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Sodium‐glucose co‐transporter (SGLT) and glucose transporter (GLUT) expression in the kidney of type 2 diabetic subjects
The sodium‐glucose co‐transporters (SGLTs) are responsible for the tubular reabsorption of filtered glucose from the kidney into the bloodstream. The inhibition of SGLT2‐mediated glucose reabsorption is a novel and highly effective strategy to alleviate hyperglycaemia in patients with type 2 diabete...
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| Published in: | Diabetes, obesity & metabolism obesity & metabolism, 2017-09, Vol.19 (9), p.1322-1326 |
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| container_end_page | 1326 |
| container_issue | 9 |
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| container_title | Diabetes, obesity & metabolism |
| container_volume | 19 |
| creator | Norton, Luke Shannon, Christopher E. Fourcaudot, Marcel Hu, Cheng Wang, Niansong Ren, Wei Song, Jun Abdul‐Ghani, Muhammad DeFronzo, Ralph A. Ren, Jimmy Jia, Weiping |
| description | The sodium‐glucose co‐transporters (SGLTs) are responsible for the tubular reabsorption of filtered glucose from the kidney into the bloodstream. The inhibition of SGLT2‐mediated glucose reabsorption is a novel and highly effective strategy to alleviate hyperglycaemia in patients with type 2 diabetes mellitus (T2DM). However, the effectiveness of SGLT2 inhibitor therapy is diminished due, in part, to a compensatory increase in the maximum reabsorptive capacity (Tm) for glucose in patients with T2DM. We hypothesized that this increase in Tm could be explained by an increase in the tubular expression of SGLT and glucose transporters (GLUT) in these patients. To examine this, we obtained human kidney biopsy specimens from patients with or without T2DM and examined the mRNA expression of SGLTs and GLUTs. The expression of SGLT1 is markedly increased in the kidney of patients with T2DM, and SGLT1 mRNA is highly and significantly correlated with fasting and postprandial plasma glucose and HbA1c. In contrast, our data demonstrate that the levels of SGLT2 and GLUT2 mRNA are downregulated in diabetic patients, but not to a statistically significant level. These important findings are clinically significant and may have implications for the treatment of T2DM using strategies that target SGLT transporters in the kidney. |
| doi_str_mv | 10.1111/dom.13003 |
| format | article |
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The inhibition of SGLT2‐mediated glucose reabsorption is a novel and highly effective strategy to alleviate hyperglycaemia in patients with type 2 diabetes mellitus (T2DM). However, the effectiveness of SGLT2 inhibitor therapy is diminished due, in part, to a compensatory increase in the maximum reabsorptive capacity (Tm) for glucose in patients with T2DM. We hypothesized that this increase in Tm could be explained by an increase in the tubular expression of SGLT and glucose transporters (GLUT) in these patients. To examine this, we obtained human kidney biopsy specimens from patients with or without T2DM and examined the mRNA expression of SGLTs and GLUTs. The expression of SGLT1 is markedly increased in the kidney of patients with T2DM, and SGLT1 mRNA is highly and significantly correlated with fasting and postprandial plasma glucose and HbA1c. In contrast, our data demonstrate that the levels of SGLT2 and GLUT2 mRNA are downregulated in diabetic patients, but not to a statistically significant level. These important findings are clinically significant and may have implications for the treatment of T2DM using strategies that target SGLT transporters in the kidney.</description><identifier>ISSN: 1462-8902</identifier><identifier>EISSN: 1463-1326</identifier><identifier>DOI: 10.1111/dom.13003</identifier><identifier>PMID: 28477418</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Biopsy ; Blood Glucose - analysis ; China ; Diabetes ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Fasting ; Female ; Gene Expression Regulation - drug effects ; Glucose ; Glucose Transporter Type 1 - genetics ; Glucose Transporter Type 1 - metabolism ; Glucose Transporter Type 2 - genetics ; Glucose Transporter Type 2 - metabolism ; glucose transporters (GLUT) ; Glycated Hemoglobin A - analysis ; Humans ; Hypoglycemic Agents - therapeutic use ; kidney ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Male ; Postprandial Period ; Reproducibility of Results ; RNA, Messenger - metabolism ; Sodium-Glucose Transporter 1 - genetics ; Sodium-Glucose Transporter 1 - metabolism ; Sodium-Glucose Transporter 2 - genetics ; Sodium-Glucose Transporter 2 - metabolism ; sodium‐glucose co‐transporters (SGLT) ; type 2 diabetes</subject><ispartof>Diabetes, obesity & metabolism, 2017-09, Vol.19 (9), p.1322-1326</ispartof><rights>2017 John Wiley & Sons Ltd</rights><rights>2017 John Wiley & Sons Ltd.</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4193-b7ab28c2518df55c28bfb9c194396b6ba340137f10145ae02f2d5583b09e87cf3</citedby><cites>FETCH-LOGICAL-c4193-b7ab28c2518df55c28bfb9c194396b6ba340137f10145ae02f2d5583b09e87cf3</cites><orcidid>0000-0002-0231-5722 ; 0000-0003-4556-1787</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fdom.13003$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fdom.13003$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28477418$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Norton, Luke</creatorcontrib><creatorcontrib>Shannon, Christopher E.</creatorcontrib><creatorcontrib>Fourcaudot, Marcel</creatorcontrib><creatorcontrib>Hu, Cheng</creatorcontrib><creatorcontrib>Wang, Niansong</creatorcontrib><creatorcontrib>Ren, Wei</creatorcontrib><creatorcontrib>Song, Jun</creatorcontrib><creatorcontrib>Abdul‐Ghani, Muhammad</creatorcontrib><creatorcontrib>DeFronzo, Ralph A.</creatorcontrib><creatorcontrib>Ren, Jimmy</creatorcontrib><creatorcontrib>Jia, Weiping</creatorcontrib><title>Sodium‐glucose co‐transporter (SGLT) and glucose transporter (GLUT) expression in the kidney of type 2 diabetic subjects</title><title>Diabetes, obesity & metabolism</title><addtitle>Diabetes Obes Metab</addtitle><description>The sodium‐glucose co‐transporters (SGLTs) are responsible for the tubular reabsorption of filtered glucose from the kidney into the bloodstream. The inhibition of SGLT2‐mediated glucose reabsorption is a novel and highly effective strategy to alleviate hyperglycaemia in patients with type 2 diabetes mellitus (T2DM). However, the effectiveness of SGLT2 inhibitor therapy is diminished due, in part, to a compensatory increase in the maximum reabsorptive capacity (Tm) for glucose in patients with T2DM. We hypothesized that this increase in Tm could be explained by an increase in the tubular expression of SGLT and glucose transporters (GLUT) in these patients. To examine this, we obtained human kidney biopsy specimens from patients with or without T2DM and examined the mRNA expression of SGLTs and GLUTs. The expression of SGLT1 is markedly increased in the kidney of patients with T2DM, and SGLT1 mRNA is highly and significantly correlated with fasting and postprandial plasma glucose and HbA1c. In contrast, our data demonstrate that the levels of SGLT2 and GLUT2 mRNA are downregulated in diabetic patients, but not to a statistically significant level. These important findings are clinically significant and may have implications for the treatment of T2DM using strategies that target SGLT transporters in the kidney.</description><subject>Adult</subject><subject>Biopsy</subject><subject>Blood Glucose - analysis</subject><subject>China</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Fasting</subject><subject>Female</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glucose</subject><subject>Glucose Transporter Type 1 - genetics</subject><subject>Glucose Transporter Type 1 - metabolism</subject><subject>Glucose Transporter Type 2 - genetics</subject><subject>Glucose Transporter Type 2 - metabolism</subject><subject>glucose transporters (GLUT)</subject><subject>Glycated Hemoglobin A - analysis</subject><subject>Humans</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>kidney</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Male</subject><subject>Postprandial Period</subject><subject>Reproducibility of Results</subject><subject>RNA, Messenger - metabolism</subject><subject>Sodium-Glucose Transporter 1 - genetics</subject><subject>Sodium-Glucose Transporter 1 - metabolism</subject><subject>Sodium-Glucose Transporter 2 - genetics</subject><subject>Sodium-Glucose Transporter 2 - metabolism</subject><subject>sodium‐glucose co‐transporters (SGLT)</subject><subject>type 2 diabetes</subject><issn>1462-8902</issn><issn>1463-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp10ctO3DAUBmCrApVLu-AFKktsYJHBtyTOsqJlijSIBbC2bOcEPE3i1E5ER-qCR-AZ-yR1mQEJJLyxrfPp15F-hA4omdF0TmrfzSgnhH9Au1QUPKOcFVtPb5bJirAdtBfjkhAiuCw_oh0mRVkKKnfRnytfu6n7-_B4207WR8DWp88YdB8HH0YI-Ohqvrg-xrqv8bN5NZ4vbtIYfg8BYnS-x67H4x3gn67uYYV9g8fVAJjh2mkDo7M4TmYJdoyf0Haj2wifN_c-ujn7fn36I1tczs9Pvy4yK2jFM1Nqw6RlOZV1k-eWSdOYytJK8KowhdFcEMrLhhIqcg2ENazOc8kNqUCWtuH76GidOwT_a4I4qs5FC22re_BTVFRWBeFFKWWih2_o0k-hT9uptAqlvOKiTOp4rWzwMQZo1BBcp8NKUaL-V6JSJeqpkmS_bBIn00H9Ip87SOBkDe5dC6v3k9S3y4t15D-2SpaE</recordid><startdate>201709</startdate><enddate>201709</enddate><creator>Norton, Luke</creator><creator>Shannon, Christopher E.</creator><creator>Fourcaudot, Marcel</creator><creator>Hu, Cheng</creator><creator>Wang, Niansong</creator><creator>Ren, Wei</creator><creator>Song, Jun</creator><creator>Abdul‐Ghani, Muhammad</creator><creator>DeFronzo, Ralph A.</creator><creator>Ren, Jimmy</creator><creator>Jia, Weiping</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0231-5722</orcidid><orcidid>https://orcid.org/0000-0003-4556-1787</orcidid></search><sort><creationdate>201709</creationdate><title>Sodium‐glucose co‐transporter (SGLT) and glucose transporter (GLUT) expression in the kidney of type 2 diabetic subjects</title><author>Norton, Luke ; Shannon, Christopher E. ; Fourcaudot, Marcel ; Hu, Cheng ; Wang, Niansong ; Ren, Wei ; Song, Jun ; Abdul‐Ghani, Muhammad ; DeFronzo, Ralph A. ; Ren, Jimmy ; Jia, Weiping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4193-b7ab28c2518df55c28bfb9c194396b6ba340137f10145ae02f2d5583b09e87cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Biopsy</topic><topic>Blood Glucose - analysis</topic><topic>China</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Fasting</topic><topic>Female</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glucose</topic><topic>Glucose Transporter Type 1 - genetics</topic><topic>Glucose Transporter Type 1 - metabolism</topic><topic>Glucose Transporter Type 2 - genetics</topic><topic>Glucose Transporter Type 2 - metabolism</topic><topic>glucose transporters (GLUT)</topic><topic>Glycated Hemoglobin A - analysis</topic><topic>Humans</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>kidney</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Male</topic><topic>Postprandial Period</topic><topic>Reproducibility of Results</topic><topic>RNA, Messenger - metabolism</topic><topic>Sodium-Glucose Transporter 1 - genetics</topic><topic>Sodium-Glucose Transporter 1 - metabolism</topic><topic>Sodium-Glucose Transporter 2 - genetics</topic><topic>Sodium-Glucose Transporter 2 - metabolism</topic><topic>sodium‐glucose co‐transporters (SGLT)</topic><topic>type 2 diabetes</topic><toplevel>online_resources</toplevel><creatorcontrib>Norton, Luke</creatorcontrib><creatorcontrib>Shannon, Christopher E.</creatorcontrib><creatorcontrib>Fourcaudot, Marcel</creatorcontrib><creatorcontrib>Hu, Cheng</creatorcontrib><creatorcontrib>Wang, Niansong</creatorcontrib><creatorcontrib>Ren, Wei</creatorcontrib><creatorcontrib>Song, Jun</creatorcontrib><creatorcontrib>Abdul‐Ghani, Muhammad</creatorcontrib><creatorcontrib>DeFronzo, Ralph A.</creatorcontrib><creatorcontrib>Ren, Jimmy</creatorcontrib><creatorcontrib>Jia, Weiping</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes, obesity & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Norton, Luke</au><au>Shannon, Christopher E.</au><au>Fourcaudot, Marcel</au><au>Hu, Cheng</au><au>Wang, Niansong</au><au>Ren, Wei</au><au>Song, Jun</au><au>Abdul‐Ghani, Muhammad</au><au>DeFronzo, Ralph A.</au><au>Ren, Jimmy</au><au>Jia, Weiping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sodium‐glucose co‐transporter (SGLT) and glucose transporter (GLUT) expression in the kidney of type 2 diabetic subjects</atitle><jtitle>Diabetes, obesity & metabolism</jtitle><addtitle>Diabetes Obes Metab</addtitle><date>2017-09</date><risdate>2017</risdate><volume>19</volume><issue>9</issue><spage>1322</spage><epage>1326</epage><pages>1322-1326</pages><issn>1462-8902</issn><eissn>1463-1326</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>The sodium‐glucose co‐transporters (SGLTs) are responsible for the tubular reabsorption of filtered glucose from the kidney into the bloodstream. The inhibition of SGLT2‐mediated glucose reabsorption is a novel and highly effective strategy to alleviate hyperglycaemia in patients with type 2 diabetes mellitus (T2DM). However, the effectiveness of SGLT2 inhibitor therapy is diminished due, in part, to a compensatory increase in the maximum reabsorptive capacity (Tm) for glucose in patients with T2DM. We hypothesized that this increase in Tm could be explained by an increase in the tubular expression of SGLT and glucose transporters (GLUT) in these patients. To examine this, we obtained human kidney biopsy specimens from patients with or without T2DM and examined the mRNA expression of SGLTs and GLUTs. The expression of SGLT1 is markedly increased in the kidney of patients with T2DM, and SGLT1 mRNA is highly and significantly correlated with fasting and postprandial plasma glucose and HbA1c. In contrast, our data demonstrate that the levels of SGLT2 and GLUT2 mRNA are downregulated in diabetic patients, but not to a statistically significant level. These important findings are clinically significant and may have implications for the treatment of T2DM using strategies that target SGLT transporters in the kidney.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>28477418</pmid><doi>10.1111/dom.13003</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-0231-5722</orcidid><orcidid>https://orcid.org/0000-0003-4556-1787</orcidid></addata></record> |
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| ispartof | Diabetes, obesity & metabolism, 2017-09, Vol.19 (9), p.1322-1326 |
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| source | Wiley-Blackwell Journals |
| subjects | Adult Biopsy Blood Glucose - analysis China Diabetes Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Fasting Female Gene Expression Regulation - drug effects Glucose Glucose Transporter Type 1 - genetics Glucose Transporter Type 1 - metabolism Glucose Transporter Type 2 - genetics Glucose Transporter Type 2 - metabolism glucose transporters (GLUT) Glycated Hemoglobin A - analysis Humans Hypoglycemic Agents - therapeutic use kidney Kidney - drug effects Kidney - metabolism Kidney - pathology Male Postprandial Period Reproducibility of Results RNA, Messenger - metabolism Sodium-Glucose Transporter 1 - genetics Sodium-Glucose Transporter 1 - metabolism Sodium-Glucose Transporter 2 - genetics Sodium-Glucose Transporter 2 - metabolism sodium‐glucose co‐transporters (SGLT) type 2 diabetes |
| title | Sodium‐glucose co‐transporter (SGLT) and glucose transporter (GLUT) expression in the kidney of type 2 diabetic subjects |
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