Ipragliflozin Ameliorates Diabetic Nephropathy Associated with Perirenal Adipose Expansion in Mice
Sodium glucose cotransporter-2 (SGLT2) inhibitors inhibit the development of diabetic nephropathy (DN). We determined whether changes in perirenal fat (PRAT) by a SGLT2 inhibitor ipragliflozin (Ipra) contribute to the suppression of DN development. High-fat diet (HFD)-fed mice were used as a DN mode...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2021-07, Vol.22 (14), p.7329, Article 7329 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 14 |
| container_start_page | 7329 |
| container_title | International journal of molecular sciences |
| container_volume | 22 |
| creator | Okuma, Hideyuki Mori, Kentaro Nakamura, Suguru Sekine, Tetsuo Ogawa, Yoshihiro Tsuchiya, Kyoichiro |
| description | Sodium glucose cotransporter-2 (SGLT2) inhibitors inhibit the development of diabetic nephropathy (DN). We determined whether changes in perirenal fat (PRAT) by a SGLT2 inhibitor ipragliflozin (Ipra) contribute to the suppression of DN development. High-fat diet (HFD)-fed mice were used as a DN model and were treated with or without Ipra for 6 weeks. Ipra treatment reduced urinary albumin excretion (UAE) and glomerular hypertrophy in HFD-fed mice. In the PRAT of Ipra-treated mice, adipocyte size was increased, and inflammation, fibrosis, and adipocyte death were suppressed. In conditioned medium made from PRAT (PRAT-CM) of Ipra-treated mice, the concentration of leptin was significantly lower than PRAT-CM of mice without Ipra treatment. Serum leptin concentration in renal vein positively correlated with UAE. PRAT-CM from HFD-fed mice showed greater cell proliferation signaling in mouse glomerular endothelial cells (GECs) than PRAT-CM from standard diet-fed mice via p38MAPK and leptin-dependent pathways, whose effects were significantly attenuated in PRAT-CM from Ipra-treated mice. These findings suggest that Ipra-induced PRAT expansion may play an important role in the improvement of DN in HFD-fed mice. In vitro experiments suggest that reduced PRAT-derived leptin by Ipra could inhibit GECs proliferation, possibly contributing to the suppression of DN development. |
| doi_str_mv | 10.3390/ijms22147329 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8304702</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_0dc3766cf40544a18052408535d49841</doaj_id><sourcerecordid>2554565712</sourcerecordid><originalsourceid>FETCH-LOGICAL-c455t-6fd77b46d476112aa17c58f670aae079adb4c216f6448091790d2d81e9ad27503</originalsourceid><addsrcrecordid>eNqNkktv1DAUhSMEou3Ajh8QiQ0SHfD7sUEaDQVGKo8FrC3HvpnxKImDnVDKr8fTqaqWFStf-Zzz6fr6VtULjN5QqtHbsO8zIZhJSvSj6hQzQpYICfn4Xn1SneW8R4hQwvXT6oQyopVm-rRqNmOy2y60XfwThnrVQxdishPk-n2wDUzB1V9g3KU42ml3Xa9yji4U3ddXYdrV3yCFBIPt6pUPY8xQX_we7ZBDHOrC-xwcPKuetLbL8Pz2XFQ_Plx8X39aXn79uFmvLpeOcT4tReulbJjwTAqMibVYOq5aIZG1gKS2vmGOYNEKxhTSWGrkiVcYikIkR3RRbY5cH-3ejCn0Nl2baIO5uYhpa2wq7-nAIO-oFMK1DHHGLFaIE4YUp9wzrRgurHdH1jg3PXgHw5Rs9wD6UBnCzmzjL6MoYrLMeVG9ugWk-HOGPJk-ZAddZweIczaEc44x0vrQ98t_rPs4pzLSGxfjgkt8AJ4fXS7FnBO0d81gZA6LYO4vQrGro_0KmthmF2BwcBdBh6UQFCtVKoTXYbJT-bF1nIepRF__f5T-BaEFxOA</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2554565712</pqid></control><display><type>article</type><title>Ipragliflozin Ameliorates Diabetic Nephropathy Associated with Perirenal Adipose Expansion in Mice</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>Web of Science - Science Citation Index Expanded - 2021<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /></source><source>PubMed Central</source><creator>Okuma, Hideyuki ; Mori, Kentaro ; Nakamura, Suguru ; Sekine, Tetsuo ; Ogawa, Yoshihiro ; Tsuchiya, Kyoichiro</creator><creatorcontrib>Okuma, Hideyuki ; Mori, Kentaro ; Nakamura, Suguru ; Sekine, Tetsuo ; Ogawa, Yoshihiro ; Tsuchiya, Kyoichiro</creatorcontrib><description>Sodium glucose cotransporter-2 (SGLT2) inhibitors inhibit the development of diabetic nephropathy (DN). We determined whether changes in perirenal fat (PRAT) by a SGLT2 inhibitor ipragliflozin (Ipra) contribute to the suppression of DN development. High-fat diet (HFD)-fed mice were used as a DN model and were treated with or without Ipra for 6 weeks. Ipra treatment reduced urinary albumin excretion (UAE) and glomerular hypertrophy in HFD-fed mice. In the PRAT of Ipra-treated mice, adipocyte size was increased, and inflammation, fibrosis, and adipocyte death were suppressed. In conditioned medium made from PRAT (PRAT-CM) of Ipra-treated mice, the concentration of leptin was significantly lower than PRAT-CM of mice without Ipra treatment. Serum leptin concentration in renal vein positively correlated with UAE. PRAT-CM from HFD-fed mice showed greater cell proliferation signaling in mouse glomerular endothelial cells (GECs) than PRAT-CM from standard diet-fed mice via p38MAPK and leptin-dependent pathways, whose effects were significantly attenuated in PRAT-CM from Ipra-treated mice. These findings suggest that Ipra-induced PRAT expansion may play an important role in the improvement of DN in HFD-fed mice. In vitro experiments suggest that reduced PRAT-derived leptin by Ipra could inhibit GECs proliferation, possibly contributing to the suppression of DN development.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms22147329</identifier><identifier>PMID: 34298949</identifier><language>eng</language><publisher>BASEL: Mdpi</publisher><subject>Adipocytes ; adipose tissue ; Albumins ; Apoptosis ; Atherosclerosis ; Biochemistry & Molecular Biology ; Cell proliferation ; Chemistry ; Chemistry, Multidisciplinary ; Diabetes ; Diabetes mellitus ; Diabetic nephropathy ; Endothelial cells ; Fatty acids ; Fibrosis ; Gene expression ; Glucose ; High fat diet ; Hyperglycemia ; Hypertension ; Hypertrophy ; Inflammation ; Insulin resistance ; Kidneys ; Kinases ; Leptin ; Life Sciences & Biomedicine ; Medical research ; Metabolism ; Nephropathy ; Pathogenesis ; Phosphorylation ; Physical Sciences ; Science & Technology ; SGLT2 inhibitors</subject><ispartof>International journal of molecular sciences, 2021-07, Vol.22 (14), p.7329, Article 7329</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>13</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000676318800001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c455t-6fd77b46d476112aa17c58f670aae079adb4c216f6448091790d2d81e9ad27503</citedby><cites>FETCH-LOGICAL-c455t-6fd77b46d476112aa17c58f670aae079adb4c216f6448091790d2d81e9ad27503</cites><orcidid>0000-0002-0834-2836</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8304702/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8304702/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,39263,53796,53798</link.rule.ids></links><search><creatorcontrib>Okuma, Hideyuki</creatorcontrib><creatorcontrib>Mori, Kentaro</creatorcontrib><creatorcontrib>Nakamura, Suguru</creatorcontrib><creatorcontrib>Sekine, Tetsuo</creatorcontrib><creatorcontrib>Ogawa, Yoshihiro</creatorcontrib><creatorcontrib>Tsuchiya, Kyoichiro</creatorcontrib><title>Ipragliflozin Ameliorates Diabetic Nephropathy Associated with Perirenal Adipose Expansion in Mice</title><title>International journal of molecular sciences</title><addtitle>INT J MOL SCI</addtitle><description>Sodium glucose cotransporter-2 (SGLT2) inhibitors inhibit the development of diabetic nephropathy (DN). We determined whether changes in perirenal fat (PRAT) by a SGLT2 inhibitor ipragliflozin (Ipra) contribute to the suppression of DN development. High-fat diet (HFD)-fed mice were used as a DN model and were treated with or without Ipra for 6 weeks. Ipra treatment reduced urinary albumin excretion (UAE) and glomerular hypertrophy in HFD-fed mice. In the PRAT of Ipra-treated mice, adipocyte size was increased, and inflammation, fibrosis, and adipocyte death were suppressed. In conditioned medium made from PRAT (PRAT-CM) of Ipra-treated mice, the concentration of leptin was significantly lower than PRAT-CM of mice without Ipra treatment. Serum leptin concentration in renal vein positively correlated with UAE. PRAT-CM from HFD-fed mice showed greater cell proliferation signaling in mouse glomerular endothelial cells (GECs) than PRAT-CM from standard diet-fed mice via p38MAPK and leptin-dependent pathways, whose effects were significantly attenuated in PRAT-CM from Ipra-treated mice. These findings suggest that Ipra-induced PRAT expansion may play an important role in the improvement of DN in HFD-fed mice. In vitro experiments suggest that reduced PRAT-derived leptin by Ipra could inhibit GECs proliferation, possibly contributing to the suppression of DN development.</description><subject>Adipocytes</subject><subject>adipose tissue</subject><subject>Albumins</subject><subject>Apoptosis</subject><subject>Atherosclerosis</subject><subject>Biochemistry & Molecular Biology</subject><subject>Cell proliferation</subject><subject>Chemistry</subject><subject>Chemistry, Multidisciplinary</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic nephropathy</subject><subject>Endothelial cells</subject><subject>Fatty acids</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>High fat diet</subject><subject>Hyperglycemia</subject><subject>Hypertension</subject><subject>Hypertrophy</subject><subject>Inflammation</subject><subject>Insulin resistance</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Leptin</subject><subject>Life Sciences & Biomedicine</subject><subject>Medical research</subject><subject>Metabolism</subject><subject>Nephropathy</subject><subject>Pathogenesis</subject><subject>Phosphorylation</subject><subject>Physical Sciences</subject><subject>Science & Technology</subject><subject>SGLT2 inhibitors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>HGBXW</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><sourceid>DOA</sourceid><recordid>eNqNkktv1DAUhSMEou3Ajh8QiQ0SHfD7sUEaDQVGKo8FrC3HvpnxKImDnVDKr8fTqaqWFStf-Zzz6fr6VtULjN5QqtHbsO8zIZhJSvSj6hQzQpYICfn4Xn1SneW8R4hQwvXT6oQyopVm-rRqNmOy2y60XfwThnrVQxdishPk-n2wDUzB1V9g3KU42ml3Xa9yji4U3ddXYdrV3yCFBIPt6pUPY8xQX_we7ZBDHOrC-xwcPKuetLbL8Pz2XFQ_Plx8X39aXn79uFmvLpeOcT4tReulbJjwTAqMibVYOq5aIZG1gKS2vmGOYNEKxhTSWGrkiVcYikIkR3RRbY5cH-3ejCn0Nl2baIO5uYhpa2wq7-nAIO-oFMK1DHHGLFaIE4YUp9wzrRgurHdH1jg3PXgHw5Rs9wD6UBnCzmzjL6MoYrLMeVG9ugWk-HOGPJk-ZAddZweIczaEc44x0vrQ98t_rPs4pzLSGxfjgkt8AJ4fXS7FnBO0d81gZA6LYO4vQrGro_0KmthmF2BwcBdBh6UQFCtVKoTXYbJT-bF1nIepRF__f5T-BaEFxOA</recordid><startdate>20210708</startdate><enddate>20210708</enddate><creator>Okuma, Hideyuki</creator><creator>Mori, Kentaro</creator><creator>Nakamura, Suguru</creator><creator>Sekine, Tetsuo</creator><creator>Ogawa, Yoshihiro</creator><creator>Tsuchiya, Kyoichiro</creator><general>Mdpi</general><general>MDPI AG</general><general>MDPI</general><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-0834-2836</orcidid></search><sort><creationdate>20210708</creationdate><title>Ipragliflozin Ameliorates Diabetic Nephropathy Associated with Perirenal Adipose Expansion in Mice</title><author>Okuma, Hideyuki ; Mori, Kentaro ; Nakamura, Suguru ; Sekine, Tetsuo ; Ogawa, Yoshihiro ; Tsuchiya, Kyoichiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-6fd77b46d476112aa17c58f670aae079adb4c216f6448091790d2d81e9ad27503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adipocytes</topic><topic>adipose tissue</topic><topic>Albumins</topic><topic>Apoptosis</topic><topic>Atherosclerosis</topic><topic>Biochemistry & Molecular Biology</topic><topic>Cell proliferation</topic><topic>Chemistry</topic><topic>Chemistry, Multidisciplinary</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetic nephropathy</topic><topic>Endothelial cells</topic><topic>Fatty acids</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Glucose</topic><topic>High fat diet</topic><topic>Hyperglycemia</topic><topic>Hypertension</topic><topic>Hypertrophy</topic><topic>Inflammation</topic><topic>Insulin resistance</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Leptin</topic><topic>Life Sciences & Biomedicine</topic><topic>Medical research</topic><topic>Metabolism</topic><topic>Nephropathy</topic><topic>Pathogenesis</topic><topic>Phosphorylation</topic><topic>Physical Sciences</topic><topic>Science & Technology</topic><topic>SGLT2 inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okuma, Hideyuki</creatorcontrib><creatorcontrib>Mori, Kentaro</creatorcontrib><creatorcontrib>Nakamura, Suguru</creatorcontrib><creatorcontrib>Sekine, Tetsuo</creatorcontrib><creatorcontrib>Ogawa, Yoshihiro</creatorcontrib><creatorcontrib>Tsuchiya, Kyoichiro</creatorcontrib><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 2021</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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Proquest Central</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>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Access via ProQuest (Open Access)</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 Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Okuma, Hideyuki</au><au>Mori, Kentaro</au><au>Nakamura, Suguru</au><au>Sekine, Tetsuo</au><au>Ogawa, Yoshihiro</au><au>Tsuchiya, Kyoichiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ipragliflozin Ameliorates Diabetic Nephropathy Associated with Perirenal Adipose Expansion in Mice</atitle><jtitle>International journal of molecular sciences</jtitle><stitle>INT J MOL SCI</stitle><date>2021-07-08</date><risdate>2021</risdate><volume>22</volume><issue>14</issue><spage>7329</spage><pages>7329-</pages><artnum>7329</artnum><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Sodium glucose cotransporter-2 (SGLT2) inhibitors inhibit the development of diabetic nephropathy (DN). We determined whether changes in perirenal fat (PRAT) by a SGLT2 inhibitor ipragliflozin (Ipra) contribute to the suppression of DN development. High-fat diet (HFD)-fed mice were used as a DN model and were treated with or without Ipra for 6 weeks. Ipra treatment reduced urinary albumin excretion (UAE) and glomerular hypertrophy in HFD-fed mice. In the PRAT of Ipra-treated mice, adipocyte size was increased, and inflammation, fibrosis, and adipocyte death were suppressed. In conditioned medium made from PRAT (PRAT-CM) of Ipra-treated mice, the concentration of leptin was significantly lower than PRAT-CM of mice without Ipra treatment. Serum leptin concentration in renal vein positively correlated with UAE. PRAT-CM from HFD-fed mice showed greater cell proliferation signaling in mouse glomerular endothelial cells (GECs) than PRAT-CM from standard diet-fed mice via p38MAPK and leptin-dependent pathways, whose effects were significantly attenuated in PRAT-CM from Ipra-treated mice. These findings suggest that Ipra-induced PRAT expansion may play an important role in the improvement of DN in HFD-fed mice. In vitro experiments suggest that reduced PRAT-derived leptin by Ipra could inhibit GECs proliferation, possibly contributing to the suppression of DN development.</abstract><cop>BASEL</cop><pub>Mdpi</pub><pmid>34298949</pmid><doi>10.3390/ijms22147329</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-0834-2836</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2021-07, Vol.22 (14), p.7329, Article 7329 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8304702 |
| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; MDPI - Multidisciplinary Digital Publishing Institute; Web of Science - Science Citation Index Expanded - 2021<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; PubMed Central |
| subjects | Adipocytes adipose tissue Albumins Apoptosis Atherosclerosis Biochemistry & Molecular Biology Cell proliferation Chemistry Chemistry, Multidisciplinary Diabetes Diabetes mellitus Diabetic nephropathy Endothelial cells Fatty acids Fibrosis Gene expression Glucose High fat diet Hyperglycemia Hypertension Hypertrophy Inflammation Insulin resistance Kidneys Kinases Leptin Life Sciences & Biomedicine Medical research Metabolism Nephropathy Pathogenesis Phosphorylation Physical Sciences Science & Technology SGLT2 inhibitors |
| title | Ipragliflozin Ameliorates Diabetic Nephropathy Associated with Perirenal Adipose Expansion in Mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-15T01%3A39%3A39IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Ipragliflozin%20Ameliorates%20Diabetic%20Nephropathy%20Associated%20with%20Perirenal%20Adipose%20Expansion%20in%20Mice&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Okuma,%20Hideyuki&rft.date=2021-07-08&rft.volume=22&rft.issue=14&rft.spage=7329&rft.pages=7329-&rft.artnum=7329&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms22147329&rft_dat=%3Cproquest_pubme%3E2554565712%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2554565712&rft_id=info:pmid/34298949&rft_doaj_id=oai_doaj_org_article_0dc3766cf40544a18052408535d49841&rfr_iscdi=true |