>Nuclear Respiratory Factor 1 - genetics</topic><topic>Nuclear Respiratory Factor 1 - metabolism</topic><topic>Obesity</topic><topic>Organic Chemistry</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation - drug effects</topic><topic>Phosphorylation - genetics</topic><topic>Protein Transport - drug effects</topic><topic>Protein Transport - genetics</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription Factors</topic><topic>Translocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qiu, Jie</creatorcontrib><creatorcontrib>Wang, Yu-mei</creatorcontrib><creatorcontrib>Shi, Chun-mei</creatorcontrib><creatorcontrib>Yue, Hong-ni</creatorcontrib><creatorcontrib>Qin, Zhen-Ying</creatorcontrib><creatorcontrib>Zhu, Guan-zhong</creatorcontrib><creatorcontrib>Cao, Xin-guo</creatorcontrib><creatorcontrib>Ji, Chen-bo</creatorcontrib><creatorcontrib>Cui, Yan</creatorcontrib><creatorcontrib>Guo, Xi-rong</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>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Materials Science Collection</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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of bioenergetics and biomembranes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qiu, Jie</au><au>Wang, Yu-mei</au><au>Shi, Chun-mei</au><au>Yue, Hong-ni</au><au>Qin, Zhen-Ying</au><au>Zhu, Guan-zhong</au><au>Cao, Xin-guo</au><au>Ji, Chen-bo</au><au>Cui, Yan</au><au>Guo, Xi-rong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NYGGF4 (PID1) effects on insulin resistance are reversed by metformin in 3T3-L1 adipocytes</atitle><jtitle>Journal of bioenergetics and biomembranes</jtitle><stitle>J Bioenerg Biomembr</stitle><addtitle>J Bioenerg Biomembr</addtitle><date>2012-12-01</date><risdate>2012</risdate><volume>44</volume><issue>6</issue><spage>665</spage><epage>671</epage><pages>665-671</pages><issn>0145-479X</issn><eissn>1573-6881</eissn><abstract>NYGGF4
(also called
PID1
) is a recently discovered gene that is involved in obesity-related insulin resistance (IR). We aimed in the present study to further elucidate the effects of
NYGGF4
on IR and the underlying mechanisms through using metformin treatment in 3T3-L1 adipocytes. Our data showed that the metformin pretreatment strikingly enhanced insulin-stimulated glucose uptake through increasing GLUT4 translocation to the PM in
NYGGF4
overexpression adipocytes.
NYGGF4
overexpression resulted in significant inhibition of tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, whereas incubation with metformin strongly activated IRS-1 and Akt phosphorylation in
NYGGF4
overexpression adipocytes. The reactive oxygen species (ROS) levels in
NYGGF4
overexpression adipocytes were strikingly enhanced, which could be decreased by the metformin pretreatment. Our data also showed that metformin increased the expressions of PGC1-α, NRF-1, and TFAM, which were reduced in the
NYGGF4
overexpression adipocytes. These results suggest that
NYGGF4
plays a role in IR and its effects on IR could be reversed by metformin through activating IRS-1/PI3K/Akt and AMPK-PGC1-α pathways.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>22968630</pmid><doi>10.1007/s10863-012-9472-x</doi><tpages>7</tpages></addata></record> |
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| ispartof | Journal of bioenergetics and biomembranes, 2012-12, Vol.44 (6), p.665-671 |
| issn | 0145-479X 1573-6881 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | 3T3-L1 Cells Adipocytes - metabolism Adipocytes - pathology Animal Anatomy Animal Biochemistry Animals Biochemistry Bioorganic Chemistry Body fat Carrier Proteins - genetics Carrier Proteins - metabolism Cell Membrane - genetics Cell Membrane - metabolism Cell Membrane - pathology Chemistry Chemistry and Materials Science DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Glucose Transporter Type 4 - genetics Glucose Transporter Type 4 - metabolism High Mobility Group Proteins - genetics High Mobility Group Proteins - metabolism Histology Hypoglycemic Agents - pharmacology Insulin Receptor Substrate Proteins - genetics Insulin Receptor Substrate Proteins - metabolism Insulin Resistance Medical treatment Metformin - pharmacology Mice Morphology Nuclear Respiratory Factor 1 - genetics Nuclear Respiratory Factor 1 - metabolism Obesity Organic Chemistry Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Phosphorylation - drug effects Phosphorylation - genetics Protein Transport - drug effects Protein Transport - genetics Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - drug effects Signal Transduction - genetics Trans-Activators - genetics Trans-Activators - metabolism Transcription Factors Translocation |
| title | NYGGF4 (PID1) effects on insulin resistance are reversed by metformin in 3T3-L1 adipocytes |
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