Lowering plasma glucose concentration by inhibiting renal sodium–glucose cotransport
Maintaining normoglycaemia not only reduces the risk of diabetic microvascular complications but also corrects the metabolic abnormalities that contribute to the development and progression of hyperglycaemia, that is insulin resistance and beta‐cell dysfunction. Progressive beta‐cell failure, in add...
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| Veröffentlicht in: | Journal of internal medicine 2014-10, Vol.276 (4), p.352-363 |
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| creator | Abdul‐Ghani, M. A. DeFronzo, R. A. |
| description | Maintaining normoglycaemia not only reduces the risk of diabetic microvascular complications but also corrects the metabolic abnormalities that contribute to the development and progression of hyperglycaemia, that is insulin resistance and beta‐cell dysfunction. Progressive beta‐cell failure, in addition to side effects associated with many current antidiabetic agents, for example hypoglycaemia and weight gain, presents major obstacles to the achievement of the recommended goal of glycaemic control in patients with type 2 diabetes mellitus (T2DM). Thus, novel effective therapies are needed for optimal glucose control in subjects with T2DM. Most recently, specific inhibitors of the renal sodium–glucose cotransporter 2 (SGLT2) have been developed to produce glucosuria and lower the plasma glucose concentration. Because of the iR unique mechanism of action, which is independent of insulin secretion and insulin action, these agents are effective in lowering the plasma glucose concentration in all stages of the disease and can be combined with all other antidiabetic agents. In this review, we will summarize the available data concerning the mechanism of action, efficacy and safety of this novel class of antidiabetic agents. |
| doi_str_mv | 10.1111/joim.12244 |
| format | Article |
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A. ; DeFronzo, R. A.</creator><creatorcontrib>Abdul‐Ghani, M. A. ; DeFronzo, R. A.</creatorcontrib><description>Maintaining normoglycaemia not only reduces the risk of diabetic microvascular complications but also corrects the metabolic abnormalities that contribute to the development and progression of hyperglycaemia, that is insulin resistance and beta‐cell dysfunction. Progressive beta‐cell failure, in addition to side effects associated with many current antidiabetic agents, for example hypoglycaemia and weight gain, presents major obstacles to the achievement of the recommended goal of glycaemic control in patients with type 2 diabetes mellitus (T2DM). Thus, novel effective therapies are needed for optimal glucose control in subjects with T2DM. Most recently, specific inhibitors of the renal sodium–glucose cotransporter 2 (SGLT2) have been developed to produce glucosuria and lower the plasma glucose concentration. Because of the iR unique mechanism of action, which is independent of insulin secretion and insulin action, these agents are effective in lowering the plasma glucose concentration in all stages of the disease and can be combined with all other antidiabetic agents. In this review, we will summarize the available data concerning the mechanism of action, efficacy and safety of this novel class of antidiabetic agents.</description><identifier>ISSN: 0954-6820</identifier><identifier>EISSN: 1365-2796</identifier><identifier>DOI: 10.1111/joim.12244</identifier><identifier>PMID: 24690096</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Abnormalities ; Animals ; Antidiabetics ; Beta cells ; Blood Glucose - metabolism ; Complications ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 1 - blood ; Diabetes Mellitus, Type 1 - drug therapy ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - drug therapy ; Glucose ; Glucose - metabolism ; Glycated Hemoglobin - metabolism ; Glycosuria ; Humans ; Hyperglycemia ; Hypoglycemia ; Hypoglycemic Agents - adverse effects ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; Insulin ; Insulin resistance ; Insulin secretion ; kidney ; Kidney - drug effects ; Kidney - metabolism ; Microvasculature ; Na+/glucose cotransporter ; Reagents ; Secretion ; SGLT2 inhibition ; Side effects ; Sodium ; Sodium-Glucose Transporter 2 Inhibitors ; sodium–glucose cotransport ; type 2 diabetes</subject><ispartof>Journal of internal medicine, 2014-10, Vol.276 (4), p.352-363</ispartof><rights>2014 The Association for the Publication of the Journal of Internal Medicine</rights><rights>2014 The Association for the Publication of the Journal of Internal Medicine.</rights><rights>Copyright © 2014 The Association for the Publication of the Journal of Internal Medicine</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4594-fda8c9a3b3647ea76398ce7bd60ec849f3113c22c31c7c9092fb0def983184dd3</citedby><cites>FETCH-LOGICAL-c4594-fda8c9a3b3647ea76398ce7bd60ec849f3113c22c31c7c9092fb0def983184dd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjoim.12244$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjoim.12244$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24690096$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Abdul‐Ghani, M. A.</creatorcontrib><creatorcontrib>DeFronzo, R. A.</creatorcontrib><title>Lowering plasma glucose concentration by inhibiting renal sodium–glucose cotransport</title><title>Journal of internal medicine</title><addtitle>J Intern Med</addtitle><description>Maintaining normoglycaemia not only reduces the risk of diabetic microvascular complications but also corrects the metabolic abnormalities that contribute to the development and progression of hyperglycaemia, that is insulin resistance and beta‐cell dysfunction. Progressive beta‐cell failure, in addition to side effects associated with many current antidiabetic agents, for example hypoglycaemia and weight gain, presents major obstacles to the achievement of the recommended goal of glycaemic control in patients with type 2 diabetes mellitus (T2DM). Thus, novel effective therapies are needed for optimal glucose control in subjects with T2DM. Most recently, specific inhibitors of the renal sodium–glucose cotransporter 2 (SGLT2) have been developed to produce glucosuria and lower the plasma glucose concentration. Because of the iR unique mechanism of action, which is independent of insulin secretion and insulin action, these agents are effective in lowering the plasma glucose concentration in all stages of the disease and can be combined with all other antidiabetic agents. In this review, we will summarize the available data concerning the mechanism of action, efficacy and safety of this novel class of antidiabetic agents.</description><subject>Abnormalities</subject><subject>Animals</subject><subject>Antidiabetics</subject><subject>Beta cells</subject><subject>Blood Glucose - metabolism</subject><subject>Complications</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 1 - blood</subject><subject>Diabetes Mellitus, Type 1 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glycated Hemoglobin - metabolism</subject><subject>Glycosuria</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Hypoglycemia</subject><subject>Hypoglycemic Agents - adverse effects</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin secretion</subject><subject>kidney</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Microvasculature</subject><subject>Na+/glucose cotransporter</subject><subject>Reagents</subject><subject>Secretion</subject><subject>SGLT2 inhibition</subject><subject>Side effects</subject><subject>Sodium</subject><subject>Sodium-Glucose Transporter 2 Inhibitors</subject><subject>sodium–glucose cotransport</subject><subject>type 2 diabetes</subject><issn>0954-6820</issn><issn>1365-2796</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kLtOwzAUQC0EoqWw8AEoEhtSil-14xFVBYqKugCr5ThOcZXEwU5UdeMf-EO-hJQU2LjLXc49ujoAnCM4Rt1cr50txwhjSg_AEBE2iTEX7BAMoZjQmCUYDsBJCGsIEYEMHoMBpkxAKNgQvCzcxnhbraK6UKFU0apotQsm0q7Spmq8aqyronQb2erVprbZod5UqoiCy2xbfr5__J10eBVq55tTcJSrIpiz_R6B59vZ0_Q-Xizv5tObRazpRNA4z1SihSIpYZQbxRkRiTY8zRg0OqEiJwgRjbEmSHMtoMB5CjOTi4SghGYZGYHL3lt799aa0Mi1a333XZAYMsyx4Bh11FVPae9C8CaXtbel8luJoNwllLuE8jthB1_slW1amuwX_WnWAagHNrYw239U8mE5f-ylX1euflk</recordid><startdate>201410</startdate><enddate>201410</enddate><creator>Abdul‐Ghani, M. A.</creator><creator>DeFronzo, R. A.</creator><general>Blackwell Publishing 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>7QL</scope><scope>C1K</scope><scope>K9.</scope></search><sort><creationdate>201410</creationdate><title>Lowering plasma glucose concentration by inhibiting renal sodium–glucose cotransport</title><author>Abdul‐Ghani, M. A. ; DeFronzo, R. A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4594-fda8c9a3b3647ea76398ce7bd60ec849f3113c22c31c7c9092fb0def983184dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Abnormalities</topic><topic>Animals</topic><topic>Antidiabetics</topic><topic>Beta cells</topic><topic>Blood Glucose - metabolism</topic><topic>Complications</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 1 - blood</topic><topic>Diabetes Mellitus, Type 1 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Glycated Hemoglobin - metabolism</topic><topic>Glycosuria</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Hypoglycemia</topic><topic>Hypoglycemic Agents - adverse effects</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin secretion</topic><topic>kidney</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Microvasculature</topic><topic>Na+/glucose cotransporter</topic><topic>Reagents</topic><topic>Secretion</topic><topic>SGLT2 inhibition</topic><topic>Side effects</topic><topic>Sodium</topic><topic>Sodium-Glucose Transporter 2 Inhibitors</topic><topic>sodium–glucose cotransport</topic><topic>type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Abdul‐Ghani, M. A.</creatorcontrib><creatorcontrib>DeFronzo, R. A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Journal of internal medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Abdul‐Ghani, M. A.</au><au>DeFronzo, R. A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lowering plasma glucose concentration by inhibiting renal sodium–glucose cotransport</atitle><jtitle>Journal of internal medicine</jtitle><addtitle>J Intern Med</addtitle><date>2014-10</date><risdate>2014</risdate><volume>276</volume><issue>4</issue><spage>352</spage><epage>363</epage><pages>352-363</pages><issn>0954-6820</issn><eissn>1365-2796</eissn><abstract>Maintaining normoglycaemia not only reduces the risk of diabetic microvascular complications but also corrects the metabolic abnormalities that contribute to the development and progression of hyperglycaemia, that is insulin resistance and beta‐cell dysfunction. Progressive beta‐cell failure, in addition to side effects associated with many current antidiabetic agents, for example hypoglycaemia and weight gain, presents major obstacles to the achievement of the recommended goal of glycaemic control in patients with type 2 diabetes mellitus (T2DM). Thus, novel effective therapies are needed for optimal glucose control in subjects with T2DM. Most recently, specific inhibitors of the renal sodium–glucose cotransporter 2 (SGLT2) have been developed to produce glucosuria and lower the plasma glucose concentration. Because of the iR unique mechanism of action, which is independent of insulin secretion and insulin action, these agents are effective in lowering the plasma glucose concentration in all stages of the disease and can be combined with all other antidiabetic agents. In this review, we will summarize the available data concerning the mechanism of action, efficacy and safety of this novel class of antidiabetic agents.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>24690096</pmid><doi>10.1111/joim.12244</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Abnormalities Animals Antidiabetics Beta cells Blood Glucose - metabolism Complications Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 1 - blood Diabetes Mellitus, Type 1 - drug therapy Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - drug therapy Glucose Glucose - metabolism Glycated Hemoglobin - metabolism Glycosuria Humans Hyperglycemia Hypoglycemia Hypoglycemic Agents - adverse effects Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use Insulin Insulin resistance Insulin secretion kidney Kidney - drug effects Kidney - metabolism Microvasculature Na+/glucose cotransporter Reagents Secretion SGLT2 inhibition Side effects Sodium Sodium-Glucose Transporter 2 Inhibitors sodium–glucose cotransport type 2 diabetes |
| title | Lowering plasma glucose concentration by inhibiting renal sodium–glucose cotransport |
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