Beyond Glycosuria: Exploring the intrarenal effects of SGLT₋₂ inhibition in diabetes.
Identifieur interne : 003128 ( PubMed/Curation ); précédent : 003127; suivant : 003129Beyond Glycosuria: Exploring the intrarenal effects of SGLT₋₂ inhibition in diabetes.
Auteurs : M C Thomas [Australie] ; K. Jandeleit-Dahm ; F. Bonnet [France]Source :
- Diabetes & metabolism [ 1878-1780 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Diabète de type 1 (métabolisme), Diabète de type 1 (sang), Diabète de type 1 (traitement médicamenteux), Diabète de type 1 (urine), Diabète de type 2 (métabolisme), Diabète de type 2 (sang), Diabète de type 2 (traitement médicamenteux), Diabète de type 2 (urine), Glycémie (métabolisme), Humains, Hypoglycémiants (effets indésirables), Hypoglycémiants (usage thérapeutique), Modulateurs du transport transmembranaire (effets indésirables), Modulateurs du transport transmembranaire (usage thérapeutique), Rein (), Rein (métabolisme), Transporteur-2 sodium-glucose (antagonistes et inhibiteurs), Transporteur-2 sodium-glucose (métabolisme), Élimination rénale ().
- MESH :
- antagonistes et inhibiteurs : Transporteur-2 sodium-glucose.
- effets indésirables : Hypoglycémiants, Modulateurs du transport transmembranaire.
- métabolisme : Diabète de type 1, Diabète de type 2, Glycémie, Rein, Transporteur-2 sodium-glucose.
- sang : Diabète de type 1, Diabète de type 2.
- traitement médicamenteux : Diabète de type 1, Diabète de type 2.
- usage thérapeutique : Diabète de type 1, Diabète de type 2, Hypoglycémiants, Modulateurs du transport transmembranaire.
- Animaux, Humains, Rein, Élimination rénale.
English descriptors
- KwdEn :
- Animals, Blood Glucose (metabolism), Diabetes Mellitus, Type 1 (blood), Diabetes Mellitus, Type 1 (drug therapy), Diabetes Mellitus, Type 1 (metabolism), Diabetes Mellitus, Type 1 (urine), Diabetes Mellitus, Type 2 (blood), Diabetes Mellitus, Type 2 (drug therapy), Diabetes Mellitus, Type 2 (metabolism), Diabetes Mellitus, Type 2 (urine), Humans, Hypoglycemic Agents (adverse effects), Hypoglycemic Agents (therapeutic use), Kidney (drug effects), Kidney (metabolism), Membrane Transport Modulators (adverse effects), Membrane Transport Modulators (therapeutic use), Renal Elimination (drug effects), Sodium-Glucose Transporter 2 (antagonists & inhibitors), Sodium-Glucose Transporter 2 (metabolism).
- MESH :
- chemical , adverse effects : Hypoglycemic Agents, Membrane Transport Modulators.
- chemical , antagonists & inhibitors : Sodium-Glucose Transporter 2.
- chemical , metabolism : Blood Glucose, Sodium-Glucose Transporter 2.
- blood : Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2.
- drug effects : Kidney, Renal Elimination.
- drug therapy : Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2.
- metabolism : Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Kidney.
- chemical , therapeutic use : Hypoglycemic Agents, Membrane Transport Modulators.
- urine : Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2.
- Animals, Humans.
Abstract
For millennia, the syndrome that has become known as diabetes was considered to be primarily a disease of the urinary system and, by association, of dysfunction in the kidneys (recognized as the source of urine). In the last decade, there has been renewed interest in the role of the kidneys in the development and maintenance of high glucose levels. This has led to the development of novel agents to inhibit sodiumglucose cotransporter 2 (SGLT-2) as a means to control glucose levels and augment calorie-wasting leading to weight loss. However, beyond actions on glycaemic control, inhibition of proximal glucose absorption via SGLT-2 has significant direct effects to attenuate hyperfiltration and reduce renal hypertrophy. Increased distal sodium delivery may also act to suppress the intrarenal renin-angiotensin-aldosterone system, although systemic activity may be modestly increased due to osmotic diuresis. Reducing proximal glucose reabsorption may also protect the tubular cells from exposure to excess glucose and glucose-induced reactive oxygen species. On the other hand, distal glucose delivery following inhibition of SGLT-2 may increase glycogen deposition, the significance of which is unclear. However, subjects with familial glycosuria appear to have a benign renal prognosis. Some studies have demonstrated significant reductions in albumin excretion in various experimental models and as post-hoc observations in clinical trials. Whether these reflect renoprotection or are simply the result of intraglomerular haemodynamic changes remains unclear. Although promising, such actions remain to be established by comprehensive clinical trials with a renal focus, many of which are currently in progress.
DOI: 10.1016/S1262-3636(14)72691-6
PubMed: 25554067
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K. Jandeleit-Dahm<affiliation><nlm:affiliation>Baker IDI Heart & Diabetes Institute, 75 Commercial Rd, Melbourne, Australia, 3004.</nlm:affiliation><wicri:noCountry code="subField">3004</wicri:noCountry></affiliation>Le document en format XML
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Bonnet</name><affiliation wicri:level="1"><nlm:affiliation>Inserm UMR 991, service endocrinologie-diabétologie, CHU Rennes, université Rennes 1, 2 rue du Thabor, CS 46510, 35065 Rennes cedex, FRANCE.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>Inserm UMR 991, service endocrinologie-diabétologie, CHU Rennes, université Rennes 1, 2 rue du Thabor, CS 46510, 35065 Rennes cedex</wicri:regionArea></affiliation></author></analytic><series><title level="j">Diabetes & metabolism</title><idno type="eISSN">1878-1780</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Blood Glucose (metabolism)</term><term>Diabetes Mellitus, Type 1 (blood)</term><term>Diabetes Mellitus, Type 1 (drug therapy)</term><term>Diabetes Mellitus, Type 1 (metabolism)</term><term>Diabetes Mellitus, Type 1 (urine)</term><term>Diabetes Mellitus, Type 2 (blood)</term><term>Diabetes Mellitus, Type 2 (drug therapy)</term><term>Diabetes Mellitus, Type 2 (metabolism)</term><term>Diabetes Mellitus, Type 2 (urine)</term><term>Humans</term><term>Hypoglycemic Agents (adverse effects)</term><term>Hypoglycemic Agents (therapeutic use)</term><term>Kidney (drug effects)</term><term>Kidney (metabolism)</term><term>Membrane Transport Modulators (adverse effects)</term><term>Membrane Transport Modulators (therapeutic use)</term><term>Renal Elimination (drug effects)</term><term>Sodium-Glucose Transporter 2 (antagonists & inhibitors)</term><term>Sodium-Glucose Transporter 2 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Diabète de type 1 (métabolisme)</term><term>Diabète de type 1 (sang)</term><term>Diabète de type 1 (traitement médicamenteux)</term><term>Diabète de type 1 (urine)</term><term>Diabète de type 2 (métabolisme)</term><term>Diabète de type 2 (sang)</term><term>Diabète de type 2 (traitement médicamenteux)</term><term>Diabète de type 2 (urine)</term><term>Glycémie (métabolisme)</term><term>Humains</term><term>Hypoglycémiants (effets indésirables)</term><term>Hypoglycémiants (usage thérapeutique)</term><term>Modulateurs du transport transmembranaire (effets indésirables)</term><term>Modulateurs du transport transmembranaire (usage thérapeutique)</term><term>Rein ()</term><term>Rein (métabolisme)</term><term>Transporteur-2 sodium-glucose (antagonistes et inhibiteurs)</term><term>Transporteur-2 sodium-glucose (métabolisme)</term><term>Élimination rénale ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Hypoglycemic Agents</term><term>Membrane Transport Modulators</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Sodium-Glucose Transporter 2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Blood Glucose</term><term>Sodium-Glucose Transporter 2</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Transporteur-2 sodium-glucose</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Diabetes Mellitus, Type 1</term><term>Diabetes Mellitus, Type 2</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Kidney</term><term>Renal Elimination</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Diabetes Mellitus, Type 1</term><term>Diabetes Mellitus, Type 2</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Hypoglycémiants</term><term>Modulateurs du transport transmembranaire</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Diabetes Mellitus, Type 1</term><term>Diabetes Mellitus, Type 2</term><term>Kidney</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Diabète de type 1</term><term>Diabète de type 2</term><term>Glycémie</term><term>Rein</term><term>Transporteur-2 sodium-glucose</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Diabète de type 1</term><term>Diabète de type 2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Hypoglycemic Agents</term><term>Membrane Transport Modulators</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Diabète de type 1</term><term>Diabète de type 2</term></keywords><keywords scheme="MESH" qualifier="urine" xml:lang="en"><term>Diabetes Mellitus, Type 1</term><term>Diabetes Mellitus, Type 2</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Diabète de type 1</term><term>Diabète de type 2</term><term>Hypoglycémiants</term><term>Modulateurs du transport transmembranaire</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Rein</term><term>Élimination rénale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">For millennia, the syndrome that has become known as diabetes was considered to be primarily a disease of the urinary system and, by association, of dysfunction in the kidneys (recognized as the source of urine). In the last decade, there has been renewed interest in the role of the kidneys in the development and maintenance of high glucose levels. This has led to the development of novel agents to inhibit sodiumglucose cotransporter 2 (SGLT-2) as a means to control glucose levels and augment calorie-wasting leading to weight loss. However, beyond actions on glycaemic control, inhibition of proximal glucose absorption via SGLT-2 has significant direct effects to attenuate hyperfiltration and reduce renal hypertrophy. Increased distal sodium delivery may also act to suppress the intrarenal renin-angiotensin-aldosterone system, although systemic activity may be modestly increased due to osmotic diuresis. Reducing proximal glucose reabsorption may also protect the tubular cells from exposure to excess glucose and glucose-induced reactive oxygen species. On the other hand, distal glucose delivery following inhibition of SGLT-2 may increase glycogen deposition, the significance of which is unclear. However, subjects with familial glycosuria appear to have a benign renal prognosis. Some studies have demonstrated significant reductions in albumin excretion in various experimental models and as post-hoc observations in clinical trials. Whether these reflect renoprotection or are simply the result of intraglomerular haemodynamic changes remains unclear. Although promising, such actions remain to be established by comprehensive clinical trials with a renal focus, many of which are currently in progress.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25554067</PMID><DateCreated><Year>2015</Year><Month>01</Month><Day>02</Day></DateCreated><DateCompleted><Year>2015</Year><Month>07</Month><Day>13</Day></DateCompleted><DateRevised><Year>2015</Year><Month>01</Month><Day>02</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1878-1780</ISSN><JournalIssue CitedMedium="Internet"><Volume>40</Volume><Issue>6 Suppl 1</Issue><PubDate><Year>2014</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Diabetes & metabolism</Title><ISOAbbreviation>Diabetes Metab.</ISOAbbreviation></Journal><ArticleTitle>Beyond Glycosuria: Exploring the intrarenal effects of SGLT₋₂ inhibition in diabetes.</ArticleTitle><Pagination><MedlinePgn>S17-22</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/S1262-3636(14)72691-6</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1262-3636(14)72691-6</ELocationID><Abstract><AbstractText>For millennia, the syndrome that has become known as diabetes was considered to be primarily a disease of the urinary system and, by association, of dysfunction in the kidneys (recognized as the source of urine). In the last decade, there has been renewed interest in the role of the kidneys in the development and maintenance of high glucose levels. This has led to the development of novel agents to inhibit sodiumglucose cotransporter 2 (SGLT-2) as a means to control glucose levels and augment calorie-wasting leading to weight loss. However, beyond actions on glycaemic control, inhibition of proximal glucose absorption via SGLT-2 has significant direct effects to attenuate hyperfiltration and reduce renal hypertrophy. Increased distal sodium delivery may also act to suppress the intrarenal renin-angiotensin-aldosterone system, although systemic activity may be modestly increased due to osmotic diuresis. Reducing proximal glucose reabsorption may also protect the tubular cells from exposure to excess glucose and glucose-induced reactive oxygen species. On the other hand, distal glucose delivery following inhibition of SGLT-2 may increase glycogen deposition, the significance of which is unclear. However, subjects with familial glycosuria appear to have a benign renal prognosis. Some studies have demonstrated significant reductions in albumin excretion in various experimental models and as post-hoc observations in clinical trials. Whether these reflect renoprotection or are simply the result of intraglomerular haemodynamic changes remains unclear. Although promising, such actions remain to be established by comprehensive clinical trials with a renal focus, many of which are currently in progress.</AbstractText><CopyrightInformation>Copyright © 2014 Elsevier Masson SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Thomas</LastName><ForeName>M C</ForeName><Initials>MC</Initials><AffiliationInfo><Affiliation>Baker IDI Heart & Diabetes Institute, 75 Commercial Rd, Melbourne, Australia, 3004; Monash University, Dept. of Epidemiology and Preventive Medicine, Melbourne, Australia. Electronic address: amerlin.thomas@bakeridi.edu.au.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jandeleit-Dahm</LastName><ForeName>K</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Baker IDI Heart & Diabetes Institute, 75 Commercial Rd, Melbourne, Australia, 3004.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bonnet</LastName><ForeName>F</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Inserm UMR 991, service endocrinologie-diabétologie, CHU Rennes, université Rennes 1, 2 rue du Thabor, CS 46510, 35065 Rennes cedex, FRANCE.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Diabetes Metab</MedlineTA><NlmUniqueID>9607599</NlmUniqueID><ISSNLinking>1262-3636</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D049990">Membrane Transport Modulators</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C089180">SLC5A2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051297">Sodium-Glucose Transporter 2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="N">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000652" MajorTopicYN="N">urine</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000652" MajorTopicYN="N">urine</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007668" MajorTopicYN="N">Kidney</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049990" MajorTopicYN="N">Membrane Transport Modulators</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D065667" MajorTopicYN="N">Renal Elimination</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051297" MajorTopicYN="N">Sodium-Glucose Transporter 2</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes</Keyword><Keyword MajorTopicYN="N">Glycosuria</Keyword><Keyword MajorTopicYN="N">Hyperfiltration</Keyword><Keyword MajorTopicYN="N">Kidney</Keyword><Keyword MajorTopicYN="N">SGLT inhibitors</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>1</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>1</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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